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Magnetic resonance spectroscopy (MRS) has been employed to investigate brain metabolite concentrations in vivo, and they vary during neuronal activation, across brain activity states, or upon disease with neurological impact. Whether resting brain metabolites correlate with functioning in behavioral tasks remains to be demonstrated in any of the widely used rodent models. This study tested the hypothesis that, in the absence of neurological disease or injury, the performance in a hippocampal-dependent memory task is correlated with the hippocampal levels of metabolites that are mainly synthesized in neurons, namely N-acetylaspartate (NAA), glutamate and GABA. Experimentally naïve rats were tested for hippocampal-dependent spatial memory performance by measuring spontaneous alternation in the Y-maze, followed by anatomical magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) in the hippocampus and cortex. Memory performance correlated with hippocampal concentrations of NAA (p = 0.024) and glutamate (p = 0.014) but not GABA. Concentrations of glutamate in the cortex also correlated with spatial memory (p = 0.035). In addition, memory performance was also correlated with the relative volume of the hippocampus (p = 0.041). Altogether, this exploratory study suggests that levels of the neuronal maker NAA and the main excitatory neurotransmitter glutamate are associated with physiological functional capacity. [ABSTRACT FROM AUTHOR]

Bilingual language process is a key factor in left side of the brain. The cognition of the learning modalities is very crucial for assimilation, organization, and interpretation of knowledge. The neurochemical events like estrogen, testosterone, dopamine 5HT, Oxytocin, nerve growth factor (NGF) play as neuro-endocrine brain axis for learning to cognition. The human cognition recognises the language in five stages that is input, status of language, getting access over the literature of that language, interaction with family, and finally social network communication. The factors influence the bilingual aspects include language exposure, genes, perception and receiving, neurochemical pathways, social communication, and environmental conditions. Apart from these elements the other external influencing factors like health humanities and technological advances and make a lot of impact on cognition processes and mental health. [ABSTRACT FROM AUTHOR]

Abstract Background While the use of orally consumed Cannabis, cannabidiol (CBD) and tetrahydrocannabinol (THC) containing products, i.e. “edibles”, has expanded, the health consequences are still largely unknown. This study examines the effects of oral consumption of whole Cannabis and a complex Cannabis extract on neurochemicals, endocannabinoids (eCB), and physiological parameters (body temperature, heart rate) in mice. Methods In this pilot study, C57BL/6 J mice were treated with one of the following every other day for 2 weeks: a complex Cannabis extract by gavage, whole Cannabis mixed with nutritional gel through free feeding, or purified THC/CBD by intraperitoneal (i.p.) injection. Treatments were conducted at 4 doses ranging from 0–100 mg/kg/day of CBD with THC levels of ≤ 1.2 mg/kg/day for free feeding and gavage and 10 mg/kg/day for i.p. Body temperature and heart rate were monitored using surgically implanted telemetry devices. Levels of neurochemicals, eCB, THC, CBD, and 11-OH-THC were measured using mass spectrometry 48 h after the final treatment. Statistical comparisons were conducted using ANOVA and t-tests. Results Differences were found between neurochemicals in the brains and plasma of mice treated by i.p. (e.g. dopamine, p

Background: While the use of orally consumed Cannabis, cannabidiol (CBD) and tetrahydrocannabinol (THC) containing products, i.e. "edibles", has expanded, the health consequences are still largely unknown. This study examines the effects of oral consumption of whole Cannabis and a complex Cannabis extract on neurochemicals, endocannabinoids (eCB), and physiological parameters (body temperature, heart rate) in mice. Methods: In this pilot study, C57BL/6 J mice were treated with one of the following every other day for 2 weeks: a complex Cannabis extract by gavage, whole Cannabis mixed with nutritional gel through free feeding, or purified THC/CBD by intraperitoneal (i.p.) injection. Treatments were conducted at 4 doses ranging from 0–100 mg/kg/day of CBD with THC levels of ≤ 1.2 mg/kg/day for free feeding and gavage and 10 mg/kg/day for i.p. Body temperature and heart rate were monitored using surgically implanted telemetry devices. Levels of neurochemicals, eCB, THC, CBD, and 11-OH-THC were measured using mass spectrometry 48 h after the final treatment. Statistical comparisons were conducted using ANOVA and t-tests. Results: Differences were found between neurochemicals in the brains and plasma of mice treated by i.p. (e.g. dopamine, p < 0.01), gavage (e.g., phenylalanine, p < 0.05) and in mice receiving whole Cannabis (e.g., 3,4-dihydroxyphenylacetic DOPAC p < 0.05). Tryptophan trended downward or was significantly decreased in the brain and/or plasma of all mice receiving Cannabis or purified CBD/THC, regardless of dose, compared to controls. Levels of the eCB, arachidonoyl glycerol (2-AG) were decreased in mice receiving lowest doses of a complex Cannabis extract by gavage, but were higher in mice receiving highest doses compared to controls (p < 0.05). Plasma and brain levels of THC and 11-OH-THC were higher in mice receiving 1:1 THC:CBD by i.p. compared to those receiving 1:5 or 1:10 THC:CBD. Nominal changes in body temperature and heart rate following acute and repeated exposures were seen to some degree in all treatments. Conclusions: Changes to neurochemicals and eCBs were apparent at all doses regardless of treatment type. Levels of neurochemicals seemed to vary based on the presence of a complex Cannabis extract, suggesting a non-linear response between THC and neurochemicals following repeated oral dosing. [ABSTRACT FROM AUTHOR]

Neurochemicals, crucial for nervous system function, influence vital bodily processes and their fluctuations are linked to neurodegenerative diseases and mental health conditions. Monitoring these compounds is pivotal, yet the intricate nature of the central nervous system poses challenges. Researchers have devised methods, notably electrochemical sensing with micro-nanoscale electrodes, offering high-resolution monitoring despite low concentrations and rapid changes. Implantable sensors enable precise detection in brain tissues with minimal damage, while microdialysis-coupled platforms allow in vivo sampling and subsequent in vitro analysis, addressing the selectivity issues seen in other methods. While lacking temporal resolution, techniques like HPLC and CE complement electrochemical sensing's selectivity, particularly for structurally similar neurochemicals. This review covers essential neurochemicals and explores miniaturized electrochemical sensors for brain analysis, emphasizing microdialysis integration. It discusses the pros and cons of these techniques, forecasting electrochemical sensing's future in neuroscience research. Overall, this comprehensive review outlines the evolution, strengths, and potential applications of electrochemical sensing in the study of neurochemicals, offering insights into future advancements in the field. [ABSTRACT FROM AUTHOR]

Magnetic resonance spectroscopy (MRS) has been employed to investigate brain metabolite concentrations in vivo, and they vary during neuronal activation, across brain activity states, or upon disease with neurological impact. Whether resting brain metabolites correlate with functioning in behavioral tasks remains to be demonstrated in any of the widely used rodent models. This study tested the hypothesis that, in the absence of neurological disease or injury, the performance in a hippocampal-dependent memory task is correlated with the hippocampal levels of metabolites that are mainly synthesized in neurons, namely N-acetylaspartate (NAA), glutamate and GABA. Experimentally naïve rats were tested for hippocampal-dependent spatial memory performance by measuring spontaneous alternation in the Y-maze, followed by anatomical magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) in the hippocampus and cortex. Memory performance correlated with hippocampal concentrations of NAA (p = 0.024) and glutamate (p = 0.014) but not GABA. Concentrations of glutamate in the cortex also correlated with spatial memory (p = 0.035). In addition, memory performance was also correlated with the relative volume of the hippocampus (p = 0.041). Altogether, this exploratory study suggests that levels of the neuronal maker NAA and the main excitatory neurotransmitter glutamate are associated with physiological functional capacity.

Understanding how neuronal networks generate complex behavior is one of the major goals of Neuroscience. Neurotransmitter and Neuromodulators are crucial for information flow between neurons and understanding their dynamics is the key to unravel their role in behavior. To understand how the brain transmits information and how brain states arise, it is essential to visualize the dynamics of neurotransmitters, neuromodulators and neurochemicals. In the last five years, an increasing number of single-wavelength biosensors either based on periplasmic binding proteins (PBPs) or on G-protein-coupled receptors (GPCR) have been published that are able to detect neurotransmitter release in vitro and in vivo with high spatial and temporal resolution. Here we review and discuss recent progress in the development of these sensors, their limitations and future directions. [ABSTRACT FROM AUTHOR]

This study investigated the protective effect of vanillin against Parkinson's disease (PD). 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 30 mg/kg) was administered s.c. for 6 consecutive days to induce PD and mice were treated with vanillin (100 and 200 mg/kg, p.o.) for 15 days. Cognitive, motor and non-motor functions were assessed to evaluate the effect of vanillin in PD mice. Levels of dopamine and glutamate and activity of monoamine oxidaseB (MAO-B) were estimated in vanillin-treated PD mice. The effect of vanillin on the level of lipid peroxidation and superoxide dismutase in brain tissue of PD mice was estimated. Data of the study revealed that vanillin reversed the altered cognitive, motor and non-motor function in PD mice. Activity of MAO-B and neurochemical level were attenuated with vanillin in PD mice. Inflammatory cytokines, nuclear factor kappa B (NF-κB) and Toll-like receptor 4 (TLR-4) levels were lower in the vanillin-treated group compared to the PD group of mice. Data of the study suggest that vanillin protects against neuronal injury and recovers the altered behaviour in PD mice by regulating neurochemical balance and the TLR-4/NF-κB pathway. [ABSTRACT FROM AUTHOR]

This study investigated the protective effect of vanillin against Parkinson’s disease (PD). 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 30 mg/kg) was administered s.c. for 6 consecutive days to induce PD and mice were treated with vanillin (100 and 200 mg/kg, p.o.) for 15 days. Cognitive, motor and non-motor functions were assessed to evaluate the effect of vanillin in PD mice. Levels of dopamine and glutamate and activity of monoamine oxidaseB (MAO-B) were estimated in vanillin-treated PD mice. The effect of vanillin on the level of lipid peroxidation and superoxide dismutase in brain tissue of PD mice was estimated. Data of the study revealed that vanillin reversed the altered cognitive, motor and non-motor function in PD mice. Activity of MAO-B and neurochemical level were attenuated with vanillin in PD mice. Inflammatory cytokines, nuclear factor kappa B (NF-kB) and Toll-like receptor 4 (TLR-4) levels were lower in the vanillin-treated group compared to the PD group of mice. Data of the study suggest that vanillin protects against neuronal injury and recovers the altered behaviour in PD mice by regulating neurochemical balance and the TLR-4/NF-kB pathway.

Migraine is a complex neurological disorder that affects a significant portion of the population. Conventional therapies for migraines have limitations and drawbacks, necessitating the exploration of novel therapeutic strategies. This review paper provides an overview of emerging therapeutic approaches for migraines, focusing on both pharmacological and non-pharmacological interventions. The review begins with an introduction that highlights the background and significance of the topic. It emphasizes the need for advancements in migraine treatment and the potential impact of emerging therapeutic strategies on patient care. The pathophysiology of migraines is discussed, providing a brief overview of the underlying mechanisms, key neurochemicals, and pathways involved. Additionally, the current understanding of migraine triggers is explored, shedding light on factors that can initiate or exacerbate migraine attacks. The paper then delves into the conventional therapies used for migraine management. An overview of commonly used treatments is provided, along with a discussion of their limitations and drawbacks. The need for the development of novel therapeutic strategies is emphasized, considering the challenges faced by existing therapies. Recent advances in migraine research are reviewed, highlighting the scientific advancements in the field. Novel insights into the pathophysiology of migraines are discussed, along with the identification of potential therapeutic targets. These advancements have the potential to reshape our understanding of migraines and guide the development of more targeted and effective treatments. Non-pharmacological approaches for migraine management are explored, including a comprehensive review of complementary and alternative therapies. The evidence-based review highlights the potential benefits of lifestyle modifications, such as dietary changes, sleep optimization, and exercise, in reducing migraine frequency and severity. Emerging pharmacological therapies are examined, focusing on the overview of novel pharmacological agents under investigation. The analysis of clinical trials and their outcomes provides insights into the efficacy and safety of these emerging therapies. The discussion also encompasses emerging drug classes and their mechanisms of action, shedding light on the potential of targeted treatments for migraines. The review concludes with a discussion of the future perspectives and challenges in migraine research. The potential implications of personalized medicine approaches are explored, considering the role of genetics and biomarkers in guiding treatment decisions and optimizing therapeutic interventions. The recommendations for future research and development highlight the need for further investigations into the underlying mechanisms of migraines, prospective studies evaluating combination therapies, and the ethical considerations associated with personalized medicine approaches. In summary, this review paper provides a comprehensive overview of the emerging therapeutic strategies for migraines. It highlights the advancements in understanding the pathophysiology of migraines, the potential of non-pharmacological interventions, and the promise of emerging pharmacological therapies. The paper emphasizes the importance of personalized medicine approaches in guiding treatment decisions and optimizing patient outcomes. The insights and recommendations provided in this review can contribute to the advancement of migraine research and improve patient care in the future. [ABSTRACT FROM AUTHOR]

Dopamine (DA) is a vital neurotransmitter for brain functions, including pleasure, memory, motivation, and movement control. Dopaminergic neuron degradation is correlated to neurological disorders such as Parkinson's disease, and changes in DA concentration are related to mental health disorders. Currently, the gold standard for monitoring DA concentrations in the brain is electrochemistry. However, although electrochemistry has high sensitivity, it has low specificity for molecules with similar molecular structures, such as DA and its metabolites. Here, we demonstrate that surface‐enhanced Raman spectroscopy (SERS), a vibrational spectroscopy that provides molecule‐specific information with excellent sensitivity, requires small sample sizes/volumes, and is non‐destructive, is optimal for the detection and differentiation of DA and its metabolites. We show that SERS combined with multivariate analysis allows for the detection and differentiation of DA and its metabolites, including 3‐O‐methyldopamine (3‐OMD), homovanillic acid (HVA), 3,4‐dihydroxyphenylacetic acid (DOPAC), and 3‐methoxytyramine (3‐MT) at physiologically relevant concentrations in artificial cerebrospinal fluid (aCSF). [ABSTRACT FROM AUTHOR]

Brain doping is a novel form of doping that involves stimulating specific brain regions to enhance sports performance. However, to the best of our knowledge, there is currently no established provision or detection method for it. As brain stimulation ultimately induces alterations in neurochemical concentrations, this study aimed to develop a diagnostic strategy for brain doping. We successfully developed and validated a sensitive simultaneous analysis method for 23 neurochemicals present in urine. Simple derivatization was employed to overcome ionization efficiency, enabling the effective detection of all the target compounds within 5 min. Additionally, we developed an animal model system using rats to replicate brain-doping scenarios and establish a diagnostic strategy. Behavior tests confirmed improved sports performance in the brain stimulation group. By examining changes in the distribution patterns of the target substances in urine samples, we observed that neurochemicals could be used as potential biomarkers for brain-doping diagnosis. The developed method allows the effective simultaneous analysis of multiple neurochemicals in biological samples and is expected to have various applications, including doping control. Thus, changes in the distribution pattern of neurochemicals could serve as a basis for brain-doping diagnosis. [ABSTRACT FROM AUTHOR]

"Psychobiotics" are a novel class of probiotics that are beneficial to the health and functional efficiency of our brain and psychology. The main hold on command in ill conditions of the brain and psychology is overtaken by these psychobiotic bacteria (a dietary supplement) via the action/determined role of bacterial neurochemicals or neuroactive substances that are released by them in the intestinal epithelium after their ingestion. Although these psychobiotics flourish in the gut of the host consuming them, the effect is widely spread to the brain due to the communication between the gut and the brain via the bidirectional gut–brain axis. The nervous system involved in this directional process includes both the enteric nervous system and the central nervous system. With time, several corroborations have proved the effectiveness of psychobiotics in terms of mental illnesses and brain disorders. In the prevailing situation of the coronavirus pandemic, psychobiotics may serve as an aid because a majority of the population worldwide is already suffering from psychological issues due to changes in lifestyle and dietary habits, and in need of an immediate solution to cope with it. Moreover, the in silico approach is also vital for the development of biological relevance to neurosubstances. [ABSTRACT FROM AUTHOR]

The gut microbiota modulates neurobiological activity in various animal lineages. This is often proposed to occur through interactions with neurotransmitters and other neuromodulatory molecules in the host. Our commentary will discuss recent research that establishes microbiota–neurotransmitter connections, gaps in current understanding, and outstanding questions that may guide future advances in the field of microbiota–nervous system interactions. [ABSTRACT FROM AUTHOR]

Bisphenol F (BPF; 4,4′-dihydroxydiphenylmethane) is one of the most frequently used compounds in the manufacture of plastics and epoxy resins. Previous studies have demonstrated that BPF affects locomotor behavior, oxidative stress, and neurodevelopment in zebrafish. However, its neurotoxic effects are controversial, and the underlying mechanisms are unclear. In order to determine whether BPF affects the motor system, we exposed zebrafish embryos to BPF and assessed behavioral, histological, and neurochemical changes. Spontaneous locomotor behavior and startle response were significantly decreased in BPF-treated zebrafish larvae compared with control larvae. BPF induced motor degeneration and myelination defects in zebrafish larvae. In addition, embryonic exposure to BPF resulted in altered metabolic profiles of neurochemicals, including neurotransmitters and neurosteroids, which may impact locomotion and motor function. In conclusion, exposure to BPF has the potential to affect survival, motor axon length, locomotor activity, myelination, and neurochemical levels of zebrafish larvae. [ABSTRACT FROM AUTHOR]

Parkinson’s disease (PD) is a neurodegenerative disease, which alters body and cognitive functions. The present study evaluates the effect of exercise on body function and neuronal injury against a 6-hydroxydopamine hydrobromide (6-OHDA) induced PD rat model and postulates a possible molecular mechanism of its action. Parkinson’s disease was induced by administration of (20 µg/5 µl at the rate of 1 µl/min) 6-OHDA and exercise training was given to mice by motorized rodent treadmill for a period of 14 days after the confirmation of PD. Behavioural changes were observed by apomorphine-induced rotation and motor function was assessed using the rotarod apparatus. The effect of exercise was observed on the levelof neurochemicals and the expression of calpain-1 (CAPN1) and kallikrein 6 (KLK6) was estimated in brain tissue of PD rats using western blot assay. A more significant improvement in the motor and cognitive function was observed in the PD + exercise group than in the PD group of rats. Exercise attenuates the altered level of g-aminobutyric acid (GABA), dopamine (DA) and glutamate in brain tissue of PD rats. Intracellular concentration of Ca+ ion was reduced significantly in brain tissue of the PD + exercise group compared to PD rats. Moreover, exercise activates the expression of KLK6 and CAPN1 protein in brain tissue of PD rats. In conclusion, data of the study reveal that exercise protects neuronal injury by reducing intracellular concentration Ca+ ion and activates KLK6 and CAPN1 in brain tissue of PD rats and thereby improves motor and cognitive functions.

Neurochemicals, crucial for nervous system function, influence vital bodily processes and their fluctuations are linked to neurodegenerative diseases and mental health conditions. Monitoring these compounds is pivotal, yet the intricate nature of the central nervous system poses challenges. Researchers have devised methods, notably electrochemical sensing with micro-nanoscale electrodes, offering high-resolution monitoring despite low concentrations and rapid changes. Implantable sensors enable precise detection in brain tissues with minimal damage, while microdialysis-coupled platforms allow in vivo sampling and subsequent in vitro analysis, addressing the selectivity issues seen in other methods. While lacking temporal resolution, techniques like HPLC and CE complement electrochemical sensing’s selectivity, particularly for structurally similar neurochemicals. This review covers essential neurochemicals and explores miniaturized electrochemical sensors for brain analysis, emphasizing microdialysis integration. It discusses the pros and cons of these techniques, forecasting electrochemical sensing’s future in neuroscience research. Overall, this comprehensive review outlines the evolution, strengths, and potential applications of electrochemical sensing in the study of neurochemicals, offering insights into future advancements in the field.

Striatal medium spiny neurons are highly susceptible in Huntington's disease (HD), resulting in progressive synaptic perturbations that lead to neuronal dysfunction and death. Non‐invasive imaging techniques, such as proton magnetic resonance spectroscopy (1H‐MRS), are used in HD mouse models and patients with HD to monitor neurochemical changes associated with neuronal health. However, the association between brain neurochemical alterations and synaptic dysregulation remains unknown, limiting our ability to monitor potential treatments that may affect synapse function. We conducted in vivo longitudinal 1H‐MRS in the striatum followed by ex vivo analyses of excitatory synapse density of two synaptic circuits disrupted in HD, thalamo‐striatal (T‐S), and cortico‐striatal (C‐S) pathways, to assess the relationship between neurochemical alterations and changes in synapse density. We used the zQ175(Tg/0) HD mouse model as well as zQ175 mice lacking one allele of CK2α'(zQ175(Tg/0):CK2α'(+/−)), a kinase previously shown to regulate synapse function in HD. Longitudinal analyses of excitatory synapse density showed early and sustained reduction in T‐S synapses in zQ175 mice, preceding C‐S synapse depletion, which was rescued in zQ175:CK2α'(+/−). Changes in T‐S and C‐S synapses were accompanied by progressive alterations in numerous neurochemicals between WT and HD mice. Linear regression analyses showed C‐S synapse number positively correlated with 1H‐MRS‐measured levels of GABA, while T‐S synapse number positively correlated with levels of phosphoethanolamine and negatively correlated with total creatine levels. These associations suggest that these neurochemical concentrations measured by 1H‐MRS may facilitate monitoring circuit‐specific synaptic dysfunction in the zQ175 mouse model and in other HD pre‐clinical studies. [ABSTRACT FROM AUTHOR]

Serotonin N-acetyltransferase (SNAT) catalyzes the biosynthesis of N-acetylserotonin (NAS) and N-acetyltryptamine (NAT), two pleiotropic molecules with neurotransmitter functions. Here, we report the identification of a SNAT protein in the genus Staphylococcus. The SNAT gene identified in Staphylococcus pseudintermedius ED99, namely SPSE_0802, encodes a 140 residues-long cytoplasmic protein. The recombinant protein SPSE_0802 was expressed in E. coli BL21 and found to acetylate serotonin (SER) and tryptamine (TRY) as well as other trace amines in vitro. The production of the neuromodulators NAS and NAT was detected in the cultures of different members of the genus Staphylococcus and the role of SPSE_0802 in this production was confirmed in an ED99 SPSE_0802 deletion mutant. A search for SNAT homologues showed that the enzyme is widely distributed across the genus which correlated with the SNAT activity detected in 22 out of the 40 Staphylococcus strains tested. The N-acetylated products of SNAT are precursors for melatonin synthesis and are known to act as neurotransmitters and activate melatonin receptors, among others, inducing various responses in the human body. The identification of SNAT in staphylococci could contribute to a better understanding of the interaction between those human colonizers and the host peripheral nervous system.

Brain doping is a novel form of doping that involves stimulating specific brain regions to enhance sports performance. However, to the best of our knowledge, there is currently no established provision or detection method for it. As brain stimulation ultimately induces alterations in neurochemical concentrations, this study aimed to develop a diagnostic strategy for brain doping. We successfully developed and validated a sensitive simultaneous analysis method for 23 neurochemicals present in urine. Simple derivatization was employed to overcome ionization efficiency, enabling the effective detection of all the target compounds within 5 min. Additionally, we developed an animal model system using rats to replicate brain-doping scenarios and establish a diagnostic strategy. Behavior tests confirmed improved sports performance in the brain stimulation group. By examining changes in the distribution patterns of the target substances in urine samples, we observed that neurochemicals could be used as potential biomarkers for brain-doping diagnosis. The developed method allows the effective simultaneous analysis of multiple neurochemicals in biological samples and is expected to have various applications, including doping control. Thus, changes in the distribution pattern of neurochemicals could serve as a basis for brain-doping diagnosis.

Different pathological conditions that begin with slow and progressive deformations, cause irreversible affliction by producing loss of neurons and synapses. Commonly it is referred to as 'protein misfolding' diseases or proteinopathies and comprises the latest definition of neurological disorders (ND). Protein misfolding dynamics, proteasomal dysfunction, aggregation, defective degradation, oxidative stress, free radical formation, mitochondrial dysfunctions, impaired bioenergetics, DNA damage, neuronal Golgi apparatus fragmentation, axonal transport disruption, Neurotrophins (NTFs) dysfunction, neuroinflammatory or neuroimmune processes, and neurohumoral changes are the several mechanisms that embark the pathogenesis of ND. Capsaicin (8-Methyl-N-vanillyl-6-nonenamide) one of the major phenolic components in chili peppers (Capsicum) distinctively triggers the unmyelinated C-fiber and acts on Transient Receptor Potential Vanilloid-1, which is a Ca2+ permeable, non-selective cation channel. Several studies have shown the neuroprotective role of capsaicin against oxidative damage, behavioral impairment, with 6-hydroxydopamine (6-OHDA) induced Parkinson's disease, pentylenetetrazol-induced seizures, global cerebral ischemia, and streptozotocin-induced Alzheimer's disease. Based on these lines of evidence, capsaicin can be considered as a potential constituent to develop suitable neuro-pharmacotherapeutics for the management and treatment of ND. Furthermore, exploring newer horizons and carrying out proper clinical trials would help to bring out the promising effects of capsaicin to be recommended as a neuroprotectant. [ABSTRACT FROM AUTHOR]

Gut microbiota depletion may result in cognitive impairment and emotional disorder. This study aimed to determine the possible association between host gut microbiota, cognitive function, and emotion in various life stages and its related underlying mechanisms. Seventy-five neonatal mice were randomly divided into five groups (n = 15 per group). Mice in the vehicle group were administered distilled water from birth to death, and those in the last four groups were administered antibiotic cocktail from birth to death, from birth to postnatal day (PND) 21 (infancy), from PND 21 to 56 (adolescence), and from PND 57 to 84 (adulthood), respectively. Antibiotic exposure consistently altered the gut microbiota composition and decreased the diversity of gut microbiota. Proteobacteria were the predominant bacteria instead of Firmicutes and Bacteroidetes after antibiotic exposure in different life stages. Long-term and infant gut microbiota depletion resulted in anxiety- and depression-like behaviors, memory impairments, and increased expression of γ-aminobutyric acid type A receptor α1 of adult mice. Long-term antibiotic exposure also significantly decreased serum interleukin (IL)-1β, IL-10, and corticosterone of adult mice. Gut microbiota depletion in adolescence resulted in anxiety-like behaviors, short-term memory decline, decreased serum interferon-γ (IFN-γ), mRNA expression of 5-hydroxytryptamine receptor 1A, and neuropeptide Y receptor Y2 in the prefrontal cortex of adult mice. Antibiotic exposure in adulthood damaged short-term memory and decreased serum IL-10, IFN-γ, and increased γ-aminobutyric acid type B receptor 1 mRNA expression of adult mice. These results suggest that antibiotic-induced gut microbiota depletion in the long term and infancy resulted in the most severe cognitive and emotional disorders followed by depletion in adolescence and adulthood. These results also suggest that gut microbes could influence host cognitive function and emotion in a life stage-dependent manner by affecting the function of the immune system, hypothalamic-pituitary-adrenal axis, and the expression of neurochemicals in the brain.

Increasing demand for cage-free eggs arises from goals to provide hens with better welfare, particularly in terms of natural behavior. However, most laying hens are kept in conventional cages, and cage-free systems can present challenges, such as injuries, floor eggs, and bacterial infections. We proposed using virtual reality (VR) as a feasible means for combining the positive attributes of natural environments while mitigating health risks. To our knowledge, no animal study has provided evidence that VR can trigger biological changes to improve animal health and well-being nor whether VR can affect the gut microbiota. In this study, we used VR technology to simulate a natural environment in laying hen housing. Early-lay White Leghorn hens were placed in pens with (VR) or without (CON) video projections displaying free-range chickens interacting with indoor and outdoor environmental features over 5 days. Using in vitro blood bactericidal assays, VR hens exhibited higher resistance against avian pathogenic Escherichia coli versus CON (p < 0.05), which was positively associated with corticosterone levels (p < 0.01). Analyzing intestinal neurochemicals via ultra-high pressure liquid chromatography, salsolinol was the only neurochemical metabolite affected by VR, being greater in CON ileal content (p < 0.0001), in VR ileal mucus (p < 0.01), and in VR ceca tissue (p < 0.05). Using 16S rRNA sequencing and QIIME2 analyses, no differences in alpha nor beta diversity were determined between groups. Although several genera (Megamonas, Ruminococcus, Slackia) were reduced in VR hens versus CON, Mucispirillum schaedleri (member of Deferribacteres Phylum) was the only taxon increased in VR hens, being elevated in ileal mucus (p < 0.05). Lastly, using the QIIME2 plugin mmvec to map microbe-metabolite co-occurrences, we identified several positive relationships between bacterial phyla and neurochemical metabolites, notably finding dopamine and salsolinol levels were related to Deferribacteres and Tenericutes levels. In conclusion, we found that several biological parameters were influenced by VR treatment in hens, suggesting that VR can be used to improve host resistance to pathogens and gut health in poultry.

Bisphenol F (BPF; 4,4′-dihydroxydiphenylmethane) is one of the most frequently used compounds in the manufacture of plastics and epoxy resins. Previous studies have demonstrated that BPF affects locomotor behavior, oxidative stress, and neurodevelopment in zebrafish. However, its neurotoxic effects are controversial, and the underlying mechanisms are unclear. In order to determine whether BPF affects the motor system, we exposed zebrafish embryos to BPF and assessed behavioral, histological, and neurochemical changes. Spontaneous locomotor behavior and startle response were significantly decreased in BPF-treated zebrafish larvae compared with control larvae. BPF induced motor degeneration and myelination defects in zebrafish larvae. In addition, embryonic exposure to BPF resulted in altered metabolic profiles of neurochemicals, including neurotransmitters and neurosteroids, which may impact locomotion and motor function. In conclusion, exposure to BPF has the potential to affect survival, motor axon length, locomotor activity, myelination, and neurochemical levels of zebrafish larvae.

(1) Objective: Considering that current knowledge of mechanisms involved in the molecular pathogenesis of Social Anxiety Disorder (SAD) is limited, we conducted a systematic review to evaluate cumulative data obtained by Proton Magnetic Resonance Spectroscopic (1H MRS) studies. (2) Methods: A computer-based literature search of Medline, EMBASE, PsycInfo, and ProQuest was performed. Only cross-sectional studies using 1H MRS techniques in participants with SAD and healthy controls (HCs) were selected. (3) Results: The search generated eight studies. The results indicated regional abnormalities in the 'fear neurocircuitry' in patients with SAD. The implicated regions included the anterior cingulate cortex (ACC), dorsomedial prefrontal cortex (dmPFC), dorsolateral prefrontal cortex (dlPFC), insula, occipital cortex (OC), as well as the subcortical regions, including the thalamus, caudate, and the putamen. (4) Conclusions: The evidence derived from eight studies suggests that possible pathophysiological mechanisms of SAD include impairments in the integrity and function of neurons and glial cells, including disturbances in energy metabolism, maintenance of phospholipid membranes, dysregulations of second messenger systems, and excitatory/inhibitory neurocircuitry. Conducting more cross-sectional studies with larger sample sizes is warranted given the limited evidence in this area of research. [ABSTRACT FROM AUTHOR]

Rationale and Objectives: Pro-inflammatory processes have been argued to play a role in conditions associated with cognitive decline and neurodegeneration, like aging and obesity. Only a limited number of studies have tried to measure both peripheral and central biomarkers of inflammation and examined their interrelationship. The primary aim of this study was to examine the hypothesis that chronic peripheral inflammation would be associated with neurometabolic changes that indicate neuroinflammation (the combined elevation of myoinositol and choline), brain gray matter volume decrease, and lower cognitive functioning in older adults. Materials and Methods: Seventy-four older adults underwent bio-impedance body composition analysis, cognitive testing with the Montreal Cognitive Assessment (MoCA), blood serum analysis of inflammatory markers interleukin-6 (IL-6) and kynurenine, magnetic resonance imaging (MRI), and proton magnetic resonance spectroscopy (1H-MRS) of the brain. Neurometabolic findings from both Tarquin and LCModel 1H-MRS post-processing software packages were compared. The regions of interest for MRI and 1H-MRS measurements were dorsal posterior cingulate cortex (DPCC), left hippocampal cortex (HPC), left medial temporal cortex (MTC), left primary sensorimotor cortex (SM1), and right dorsolateral prefrontal cortex (DLPFC). Results: Elevated serum kynurenine levels were associated with signs of neuroinflammation, specifically in the DPCC, left SM1 and right DLPFC, and signs of neurodegeneration, specifically in the left HPC, left MTC and left SM1, after adjusting for age, sex and fat percentage (fat%). Elevated serum IL-6 levels were associated with increased Glx levels in left HPC, left MTC, and right DLPFC, after processing the 1H-MRS data with Tarquin. Overall, the agreement between Tarquin and LCModel results was moderate-to-strong for tNAA, tCho, mIns, and tCr, but weak to very weak for Glx. Peripheral inflammatory markers (IL-6 and kynurenine) were not associated with older age, higher fat%, decreased brain gray matter volume loss or decreased cognitive functioning within a cohort of older adults. Conclusion: Our results suggest that serum kynurenine may be used as a peripheral inflammatory marker that is associated with neuroinflammation and neurodegeneration, although not linked to cognition. Future studies should consider longitudinal analysis to assess the causal inferences between chronic peripheral and neuroinflammation, brain structural and neurometabolic changes, and cognitive decline in aging. [ABSTRACT FROM AUTHOR]

The study of human neurons and their interaction with neurochemicals is difficult due to the inability to collect primary biomaterial. However, recent advances in the cultivation of human stem cells, methods for their neuronal differentiation and chimeric fluorescent calcium indicators have allowed the creation of model systems in vitro. In this paper we report on the development of a method to obtain human neurons with the GCaMP6s calcium indicator, based on a human iPSC line with the TetON–NGN2 transgene complex. The protocol we developed allows us quickly, conveniently and efficiently obtain significant amounts of human neurons suitable for the study of various neurochemicals and their effects on specific neurophysiological activity, which can be easily registered using fluorescence microscopy. In the neurons we obtained, glutamate (Glu) induces rises in [Ca2+]i which are caused by ionotropic receptors for Glu, predominantly of the NMDA-type. Taken together, these facts allow us to consider the model we have created to be a useful and successful development of this technology. [ABSTRACT FROM AUTHOR]

Rationale and ObjectivesPro-inflammatory processes have been argued to play a role in conditions associated with cognitive decline and neurodegeneration, like aging and obesity. Only a limited number of studies have tried to measure both peripheral and central biomarkers of inflammation and examined their interrelationship. The primary aim of this study was to examine the hypothesis that chronic peripheral inflammation would be associated with neurometabolic changes that indicate neuroinflammation (the combined elevation of myoinositol and choline), brain gray matter volume decrease, and lower cognitive functioning in older adults.Materials and MethodsSeventy-four older adults underwent bio-impedance body composition analysis, cognitive testing with the Montreal Cognitive Assessment (MoCA), blood serum analysis of inflammatory markers interleukin-6 (IL-6) and kynurenine, magnetic resonance imaging (MRI), and proton magnetic resonance spectroscopy (1H-MRS) of the brain. Neurometabolic findings from both Tarquin and LCModel 1H-MRS post-processing software packages were compared. The regions of interest for MRI and 1H-MRS measurements were dorsal posterior cingulate cortex (DPCC), left hippocampal cortex (HPC), left medial temporal cortex (MTC), left primary sensorimotor cortex (SM1), and right dorsolateral prefrontal cortex (DLPFC).ResultsElevated serum kynurenine levels were associated with signs of neuroinflammation, specifically in the DPCC, left SM1 and right DLPFC, and signs of neurodegeneration, specifically in the left HPC, left MTC and left SM1, after adjusting for age, sex and fat percentage (fat%). Elevated serum IL-6 levels were associated with increased Glx levels in left HPC, left MTC, and right DLPFC, after processing the 1H-MRS data with Tarquin. Overall, the agreement between Tarquin and LCModel results was moderate-to-strong for tNAA, tCho, mIns, and tCr, but weak to very weak for Glx. Peripheral inflammatory markers (IL-6 and kynurenine) were not associated with older age, higher fat%, decreased brain gray matter volume loss or decreased cognitive functioning within a cohort of older adults.ConclusionOur results suggest that serum kynurenine may be used as a peripheral inflammatory marker that is associated with neuroinflammation and neurodegeneration, although not linked to cognition. Future studies should consider longitudinal analysis to assess the causal inferences between chronic peripheral and neuroinflammation, brain structural and neurometabolic changes, and cognitive decline in aging.

Background: The literature survey shows improvement in cognitive performance following acute bouts of physical exercise and chronic exercise patterns. However, neurocognitive growth through karate, a moderate intensity physical activity, is very limited. The synchronization of the nervous and endocrine system can be best reflected through this martial art form through neurogenesis and cognitive potentiation. Numerous outstanding reviews have summarized these findings for martial arts like judo and taekwondo. This review tries to orchestrate the efficiency of karate in neurocognition. Objective of the Study: The specific aim of this review paper is to magnify the efficiency of karate training in cognitive functions, through its response to neurochemical transmissions and electrophysiological signaling Materials and Method: Numerous related literature were evaluated, screened, and selected using the Preferred Reporting Items for Systematic reviews and Meta-Analyses eligibility criteria. All appropriate publications that satisfied the primary objective of the study were scientifically and schematically presented in this review paper. Results: The psychophysiological effect of karate training and their relation with brain functions have been elaborated. This review compiles the few studies established on the cognitive benefits of karate through the electrical stimuli and neurochemical release. Conclusion: Karate may be effective in advancement of particular brain functions and neurocognitive actions through a life time. Electrophysiological studies have unraveled improved neural efficiency, stress tolerance, working and muscle memory but need further exploration. Similarly, to better understand the effects of karate on neurochemical secretions, further research involvement is required. [ABSTRACT FROM AUTHOR]

Objective: To uncover the underlying mechanism of Hewei Jiangni granule (HWJNG) on non-erosive reflux disease (NERD) treatment by examining histological changes, gastrointestinal neurochemicals release and visceral hypersensitivity-related receptor expression in NERD model rats. Methods: A NERD rat model was established via a combination of basal sensitization and acid perfusion. HWJNG treatments at different doses were then administered. Pathological changes to tissues, mast cell (MC) activation, serum levels of esophageal visceral hypersensitivity-related neurochemicals, and transient receptor potential (TRP) receptor mRNA and protein levels were investigated. Results: Compared with the control group, the expression of tryptase in MCs, the changes of intercellular space, and the serum levels of substance P (SP), calcitonin gene-related peptides (CGRP) and proteinase-activated receptor 2 (PAR2) increased in the model group (all P

Hyperthermia is a common confounding factor for assessing the neurotoxic effects of methamphetamine (METH) in mammalian models. The development of new models of methamphetamine neurotoxicity using vertebrate poikilothermic animals should allow to overcome this problem. The aim of the present study was to develop a zebrafish model of neurotoxicity by binge-like methamphetamine exposure. After an initial testing at 20 and 40 mg/L for 48 h, the later METH concentration was selected for developing the model and the effects on the brain monoaminergic profile, locomotor, anxiety-like and social behaviors as well as on the expression of key genes of the catecholaminergic system were determined. A concentration- and time-dependent decrease in the brain levels of dopamine (DA), norepinephrine (NE) and serotonin (5-HT) was found in METH-exposed fish. A significant hyperactivity was found during the first hour of exposure, followed 3 h after by a positive geotaxis and negative scototaxis in the novel tank and in the light/dark paradigm, respectively. Moreover, the behavioral phenotype in the treated fish was consistent with social isolation. At transcriptional level, th1 and slc18a2 (vmat2) exhibited a significant increase after 3 h of exposure, whereas the expression of gfap , a marker of astroglial response to neuronal injury, was strongly increased after 48 h exposure. However, no evidences of oxidative stress were found in the brain of the treated fish. Altogether, this study demonstrates the suitability of the adult zebrafish as a model of METH-induced neurotoxicity and provides more information about the biochemical and behavioral consequences of METH abuse. [ABSTRACT FROM AUTHOR]

Hyperthermia is a common confounding factor for assessing the neurotoxic effects of methamphetamine (METH) in mammalian models. The development of new models of methamphetamine neurotoxicity using vertebrate poikilothermic animals should allow to overcome this problem. The aim of the present study was to develop a zebrafish model of neurotoxicity by binge-like methamphetamine exposure. After an initial testing at 20 and 40 mg/L for 48 h, the later METH concentration was selected for developing the model and the effects on the brain monoaminergic profile, locomotor, anxiety-like and social behaviors as well as on the expression of key genes of the catecholaminergic system were determined. A concentration- and time-dependent decrease in the brain levels of dopamine (DA), norepinephrine (NE) and serotonin (5-HT) was found in METH-exposed fish. A significant hyperactivity was found during the first hour of exposure, followed 3 h after by a positive geotaxis and negative scototaxis in the novel tank and in the light/dark paradigm, respectively. Moreover, the behavioral phenotype in the treated fish was consistent with social isolation. At transcriptional level, th1 and slc18a2 (vmat2) exhibited a significant increase after 3 h of exposure, whereas the expression of gfap, a marker of astroglial response to neuronal injury, was strongly increased after 48 h exposure. However, no evidences of oxidative stress were found in the brain of the treated fish. Altogether, this study demonstrates the suitability of the adult zebrafish as a model of METH-induced neurotoxicity and provides more information about the biochemical and behavioral consequences of METH abuse.

Vascular dementia (VaD), a diverse group of brain disorders with cognitive decline is attributable to cerebrovascular pathologies. Recent studies have shown that mitochondrial dysfunctions and oxidative stress are involved in cognitive decline. Several studies consider that oxidative stress is the main pathogenic factor in VaD. However, curcumin is having a therapeutic potential in oxidative stress and is limited due to its compromised bioavailability (BA). The current study aims to evaluate the neuroprotective effects of curcumin loaded solid lipid nanoparticles (Cur-SLNP) on homocysteine (HCY) induced oxidative stress in vascular dementia (VaD) by behavioural, biochemical, neurochemical, and histopathological alterations in different regions of the brain. Male sprague dawley rats were divided in to six groups. Group I was normal control and group II received HCY at 400 µg/kg/day, i.v for 14 days. Group III and IV received (Cur – 25 mg/kg, p.o + HCY- 400 µg/kg/day, i.v) and (Cur – 50 mg/kg, p.o + HCY- 400 µg/kg/day, i.v) . Group V and VI received Cur-SLNP at the dose (Cur – SLNP – 10 mg/kg, p.o + HCY - 400 µg/kg/day, i.v) and (Cur – SLNP – 25 mg/kg, p.o + HCY - 400 µg/kg/day, i.v) for 14 days. Subsequently, rats were tested for behavioral assessments on 0th, 7th, and 14th days and then sacrificed for biochemical, neurochemical, and histopathological assays in different regions of the brain. In the present study, the treatment with Cur-SLNP at high dose (Cur – SLNP – 25 mg/kg, p.o + HCY - 400 µg/kg/day, i.v) successfully ameliorated the oxidative stress in VaD by the estimations of biochemical, neurochemical and histological alterations. Thus, Cur-SLNP at high dose can be considered as a potential therapeutic strategy for the treatment of oxidative stress in vascular dementia induced by homocysteine in different regions of the brain. To the best of our knowledge, based on the results, this is the first study to reveal the neuroprotective effects of Cur-SLNP on HCY induced oxidative stress in vascular dementia.

Busulfan is a popular antileukemia chemotherapeutic alkylating agent widely known to induce variety of serious adverse effects including chemobrain-related cognitive impairments and dysfunction in male reproductive system. Whether kolaviron, a neuro- and repro-active compound obtained from Garcinia kola, with neuroprotective and reproductive-promoting activities, mitigates busulfan-induced cognitive and male reproductive impairments remain unknown. Hence, we investigated the reversal effects of kolaviron on busulfan-induced episodic memory deficit and testicular dysfunction, and its underlying mechanisms in male rats. In the treatment-protocol, rats in groups 1 and 2 received saline (10 mL/kg/p.o./day) and DMSO (10 mL/kg/p.o./day) respectively, group 3 was given kolaviron (200 mg/kg/p.o./day), group 4 received busulfan (50 mg/kg/p.o./day) and group 5 was pretreated with busulfan (50 mg/kg/p.o./day) consecutively for 56 days prior to kolaviron treatment (200 mg/kg/p.o./day) from days 29–56. Episodic memory deficit was assessed using passive avoidance task (PAT). Following euthanization, blood samples, epididymal sperm, testes and brain were harvested and hormonal and neurochemical contents and their metabolizing enzymes were assayed. Kolaviron reversed busulfan-induced episodic cognitive deficit in the PAT. The reduced serotonin, dopamine, noradrenaline concentrations, elevated glutamate levels, acetylcholinesterase, monoamine oxidase-A and B activities were normalized by kolaviron. Kolaviron also reversed the busulfan-induced decreased testicular/body weights and spermatogenesis. Kolaviron abated busulfan-induced changes in androgenic hormones (testosterone, FSH, LH), dehydrogenase enzymes (3ß-HSD and 17ß-HSD), altered sperm-chromatin, sperm-membrane integrity and sperm-acrosomal reaction and capacitation impairments. Our findings suggest that kolaviron could mitigate busulfan-induced episodic memory deficit and dysfunction in male reproductive system via neurochemical modulations and increase testicular androgenic hormones/enzymes in rats.

Neurochemical profile and brain connectivity are both critical aspects of brain function. However, our knowledge of their interplay across development is currently poor. We combined single‐voxel magnetic resonance spectroscopy and resting functional magnetic resonance imaging in a cross‐sectional sample spanning from childhood to adulthood which was reassessed in ~1.5 years (N = 293). We revealed the developmental trajectories of 20 neurochemicals in two key developmental brain regions (the intraparietal sulcus, IPS, and the middle frontal gyrus, MFG). We found that certain neurochemicals exhibited similar developmental trajectories across the two regions, while other trajectories were region‐specific. Crucially, we mapped the connectivity of the brain regions IPS and MFG to the rest of the brain across development as a function of regional glutamate and GABA concentration. We demonstrated that glutamate concentration within the IPS is modulated by age in explaining IPS connectivity with frontal, temporal and parietal regions. In mature participants, higher glutamate within the IPS was related to more negative connectivity while the opposite pattern was found for younger participants. Our findings offer specific developmental insights on the interplay between the brain's resting activity and the glutamatergic system both of which are crucial for regulating normal functioning and are dysregulated in several clinical conditions. [ABSTRACT FROM AUTHOR]

As the most important part of the central nervous system, the brain is extremely complex in structure and function. In vivo analysis of chemical signals is an essential way to investigate brain activity and function. Although functional magnetic resonance imaging (fMRI) or electrophysiology can be used to record brain activity, they are usually limited by low spatiotemporal fidelity or the difficulty of distinguishing the contributions of various neurochemicals. In addition, the development of in vivo biosensors with high selectivity and accuracy is essential to understand the roles that neurochemicals play in the brain. In this review, we focus on the development of instruments and devices for recording chemical signals in the live brain. Meanwhile, the strategies for development of electrochemical and fluorescent probes with high selectivity, high accuracy and good stability are also summarized. In particular, this review highlighted the contributions of our research group to this field. The development of techniques and probes enable us to understand the brain structure and function, and the mechanism of brain diseases, providing the solution for preventing and treating brain diseases. [ABSTRACT FROM AUTHOR]

Neurochemicals are essential molecules presented in the central nervous system that are primarily involved in neural activity and signaling. Neurochemical abnormalities resulted from genetic or environmental changes can lead to several behavioral and neurological disorders, including Alzheimer's and Parkinson's diseases. It is therefore imperative to employ detection systems of the optimal selectivity and spatio‐temporal resolution to ascertain the specific molecular basis particular to the pathological process. Electrochemical systems featuring excellent temporal‐spatial resolution and designable electrode interface are arguably the most versatile and widely used approaches for sensing of neurochemicals in living brain environment. Nevertheless, there are still many challenges that must be addressed to enable highly selective, sensitive, and stable in vivo electrochemical sensors and facilitate their development for emerging applications ranging from early diagnosis of brain diseases to designing potential curative treatments. Here, we provide a brief overview of the application of electrochemical sensors and biosensors in the analysis of neurochemicals in living animals. In particular, we highlight recent advances in modulating the physicochemical properties of electrode that can lead to in vivo sensors with exceptional selectivity. In addition, future trends of highly selective in vivo electrochemical systems are prospected. [ABSTRACT FROM AUTHOR]

Objectives This study aimed to evaluate the effect of duloxetine (10 and 20 mg/kg) against chronic immobilisation stress (CIS)-induced anxiety, depression, cognitive impairment and neurodegeneration in mice. Methods CIS, 2 h/10 days (11:00 AM-1:00 PM) was applied after 30 min of pretreatment with saline, duloxetine 10 mg/kg and 20 mg/kg to the respective groups of animals, except the control group. Animals were examined for physiological (body weight, locomotion and grip strength), psychological (memory impairment, anxiety and depression), neurochemical (GABA and glutamate), biochemical (MDA, catalase, glutathione, superoxide dismutase) and histopathological changes. Key findings CIS exposure revealed anxiety-like behaviour, depression-like behaviour, motor in-coordination and learning and memory impairment in mice. Besides, CIS induction decreased the antioxidant enzymes (GSH, SOD and catalase), GABA and the viable neuronal cell count, whereas CIS exposure significantly elevated the MDA, AChE activity and glutamate content in the cortex and hippocampus. Pretreatment with duloxetine10 and 20 mg/kg showed dose-dependent ameliorated effect against the CIS-induced alterations in mice. Conclusion In conclusion, the results of this study demonstrated the protective effect of duloxetine against neuropsychiatric symptoms, memory impairment caused by CIS-induction through inhibition of oxidative stress, AChE activity and glutamate release. [ABSTRACT FROM AUTHOR]

Much emphasis has been placed on the biological activities of citrus peel's essential oils (CPEOs) against human ailments. This study investigated the effect of Citrus limon and Citrus reticulata peel's essential oils (EOs) on behavioral and neurochemical imbalance in transgenic and Harwish (Wild) fruit flies. Flies were divided into seven groups comprising of the control and those that were fed with 0.1, 0.5, and 1.0 µg/ml of the dietary inclusions of study CPEOs for 7 days. Thereafter, behavioral profile was examined using lethality response and negative geotaxis assays. Effect of the EOs on cholinesterase and monoamine oxidase (MAO) activities, and antioxidative parameters were determined. The result showed a significant improvement of behavioral pattern and biochemical parameters of the flies fed with studied CPEOs inclusive diets. Conclusively, both EOs exert neuroprotective capability by reducing cholinesterases and monoamine activities, and also prevent oxidative stress, which are implicated in neuronal dysfunction in humans. Practical applications: With the growing increase in the search for safer alternatives, having no side effects, for the management of neurodegenerative diseases, a large proportion of the populace is beginning to find solace in the use of natural products. Also, the wide array of similarities between the humans and the dipteran insects, fruit flies is a perfect organism for the study of neurodegenerative diseases. Therefore, this study presents the neuroprotective potentials of lemon and tangerine peels‐derived EOs, and the possibility of their exploration as neuroactive agents and alternative in the management of Alzheimer's disease (AD). [ABSTRACT FROM AUTHOR]

(1) Objective: Considering that current knowledge of mechanisms involved in the molecular pathogenesis of Social Anxiety Disorder (SAD) is limited, we conducted a systematic review to evaluate cumulative data obtained by Proton Magnetic Resonance Spectroscopic (1H MRS) studies. (2) Methods: A computer-based literature search of Medline, EMBASE, PsycInfo, and ProQuest was performed. Only cross-sectional studies using 1H MRS techniques in participants with SAD and healthy controls (HCs) were selected. (3) Results: The search generated eight studies. The results indicated regional abnormalities in the ‘fear neurocircuitry’ in patients with SAD. The implicated regions included the anterior cingulate cortex (ACC), dorsomedial prefrontal cortex (dmPFC), dorsolateral prefrontal cortex (dlPFC), insula, occipital cortex (OC), as well as the subcortical regions, including the thalamus, caudate, and the putamen. (4) Conclusions: The evidence derived from eight studies suggests that possible pathophysiological mechanisms of SAD include impairments in the integrity and function of neurons and glial cells, including disturbances in energy metabolism, maintenance of phospholipid membranes, dysregulations of second messenger systems, and excitatory/inhibitory neurocircuitry. Conducting more cross-sectional studies with larger sample sizes is warranted given the limited evidence in this area of research.

Cross-talk between the gut microbiota and neurochemicals affects health and well-being of animals. However, little is known about this interaction in chickens despite their importance in food production. Probiotics and live Salmonella vaccines are microbial products commonly given orally to layer pullets to improve health and ensure food safety. This study’s objective was to determine how these oral treatments, individually or in combination, would impact the gut environment of chickens. White Leghorn chicks were either non-treated (CON) or orally given probiotics (PRO), a recombinant attenuated Salmonella vaccine (RASV; VAX), or both (P+V). Birds were fed with probiotics daily beginning at 1-day-old and orally immunized with RASV at 4-days-old and boosted 2 weeks post-primary vaccination. At 5 weeks, ceca content, ceca tissues, and small intestinal scrapings (SISs) were collected from ten birds/group post-euthanasia for analyses. Catecholamine, but not serotonergic, metabolism was affected by treatments. Dopamine metabolism, indicated by L-DOPA and DOPAC levels, were increased in P+V birds versus CON and PRO birds. Based on 16S sequencing, beta diversity was more similar among vaccinated birds versus birds given probiotics, suggesting live Salmonella vaccination has a major selective pressure on microbial diversity. Abundances of Akkermansia muciniphila and Enterobacteriaceae positively correlated with levels of tyrosine and norepinephrine, respectively. Both enumeration and 16S sequencing, determined that PRO exhibited the greatest levels of Enterobacteriaceae in the ceca and feces, which was associated with greater IgA production against E. coli virulence factors as tested by ELISA. In summary, we demonstrate that using probiotics alone versus in combination with a live vaccine has major implications in catecholamine production and the microbiota of layer pullets. Additionally, unique correlations between changes in some neurochemicals and specific bacteria have been shown.

In this study, an efficient and sensitive assay for the detection of 42 polar neurochemicals, including neurotransmitters, amino acids, and biogenic amines, was established by combining reversed‐phase liquid chromatography tandem mass spectrometry with chemical derivatization. An optimally designed benzoyl chloride derivatization was easily conducted in a one‐pot reaction and stable neurochemical derivatives were obtained under mild conditions within 5 min (except for acetylcholine and melatonin). Derivatization also enabled the introduction of heavy labeling of the analytes through the use of labeled derivatization agents. Chromatography separation was performed on an HSS T3 column within 15 min by gradient elution. Multiple reaction monitoring acquisition mode enabled quantitation of neurochemicals with limits of detection of 0.05 to 11.63 nM and lower limits of quantitation of 0.09 to 46.50 nM in rat serum. The assay was well validated in terms of linearity and extraction recovery. Furthermore, the instrumental precision, specificity, matrix effect, accuracy, precision, stability, dilution effect, and carry‐over effect were also validated. Finally, the overall efficacy of the assay was experimentally tested using serum from six Sprague–Dawley rats. The results demonstrated that the developed method is effective for broad targeted analysis of 42 neurochemicals in serum. [ABSTRACT FROM AUTHOR]

The selective sensing of neurochemicals is essential for understanding the chemical basis of brain function and pathology. Interfacing the excellent recognition features of aptamers with in vivo compatible carbon fiber microelectrode (CFE)‐based electroanalytical systems offers a plausible means to achieve this end. However, this is challenging in terms of coupling chemistry, stability, and versatility. Here, we present a new interfacial functionalization strategy based on the assembly of aptamer cholesterol amphiphiles (aptCAs) on the alkyl chain‐functionalized CFE. The noncovalent cholesterol‐alkyl chain interactions effectively immobilize aptamers onto the CFE surface, allowing the generation of a highly selective system for probing neurochemical dynamics in living systems and opening up a vast array of new opportunities for designing in vivo sensors for exploring brain chemistry. [ABSTRACT FROM AUTHOR]

Sleep maintains the function of the entire body through homeostasis. Chronic sleep deprivation (CSD) is a prime health concern in the modern world. Previous reports have shown that CSD has profound negative effects on brain vasculature at both the cellular and molecular levels, and that this is a major cause of cognitive dysfunction and early vascular ageing. However, correlations among sleep deprivation (SD), brain vascular changes and ageing have barely been looked into. This review attempts to correlate the alterations in the levels of major neurotransmitters (acetylcholine, adrenaline, GABA and glutamate) and signalling molecules (Sirt1, PGC1α, FOXO, P66shc, PARP1) in SD and changes in brain vasculature, cognitive dysfunction and early ageing. It also aims to connect SD-induced loss in the number of dendritic spines and their effects on alterations in synaptic plasticity, cognitive disabilities and early vascular ageing based on data available in scientific literature. To the best of our knowledge, this is the first article providing a pathophysiological basis to link SD to brain vascular ageing. [ABSTRACT FROM AUTHOR]

Earlier, we reported that chronic exposure to pesticides causes a reduction in the acetylcholinesterase activity and hematological and biochemical alterations in agriculture workers. In continuation with that, the present study aimed to investigate the pesticide‐induced neurochemical imbalance and its association with behavior alterations in agricultural workers. A significant increase in depressive symptoms, assessed by the Beck Depression Inventory‐II was observed in pesticide exposed workers as compared to the unexposed. A decrease in the level of dopamine in plasma and levels of dopamine, 3,4‐dihydroxyphenylacetic acid, homovanillic acids, norepinephrine, serotonin, and hydroxyindoleacetic acid in urine was also observed. An increase in the levels of MAO‐A and MAO‐B has also been observed in these individuals. The decreased levels of neurotransmitters in the blood and urine have been linked with increased levels of MAO and pesticide residues in plasma and urine. Furthermore, these changes were associated with a higher incidence of depression in agricultural workers. Research Highlights: Extensive use of pesticide leads to inevitable exposure in farmworkers.In the last few decades, a large number of cases of suicide in farmworkers has been reported.Adverse clinical effects in pesticide exposed farmworkers have been observed.Neurobehavioral toxicity associated with neurochemical alterations was found in the exposed population as compared to controlsNeurochemical alteration was found to be associated with pesticide residues in chronically exposed farmworkers. [ABSTRACT FROM AUTHOR]