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The positive and protective effects of regular exercise on the learning and memory impairments induced by sleep deprivation (SD) have been demonstrated in previous studies, and recently, it was found that miR-191-5p by targeting BDNF as an essential factor in cognitive function causes memory and learning impairments in sleep deprivation conditions. This study aims to investigate the effects of regular treadmill exercise on the expression of miR-191-5p in sleep-deprived rats. Ovariectomized (OVX) rats are more vulnerable to the effects of sleep deprivation than intact rats. In this study, we performed our experiments on OVX female rats. MiRNAs are vital regulators of many biological functions, mainly brain functions such as learning and memory. The effect of 72 hours of sleep deprivation and four weeks of treadmill exercise on the expression of miR-191-5p and BDNF was investigated. Seventy-two hours of sleep deprivation was performed using the multiple platform method, and the exercise protocol was four weeks of regular treadmill exercise. Expression of miR-191-5p and BDNF was done using the Real-time PCR method. Sleep deprivation downregulated the level of miR-191-5p and BDNF, all of which were ameliorated by four weeks of treadmill exercise. Despite increased BDNF expression in exercised rats, miR-191-5p did not show significant changes. The mechanism of the possible effect of exercise on the expression of BDNF was independent of its effect on the expression of miR-191-5p. [ABSTRACT FROM AUTHOR]

Cortical lesions can cause major sensory and motor impairments, representing a significant challenge in neuroscience and clinical medicine. Limbal mesenchymal stem cells (LMSCs), renowned for their remarkable ability to proliferate and distinct characteristics within the corneal epithelium, offer a promising opportunity for regenerative treatments. This study aimed to assess whether the transplantation of LMSCs could improve tactile ability in rats with lesions of the barrel cortex.

Background and Objectives: Studies have indicated that sleep is essential for the development and survival of the brain and increases the brain's capacity for cognitive functions, and sleep loss disrupts cognitive performance. The present review study aimed to investigate the effects of sleep deprivation on learning and memory with an emphasis on the role of sex hormones. Materials and Methods: In order to investigate this topic, the articles were searched for in the following databases: PubMed, Scopus Database, Science Direct and Google Scholar. The words used while searching were "sleep deprivation, sleep, learning and memory, sex hormones, synaptic plasticity, and cognitive functions" that finally, ninety one references on these topics were reviewed. Results: Researches have shown that sleep deprivation can disrupt learning and memory long-term potentiation (LTP), gene expression, and the rate of proteins in the hippocampus that are important in learning, memory and synaptic plasticity. Studies have shown that cognitive performances such as memory and learning and also different aspects of sleep, including quality and pattern, are different in sexes. A Change in sleep pattern is often associated with hormonal factors, especially sex hormones. Conclusion: Therefore, sex hormones affect the structure of the brain, behavior, learning, and memory in both sexes. The loss of hormonal function is associated with sleep disorders, and reduces learning and memory, especially in female subjects. It can be concluded that ovarian hormones might play a protective role against the deterioration in learning and memory in women with sleep loss. [ABSTRACT FROM AUTHOR]

Transient cerebral ischemia is a pandemic neurological disorder and the main aim of medical intervention is to reduce complications. Human umbilical cord mesenchymal cells (hUCMs) are capable of differentiating into neural-like cells (NLC) in vitro, therefore we investigated the neuroprotective potential of these cells in comparison to aspirin and in combination (NLC-Aspirin) on spatial memory and neural morphologic changes in male rats submitted to transient cerebral ischemia.

Impaired decision-making constitutes a fundamental issue in numerous psychiatric disorders. Extensive research has established that early life adversity (ELA) increases vulnerability to psychiatric disorders later in life. ELA in human neonates is associated with changes in cognitive, emotional, as well as reward-related processing. Maternal separation (MS) is an established animal model of ELA and has been shown to be associated with decision-making deficits. On the other hand, enriched environment (EE) and intranasal oxytocin (OT) administration have been demonstrated to have beneficial effects on decision-making in humans or animals. Given these considerations, our investigation sought to explore the impact of brief exposure to EE and intranasal OT administration on the decision-making abilities of adolescent rats that had experienced MS during infancy. The experimental protocol involved subjecting rat pups to the MS regimen for 180 min per day from postnatal day (PND) 1 to PND 21. Then, from PND 22 to PND 34, the rats were exposed to EE and/or received intranasal OT (2 μg/μl) for seven days. The assessment of decision-making abilities, using a rat gambling task (RGT), commenced during adolescence. Our findings revealed that MS led to impaired decision-making and a decreased percentage of advantageous choices. However, exposure to brief EE or intranasal OT administration mitigated the deficits induced by MS and improved the decision-making skills of maternally-separated rats. Furthermore, combination of these treatments did not yield additional benefits. These results suggest that EE and OT may hold promise as therapeutic interventions to enhance certain aspects of cognitive performance., Competing Interests: Declaration of Competing Interest The authors declare no conflicts of interest., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Asthma is an inflammatory disorder with significant health problems. It generally affects the lungs but can also impact brain performance via several mechanisms. Some investigations have proposed that asthma impairs cognition. This study assessed the impacts of myrtenol as a monoterpene on cognitive disorders following asthma at behavioral, molecular, and synaptic levels. Asthma was induced by injection and inhalation of ovalbumin (OVA). Male Wistar rats were allocated to five groups: control, asthma, asthma/vehicle, asthma/myrtenol, and asthma/budesonide. Myrtenol (8 mg/kg) or budesonide (160 μg/kg) was administered through inhalation once a day for 1 week, and at the end of the inhalation period, behavioral tests (MWM and Open Field), field potential recording, hippocampal brain-derived neurotrophic factor (BDNF), IL1β (ELISA), and NFκB measurement (Western blot) were performed to evaluate cognitive performance. Moreover, H&E (hematoxylin and eosin) staining was used for hippocampus histological evaluation. Myrtenol improved spatial learning, memory, LTP (long-term potentiation) impairments, and anxiety-like behaviors following asthma. Myrtenol inhalation increased the BDNF level and decreased the IL1β level and NFκB expression in the hippocampus of the asthmatic rats. The neuronal damage in the hippocampus following allergic asthma was alleviated via myrtenol administration. Myrtenol, as an herbal extract, protects the hippocampus from asthma consequences. Our observations revealed that myrtenol can improve spatial learning, memory, synaptic plasticity impairments, and anxiety-like behaviors following asthma. We believe that these ameliorating effects of myrtenol can be attributed to inflammation suppression and increased BDNF in the hippocampus., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Monitoring errors consumes limited cognitive resources and can disrupt subsequent task performance in multitasking scenarios. However, there is a dearth of empirical evidence concerning this interference with prospective estimation of time. In this study, we sought to investigate this issue through a serial multitasking experiment, employing a temporal bisection task as the primary task. We introduced two task contexts by implementing two different concurrent tasks. In one context, participants were tasked with discriminating the size difference between two visual items, while in the other context, they were required to judge the temporal order of similar visual items. The primary task remained the same for the entire experiment. Psychophysical metrics, including subjective bias (determined by the bisection point) and temporal sensitivity (measured by the Weber ratio), in addition to reaction time, remained unaltered in the primary task regardless of the perceptual context exerted by the concurrent tasks. However, commission of error in the concurrent tasks (i.e., non-specific errors) led to a right-ward shift in the bisection point, indicating underestimation of time after errors. Applying a drift-diffusion framework for temporal decision making, we observed alterations in the starting point and drift rate parameters, supporting the error-induced underestimation of time. The error-induced effects were all diminished with increasing a delay between the primary and concurrent task, indicating an adaptive response to errors at a trial level. Furthermore, the error-induced shift in the bisection point was diminished in the second half of the experiment, probably because of a decline in error significance and subsequent monitoring response. These findings indicate that non-specific errors impact the prospective estimation of time in multitasking scenarios, yet their effects can be alleviated through both local and global reallocation of cognitive resources from error processing to time processing., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Aim: Disruption in cerebellar inputs, as well as dysfunction of Purkinje cells (PCs), causes a change in the timing of electrical signaling in the cerebellum resulting in disorders such as cerebellar ataxia. Although much clinical and molecular genetics research has been conducted to understand this disorder, there is no specific treatment for cerebellar ataxia. As cannabinoid type 1 receptors (CB1Rs) are highly expressed in the cerebellum and have been suggested as a therapeutic strategy, we determined whether AM251, a cannabinoid receptor antagonist, was neuroprotective of PCs in a rat cerebellar ataxic model. Materials and methods: To this end, we conducted behavioral and histological tests in the 3-acetylpyridine (3AP) rat cerebellar ataxia model, to explore whether AM251 was protective against induction of ataxia and cell death. Results : Rats with chemical degeneration of the inferior olive induced by 3AP (55 mg/kg, i.p.) clearly showed cerebellar ataxic symptoms. The locomotor activity and motor coordination of the ataxic animals were clearly disrupted compared to the control group. Further, histological analysis showed cell death and PCs degenerated with loss of cell membrane integrity associated with 3AP. Pre-treatment by AM251 improved the locomotor activity of the ataxic animals, and AM251 almost prevented PCs neuronal degeneration. Conclusion: Our data which show protection of cerebellar PCs and motor improvement in the ataxic rat model by treatment with AM251 suggests that targeting cannabinoid receptors should be considered for therapeutic intervention in cerebellar ataxia.HIGHLIGHTS:AM251 was protective against induction of ataxia and cell death.CBR antagonist typically ameliorated 3AP induced Ataxia.AM251 affected explorative and gait disturbances induced by 3AP.CBR antagonist improved impairments of anxiety-like behaviors following 3AP.

Introduction: In this study, we aimed to investigate the inflammatory factors, oxidative stress, and histopathological consequences of the brain-gut axis in male and female rats prenatally exposed to VPA., Methods: Pregnant Wistar rats were randomly divided into two groups. The animals received saline, and valproic acid (VPA) (600 mg/kg, i.p.) on embryonic day 12.5 (E12.5). All offspring were weaned on postnatal day 21, and the experiments were done in male and female rats on day 60. The brain and intestine tissues were extracted to assess histopathology, inflammation, and oxidative stress., Results: An increase of interleukin-1β (IL-1β) and interleukin-6 (IL-6) and a decrease of interleukin-10 (IL-10) were observed in the two sexes and two tissues of the autistic rats. In the VPA-exposed animals, malondialdehyde (MDA) and protein carbonyl (PC) increased in the brain of both sexes and the intestines of only the males. The total antioxidant capacity (TAC), superoxide dismutase (SOD), and catalase (CAT) significantly decreased in both tissues of male and female autistic groups. Histopathological evaluation showed that the %apoptosis of the cortex in the autistic male and female groups was more than in controls whereas this parameter in the CA1 and CA3 was significant only in the male rats. In the intestine, histopathologic changes were seen only in the male autistic animals., Conclusion: The inflammatory and antioxidant factors were in line in the brain-gut axis in male and female rats prenatally exposed to VPA. Histopathological consequences were more significant in the VPA-exposed male animals., (© 2024 Wiley Periodicals LLC.)

Objectives: Mild cognitive impairment (MCI) is a neurocognitive disorder in which the cognitive and mental abilities of humans are declined. Transcranial direct-current stimulation (tDCS) is an emerging noninvasive brain stimulation technique aimed at neuromodulation. In this study, we investigate whether high-definition anodal tDCS stimulation (anodal HD-tDCS) in MCI patients in two different brain regions will be effective in improving cognitive function., Methods: This study was done as a randomized, double-blind clinical trial. Sixty MCI patients (clinically diagnosed by expert neurologists) were randomly divided into three groups. Two groups received 2-mA anodal HD-tDCS for 20 min for 2 weeks (5 consecutive days in each week, 10 days in total). In the first group (twenty patients), the left dorsolateral prefrontal cortex (left DLPFC) was targeted. In the second group (twenty patients), the target zone was the dominant anterior temporal lobe (DATL). The third group (twenty patients) formed the Sham group. The Montreal Cognitive Assessment (MoCA) and Quality of Life in Alzheimer's Disease (QoLAD) were considered as the outcome measures., Results: MCI patients obtained the highest MoCA mean scores in both left DLPFC and DATL groups versus the study baseline 2 weeks after the intervention. In addition, the MoCA mean scores of MCI patients were greater in both intervention groups compared to the Sham group up to 3 months post-stimulation (p-value ≤ 0.05). However, as we moved away from the first stimulation day, a decreasing trend in the MoCA mean scores was observed. Moreover, in the left DLPFC and DATL groups, higher QoLAD mean scores were observed 3-month post-stimulation, highlighting the effectiveness of anodal HD-tDCS in improving the quality of life in MCI patients., Conclusion: In this research, it was shown that applying anodal HD-tDCS at left DLPFC and DATL brain regains for two successive weeks improves cognitive function in MCI patients (by obtaining higher values of MoCA scores) up to 3 months after the intervention compared to the Sham group. This illustrates the positive effects of HD-tDCS, as a non-pharmacological intervention, for improving cognitive function and quality of life in MCI patients., Significance: Two weeks after anodal HD-tDCS of the DLPFC and DATL brain regions, the MCI patients achieved the highest MoCA mean scores compared to the Sham group across all measurement intervals., (© 2024. The Author(s).)

Humans demonstrate significant behavioural advantages with particular perceptual dimensions (such as colour or shape) and when the relevant dimension is repeated in consecutive trials. These dimension-related behavioural modulations are significantly altered in neuropsychological and addiction disorders; however, their underlying mechanisms remain unclear. Here, we studied whether these behavioural modulations exist in other trichromatic primate species and whether repeated exposure to opioids influences them. In a target detection task where the target-defining dimension (colour or shape) changed trial by trial, humans exhibited shorter response time (RT) and smaller event-related electrodermal activity with colour dimension; however, macaque monkeys had shorter RT with shape dimension. Although the dimensional biases were in the opposite directions, both species were faster when the relevant dimension was repeated, compared with conditions when it changed, across consecutive trials. These indicate that both species formed dimensional sets and that resulted in a significant 'switch cost'. Scheduled and repeated exposures to morphine, which is analogous to its clinical and recreational use, significantly augmented the dimensional bias in monkeys and also changed the switch cost depending on the relevant dimension. These cognitive effects occurred when monkeys were in abstinence periods (not under acute morphine effects) but expressing significant morphine-induced conditioned place preference. These findings indicate that significant dimensional biases and set formation are evolutionarily preserved in humans' and monkeys' cognition and that repeated exposure to morphine interacts with their manifestation. Shared neural mechanisms might be involved in the long-lasting effects of morphine and expression of dimensional biases and set formation in anthropoids., (© 2024 The Authors. Addiction Biology published by John Wiley & Sons Ltd on behalf of Society for the Study of Addiction.)

The likelihood of substance dependency in offspring is increased in cases when there is a family history of drug or alcohol use. Mothering is limited by maternal addiction because of the separation. Maternal separation (MS) leads to the development of behavioural and neuropsychiatric issues in the future. Despite the importance of this issue, empirical investigations of the influences of maternal substance use and separation on substance use problems in offspring are limited, and studies that consider both effects are rare. This study aims to review a few studies on the mechanisms, treatments, genetics, epigenetics, molecular and psychological alterations, and neuroanatomical regions involved in the dependence of offspring who underwent maternal addiction and separation. The PubMed database was used. A total of 95 articles were found, including the most related ones in the review. The brain's lateral paragigantocellularis (LPGi), nucleus accumbens (NAc), caudate-putamen (CPu), prefrontal cortex (PFC), and hippocampus, can be affected by MS. Dopamine receptor subtype genes, alcohol biomarker minor allele, and preproenkephalin mRNA may be affected by alcohol or substance use disorders. After early-life adversity, histone acetylation in the hippocampus may be linked to brain-derived neurotrophic factor (BDNF) gene epigenetics and glucocorticoid receptors (GRs). The adverse early-life experiences differ in offspring›s genders and rewire the brain›s dopamine and endocannabinoid circuits, making offspring more susceptible to dependence. Related psychological factors rooted in early-life stress (ELS) and parental substance use disorder (SUD). Treatments include antidepressants, histone deacetylase inhibitors, lamotrigine, ketamine, choline, modafinil, methadone, dopamine, cannabinoid 1 receptor agonists/antagonists, vitamins, oxytocin, tetrahydrocannabinol, SR141716A, and dronabinol. Finally, the study emphasizes the need for multifaceted strategies to prevent these outcomes., Competing Interests: Competing Interests The authors declare no competing or conflicting interests., (© 2024 Kerman University of Medical Sciences.)

Background: Autism spectrum disorder (ASD) represents an inheritable neurodevelopmental condition characterized by social communication deficits and repetitive behaviors. Numerous studies have underscored the significant roles played by genetic and environmental factors in the etiology of ASD, and these factors are known to perpetuate behavioral impairments across generations., Objectives: The primary objective of this study was to assess the behavioral and cognitive attributes in the second filial (F2) generation of male and female rats, with a particular focus on those whose parents had been exposed to valproic acid (VPA) during embryonic development., Methods: In this study, a cohort of 32 male and 32 female rats from the second filial (F2) generation, referred to as Mother.ASD, Father.ASD, or Both.ASD, was examined. These designations indicate whether the mother, father, or both parents had experienced embryonic exposure to valproic acid (600 mg/kg, i.p.). During adolescence, the F2 pups underwent behavioral and cognitive assessments, including open field testing, marble burying, social interaction evaluations, and Morris water maze tasks., Results: Our data revealed that while both the Mother.ASD and Father.ASD groups, regardless of sex, exhibited elevated anxiety-like behavior in the open field test. Only the Mother.ASD group displayed repetitive behaviors and deficits in social memory. Additionally, spatial memory impairments were observed in both sexes. These findings highlight the transmission of autistic-like behaviors in the offspring of Mother.ASD rats from both sexes. Nevertheless, future research endeavors should be more targeted in identifying the specific genes responsible for this transmission., Conclusion: In summary, our findings underscore the transmission of autistic-like behaviors, including anxiety-like behavior, repetitive actions, impairments in social interactions, and deficits in memory, to the offspring of the Mother.ASD group, irrespective of their sex., (© 2024 Wiley Periodicals LLC.)

Glioblastoma multiforme (GBM) is a highly aggressive malignant primary tumor in the central nervous system. Despite extensive efforts in radiotherapy, chemotherapy, and neurosurgery, there remains an inadequate level of improvement in treatment outcomes. The development of large-scale genomic and proteomic analysis suggests that GBMs are characterized by transcriptional heterogeneity, which is responsible for therapy resistance. Hence, knowledge about the genetic and epigenetic heterogeneity of GBM is crucial for developing effective treatments for this aggressive form of brain cancer. Tyrosine kinases (TKs) can act as signal transducers, regulate important cellular processes like differentiation, proliferation, apoptosis and metabolism. Therefore, TK inhibitors (TKIs) have been developed to specifically target these kinases. TKIs are categorized into allosteric and non-allosteric inhibitors. Irreversible inhibitors form covalent bonds, which can lead to longer-lasting effects. However, this can also increase the risk of off-target effects and toxicity. The development of TKIs as therapeutics through computer-aided drug design (CADD) and bioinformatic techniques enhance the potential to improve patients' survival rates. Therefore, the continued exploration of TKIs as drug targets is expected to lead to even more effective and specific therapeutics in the future., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2024 Rahban, Joushi, Bashiri, Saso and Sheibani.)

Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairment in reciprocal social interactions, deficits in communication, and restrictive and repetitive behaviors and interests. In previous studies, music has been identified as an intervention therapy for children with ASD., Objectives: The present study evaluated the effects of music on cognitive behavioral impairments in both sexes of adult rats exposed prenatally to Valproic acid., Methods: For induction of autism, pregnant female rats were pretreated with either saline or VPA (600 mg/kg.i.p.) at gestational day (GD) 12.5. Male and female offspring were divided into Saline.Non-Music, VPA.Non-Music, Saline.Music, and VPA.Music groups. The adult rats in the music groups were exposed to Mozart's piano sonata K.448 for 30 days (4 h/day), from postnatal day (PND) 60 to 90. Social interaction and Morris water maze (MWM) tasks were tested at PND 90., Results: Our results revealed that prenatal exposure to VPA decreased sociability and social memory performance in both sexes of adult rats. Moreover, prenatal exposure to VPA created learning and memory impairments in both sexes of adult rats in the MWM task. Music intervention improved sociability in both sexes of VPA-exposed rats and social memory in both sexes of VPA-exposed rats, especially in females. Furthermore, our results revealed that music ameliorated learning impairments in VPA-exposed female rats in the MWM task. In addition, music improved spatial memory impairments in VPA-exposed rats of both sexes, especially in females, which needs more investigation in molecular and histological fields in future studies., Conclusion: Music intervention improved sociability and social memory in adult VPA-exposed rats, especially in female animals. Furthermore, music improved memory impairments in VPA-exposed rats of both sexes. It seems that music had a better influence on female rats. However, future studies need more investigations in molecular and histological fields., (© 2024 Wiley Periodicals LLC.)

Introduction: Both sleep deprivation (SD) and inflammation can negatively affect cognitive function. This study aimed to investigate how SD impacts the brain's inflammatory response to lipopolysaccharide (LPS) and its subsequent effects on cognitive functions., Methods: To this end, male rats were tested through a Morris water maze (MWM) to assess their spatial learning and memory. Also, in vivo field potential recordings (to evaluate synaptic plasticity) were done in the Saline, SD, LPS1 (1 mg/kg/7 days), and LPS1+SD groups. Cytokine levels were measured using an enzyme-linked immunosorbent assay (ELISA)., Results: Based on the results, the LPS1+SD group showed increased total distance and escape latency compared to the other groups in the MWM test. Besides, the LPS1+SD group exhibited a significant decrease in long-term potentiation (LTP) induction and maintenance in the CA1 area of the brain. Finally, the inflammatory cytokine interleukin-1β (IL-1β) levels were significantly higher in the LPS1+SD group than in the Saline group., Conclusion: These findings suggest that the combined effects of SD and brain inflammatory response can have more harmful effects on cognitive function, LTP, and inflammatory factors than either SD or LPS1 alone., (© 2023 The Author(s). Published by S. Karger AG, Basel.)

Objective: Stem cells (SCs) can improve the functional defects of brain injury. Rodents use their whiskers to get tactile information from their surroundings. The aim of this study was to investigate whether the transplantation of SCs into the lesioned barrel cortex can help neuronal function in the contralateral cortex., Materials and Methods: Sixteen male Wistar rats (200-230 g) were used in this experimental study. We induced a mechanical lesion in the right barrel cortex area of rats by removing this area by a 3 mm skin punch. Four groups containing one intact group of rats: group 1: control, and three lesion groups, group 2: lesion+un-differentiated dental pulp SCs (U-DPSCs), group 3: lesion+differentiated dental pulp SCs (D-DPSCs), and group 4: cell medium (vehicle) that were injected in the lesion area. Three weeks after transplantation of SCs or cell medium, the rats' responses of left barrel cortical neurons to controlled deflections of right whiskers were recorded by using the extracellular single-unit recordings technique., Results: The results showed that the neural spontaneous activity and response magnitude of intact barrel cortex neurons in the lesion group decreased significantly (P<0.05) compared to the control group while ON and OFF responses were improved in the D-DPSCs (P<0.001) group compared to the vehicle group three weeks after transplantation., Conclusion: Transplantation of dental pulp mesenchymal SCs significantly improved the neural responses of the left barrel cortex that was depressed in the vehicle group.

Background: Parkinson's disease (PD) is one of the most common neurodegenerative diseases in the elderly. Cognitive dysfunction represents a common and challenging non-motor symptom for people with Parkinson's disease. The number of neurotrophic proteins in the brain is critical in neurodegenerative diseases such as Parkinson's. This research aims to compare the effects of two types of exercise, forced and voluntary, on spatial memory and learning and neurochemical factors (CDNF and BDNF)., Methods: In this research, 60 male rats were randomly divided into six groups (n = 10): the control (CTL) group without exercise, the Parkinson's groups without and with forced (FE) and voluntary (VE) exercises, and the sham groups (with voluntary and forced exercise). The animals in the forced exercise group were placed on the treadmill for four weeks (five days a week). At the same time, voluntary exercise training groups were placed in a special cage equipped with a rotating wheel. At the end of 4 weeks, learning and spatial memory were evaluated with the Morris water maze test. BDNF and CDNF protein levels in the hippocampus were measured by the ELISA method., Results: The results showed that although the PD group without exercise was at a significantly lower level than other groups in terms of cognitive function and neurochemical factors, both types of exercise, could improve these problems., Conclusion: According to our results, 4 weeks of voluntary and forced exercises were all found to reverse the cognitive impairments of PD rats., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interests., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Maternal morphine exposure has negative consequences for learning and memory in the offspring. Interaction between mothers and pups has a crucial effect on the mammal's development. Maternal Separation (MS) can cause behavioral and neuropsychiatric problems later in life. It seems that adolescents are more susceptible to the effects of early life stress; evidence for the combinatory effects of oral chronic maternal morphine exposure and MS in the CA1 area of the hippocampus in the male adolescent offspring is not found. Therefore, this study aimed to evaluate the effects of chronic maternal morphine consumption (21 days before and after mating, and gestation), and MS (180 min/day from postnatal day (PND) 1-21) on the synaptic plasticity of male offspring in mid-adolescence. Control, MS, Vehicle (V), Morphine, V + MS, and Morphine + MS groups were tested for in vivo field potential recording from the CA1 area of the hippocampus. The current results demonstrated that chronic maternal morphine exposure impaired the induction of early long-term potentiation (LTP). MS impaired average fEPSPs, induction of early-LTP and maintenance. Chronic maternal morphine exposure in combination with MS impaired the induction of early LTP but didn't deteriorate maintenance and the average field excitatory post-synaptic potentials (fEPSPs) measured in two hours. Prepulse facilitation ratios remained undisturbed and I/O curves showed decreased fEPSP slopes at high stimulus intensities in combinatory group. We concluded that chronic maternal morphine exposure in combination with MS negatively affects synaptic plasticity in the CA1 area in male adolescent offspring., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by core symptoms including impairment in social communication and restrictive and repetitive behaviors and interests. Music has emerged in the past decade as an intervention therapy for children with ASD. The aim of the present study was to evaluate the effects of music on cognition impairments in the valproic acid (VPA) rat model of autism. The VPA was administered for animal modeling of autism on embryonic day 12.5 (E12.5) (600 mg/kg). Male and female pups were sub divided into four main groups (Saline.Non-music, VPA.Non-music, Saline.Music, and VPA.Music). The rats in the music groups were exposed to Mozart's piano sonata K.448 for 30 days (4 h/day), from postnatal day (PND) 21 to 50. Autistic-like behaviors were tested using a social interaction, the Morris water maze (MWM), and a passive avoidance tasks at the end of the PND 50. Our results demonstrated that VPA-exposed rat pups had significantly lower sociability and social memory performance compared with the saline-exposed rats in both sexes. VPA-exposed rat pups exhibited learning and memory impairments in the MWM and passive avoidance tasks. Our results demonstrated that music improved sociability in VPA-exposed rats, especially in males. Furthermore, our findings revealed that music improved learning impairments in VPA-exposed male rats in MWM task. In addition, music improved spatial memory impairments in VPA-exposed rats of both sexes. We also found that music improved passive avoidance memory impairments in VPA-exposed rats of both sexes, especially in females. More investigation in future studies are needed., (© 2023 International Society for Developmental Neuroscience.)

There are general inhibitory effects of exo-cannabinoids on dopamine-mediated behaviors. Many studies suggested the interaction between cannabinoid receptors and dopamine receptors in the brain that affect cognition behaviors. In this paper, we investigate the effects of marijuana on 6-OHDA-induced cognitive impairments and the expression of dopamine and cannabinoid receptors in the hippocampus of male rats. 42 rats were divided into six groups. 6-hydroxy dopamine (6-OHDA) was administrated into the substantia nigra. Marijuana (60 mg/kg; i.p.) was administered 28 days, one week after the 6-OHDA injection. Morris water maze (MWM) and novel object recognition tests were performed. The hippocampal expression levels of cannabinoid receptors and D1 and D2 dopamine receptors evaluate by real-time PCR. The results showed marijuana improved the spatial learning and memory disorders caused by 6-OHDA in the MVM task and novel object recognition test. Additionally, the level of both D1 and D2 mRNA was decreased in 6-OHDA-treated animals and marijuana consumption only increased the hippocampal level of D1 mRNA. Moreover, the level of hippocampal CB1 mRNA in 6-OHDA- treated rats was higher than in control rats. However, the hippocampal level of CB2 mRNA was decreased in 6-OHDA- treated rats. Marijuana consumption caused a significant decrease in CB1 mRNA level and an increase in CB2 mRNA level in 6-OHDA + marijuana group. Therefore, marijuana may be helpful for learning & memory disorders, D1, and D2 dopamine receptors, and cannabinoid receptor alteration in patients with Parkinson's disease., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Autism spectrum disorder is a neurodevelopmental disorder characterized by deficits in social communication and repetitive behavior. Many studies show that the number of cognitive impairmentscan be reduced by antagonists of the histamine H3 receptor (H3R). In this study, the effects of ciproxifan (CPX) (1 and 3 mg/kg, intraperitoneally) on cognitive impairments in rat pups exposed to valproic acid (VPA) (600 mg/kg, intraperitoneally) wereexamined on postnatal day 48-50 (PND 48-50) using marble-burying task (MBT), open field, novel object recognition (NOR), and Passive avoidance tasks. Famotidine (FAM) (10, 20, and 40 mg/kg, intraperitoneally) was also used to determine whether histaminergic neurotransmission exerts its procognitive effects via H2 receptors (H2Rs). Furthermore, a histological investigation was conducted to assess the degree of degeneration of hippocampal neurons. The results revealed that repetitive behaviors increased in VPA-exposed rat offspring in the MBT. In addition, VPA-exposed rat offspring exhibited more anxiety-like behaviors in the open field than saline-treated rats. It was found that VPA-exposed rat offspring showed memory deficits in NOR and Passive avoidance tasks. Our results indicated that 3 mg/kg CPX improved cognitive impairments induced by VPA, while 20 mg/kg FAM attenuated them. We concluded that 3 mg/kg CPX improved VPA-induced cognitive impairments through H3Rs. The histological assessment showed that the number of CA1 neurons decreased in the VPA-exposed rat offspring compared to the saline-exposed rat offspring, but this decrease was not significant. The histological assessment also revealed no significant differences in CA1 neurons in VPA-exposed rat offspring compared to saline-exposed rat offspring. However, CPX3 increased the number of CA1 neurons in the VPA + CPX3 group compared to the VPA + Saline group, but this increase was not significant. This study showed that rats prenatally exposed to VPA exhibit cognitive impairments in the MBT, open field, NOR, and Passive avoidance tests, which are ameliorated by CPX treatment on PND 48-50. In addition, morphological investigations showed that VPA treatment did not lead to neuronal degeneration in the CA1 subfield of the hippocampus in rat pups., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)