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Anxiety, hippocampus synaptic plasticity deficit, as well as pro-inflammatory cytokines, are involved in Alzheimer's disease (AD). The present study is designed to evaluate the possible therapeutic effect of crocin on anxiety-like behaviours, hippocampal synaptic plasticity and neuronal shape, as well as pro-inflammatory cytokines in the hippocampus using in vivo amyloid-beta (Aβ) models of AD. The Aβ peptide (1-42) was bilaterally injected into the frontal-cortex. Five hours after the surgery, the rats were given intraperitoneal (IP) crocin (30 mg/kg) daily up to 12 days. Elevated plus maze results showed that crocin treatment after bilateral Aβ injection significantly increased the percentage of spent time into open arms, frequency of entries, and percentage of entries into open arms as compared with the Aβ group. In the open field test, the Aβ+crocin group showed a higher percentage of spent time in the centre and frequency of entries into central zone as compare with the Aβ treated animals. Administering crocin increased the number of soma, dendrites and axonal arbores in the CA1 neurons among the rats with Aβ neurotoxicity. Cresyl violet (CV) staining showed that crocin increased the number of CV-positive cells in the CA1 region of the hippocampus compared with the Aβ group. Silver-nitrate staining indicated that crocin reduced neurofibrillary tangle formation induced by Aβ. Crocin treatment attenuated the expression of TNF-α and IL-1β mRNA in the hippocampus compared with the Aβ group. Our results suggest that crocin attenuated Aβ-induced anxiety-like behaviours and neuronal damage, and synaptic plasticity loss in hippocampal CA1 neurons may via its anti-inflammatory effects., (© 2021 John Wiley & Sons Australia, Ltd.)

Objective(s): Alzheimer’s disease (AD) is a neurodegenerative disease that results in the gradual breakdown of brain tissue, causing the deterioration of intellectual function and ability. Crocin is a saffron carotenoid compound proven to have excellent neuroprotective and anti-inflammation properties, although it has some limitations such as low stability and bioavailability. Therefore, in the current research, we tried to improve these limitations by using nanotechnology and chitosan as the carrier. Our study examined the therapeutic effects of crocin nano-chitosan-coated compound and compared it with intact crocin in lower dosages than other studies in AD rat models. Materials and Methods: Encapsulating crocin into chitosan nanoparticles was done through a modified technique to improve its limitations. The AD rat model was induced by bilaterally injecting beta-amyloid (Aβ) peptide into the frontal lobe using a stereotaxic device. To evaluate memory, we conducted the Barnes maze test, and to evaluate anxiety, we used the elevated plus maze test. Also, histological tests were conducted to evaluate neuronal damage in each group. Results: Crocin nano-chitosan-coated administration significantly improved specific memory indicators compared to the Aβ and other treated groups. A significant decrease in anxiety indicators was detected compared to the Aβ and other treated groups. Finally, the results of hippocampus staining indicated a meaningful difference between the Aβ group and other treated groups, compared to the crocin nano-chitosan-coated group. Conclusion: Treatment with low dosages of crocin in the nano-coated form exhibited great efficacy in reducing AD’s adverse effects compared to the same dosage of intact crocin. [ABSTRACT FROM AUTHOR]

Background and Aim: Emotion regulation is an important and determining factor in psychological wellbeing and effective behavior of people, which plays an essential role in adapting to stressful life events. People who experience emotion dysregulation may show symptoms such as impulsive behaviors, severe anxiety, aggression, and problems with metacognition. This study aims to investigate the effectiveness of high-definition transcranial direct current stimulation (HD-tDCS) in the dorsolateral prefrontal cortex (DLPFC) of the brain in improving emotion dysregulation and the speed of brain information processing. Methods: This study is pre-post-test research. In this study, 20 healthy participants (male, right-handed) were used. The participants were randomly assigned to two anodal stimulation groups and sham (control) groups. By completing the ERQ and DTS questionnaires, as well as performing the Paced Auditory Serial Addition Test (PASAT) before and after electrical stimulation of the brain by the HD-tDCS method in the L-DLPFC area, this study was followed up and carried out. Results: After the intervention (stimulation) in the pre-post test comparison between the stimulation group and the control group, there was a difference in terms of evaluation variables, suppression, being absorbed by negative emotions, regulating efforts to relieve distress, the number of correct answers in the PASAT test and the time to answer the PASAT test. There was significance (P<0.05). This shows the effectiveness of the intervention (anodal stimulation) on these components between the stimulation and control groups. However, there was no significant difference between the stimulation and control groups in terms of emotional distress tolerance, subjective estimation of distress, and the number of incorrect answers in the PASAT test (P>0.05). Also, in the comparison of the pre-post test, time was not recognized as a significant factor in any of the research components. Conclusion: High-definition transcranial direct current stimulation (HD-tDCS) in the left dorsolateral prefrontal cortex (DLPFC) improves some components of emotion dysregulation and also improves brain information processing speed. [ABSTRACT FROM AUTHOR]

Behavioral and functional studies describe hemispheric asymmetry in anxiety and metabolic behaviors in responses to stress. However, no study has reported serotonergic receptor (the 5-HT1A receptor) lateralization in the basolateral amygdala (BLA) in vivo on anxiety and metabolic behaviors under stress. In the present study, the effect of unilateral and bilateral suppression of the 5-HT1A receptor in the BLA on anxiety, and metabolic responses to chronic restraint stress was assessed. Male Wistar rats 7 days after cannulation into the BLA received chronic restraint stress for 14 consecutive days. 20 minutes before induction of stress, WAY-100–635 (selective 5-HT1A antagonist) or sterile saline (vehicle) was administered either uni- or bi-laterally into the BLA. Behavioral (elevated plus maze; EPM, and open field test), and metabolic parameter studies were performed. Results showed that stress causes a significant increase in weight gain compared to control. In the non-stress condition, the left and bilaterally, and in the stress condition the right, left, and both sides, inhibition of 5-HT1A in the BLA reduced weight gain. In the restraint stress condition, only inhibition of the 5-HT1A receptor in the left BLA led to decreased food intake compared to the control group. In stress conditions, inhibition of the 5-HT1A receptor on the right, left, and bilateral BLA increased water intake compared to the stress group. Inhibition of the 5-HT1A receptor on the left side of the BLA by WAY-100–635 induced anxiety-like behaviors in stressed rats. Similarly, WAY-100–635 on the left BLA effectively caused anxiety-like behaviors in both EPM and open field tests in the control animals. In conclusion, it seems that 5-HT1A receptors in the left BLA are more responsible for anxiety-like behaviors and metabolic changes in responses to stress. [ABSTRACT FROM AUTHOR]

Chronic restraint stress induces anxiety‐like behaviors and emotional abnormalities via an alteration of synaptic remodeling in the amygdala and the hippocampus. Given that the date palm spathe has been shown to have neuroprotective effects on different experimental models, this study aimed to address whether the date palm spathe extract (hydroalcoholic extract of date palm spathe [HEDPP]) can reduce chronic restraint stress‐induced behavioral, electrophysiological, and morphological changes in the rat model. Thirty‐two male Wistar rats (weight 200–220 g) were randomly divided into control, stress, HEDPP, and stress + HEDPP for 14 days. Animals were submitted to restraint stress for 2 h per day for 14 consecutive days. The animals of the HEDPP and stress + HEDPP groups were supplemented with HEDPP (125 mg/kg) during these 14 days, 30 min before being placed in the restraint stress tube. We used passive avoidance, open‐field test, and field potential recording to assess emotional memory, anxiety‐like behavioral and long‐term potentiation in the CA1 region of the hippocampus, respectively. Moreover, Golgi–Cox staining was used to investigate the amygdala neuron dendritic arborization. Results showed that stress induction was associated with behavioral changes (anxiety‐like behavioral and emotional memory impairment), and the administration of HEDPP effectively normalized these deficits. HEDPP remarkably amplified the slope and amplitude of mean‐field excitatory postsynaptic potentials (fEPSPs) in the CA1 area of the hippocampus in stressed rats. Chronic restraint stress significantly decreased the dendritic arborization in the central and basolateral nucleus of the amygdala neuron. HEDPP suppressed this stress effect in the central nucleus of the amygdala. Our findings indicated that HEDPP administration improves stress‐induced learning impairment and memory and anxiety‐like behaviors by preventing adverse effects on synaptic plasticity in the hippocampus and amygdala. [ABSTRACT FROM AUTHOR]

The article highlights a study on the effects of intra-ventral hippocampal memantine administration in male NMRI stressed mice were studied. It could be concluded that N-Methyl-D-aspartic acid glutamate receptors in the ventral hippocampus may play a pivotal role in the mediation of maintenance of anxiety and depression induced by stress in the mice.

Subclinical hypothyroidism tends to be more prevalent due to having a deficiency in iodine intake, which could lead to it. The role of sex differentiation in the susceptibility for anxiety-like behaviors of adult rats with mild neonatal hypothyroidism and then levothyroxine therapy is aimed to be investigated. Data showed that in both genders, reduced social performance and increased anxiety-like behaviors were revealed in a dose-dependent manner to propylthiouracil exposure in hypothyroid groups and levothyroxine therapy reversed the impairment performance and increased anxiety-like in the behavioral tests. Therefore, levothyroxine therapy can also be used as therapeutic methods for adult subject treatment. [ABSTRACT FROM AUTHOR]

• Epinephrine injection into BLA resulted in a considerable impairment of fear memory in stressed rats. • Under stress conditions, epinephrine in the BLA increased anxiety-like behaviors. • Infusion of epinephrine into the BLA increases the slope of fEPSP in the CA1 region of the hippocampus. • Epinephrine infusion into the BLA in the stress didn't change the dendritic length in the CA1 region of the hippocampus. The amygdala is known to mediate in moderating the impacts of emotional arousal and stress on memory. According to a growing body of research, the basolateral amygdala (BLA) is an important locus for integrating neuromodulator influences coordinating the retrieval of different types of memory and anxiety. This study aimed to investigate how the epinephrine in the BLA affects hippocampal fear memory, anxiety, and plasticity in control and stressed rats. For four days, male Wistar rats were exposed to electrical foot-shock stress. Animals received bilateral micro-injections of either vehicle or epinephrine (1 µg/side) into the BLA over four days (5 min before foot-shock stress). Behavioral characteristics (fear memory and anxiety-like behavior), histological features and electrophysiological parameters were investigated. Epinephrine injection into BLA resulted in a considerable impairment of fear memory in stressed rats. On the other hand, epinephrine effectively affected fear memory in control rats. Under stress conditions, epinephrine in the BLA is thought to increase anxiety-like behaviors. Treatment with epinephrine significantly increases the slope of fEPSP in the CA1 region of the hippocampus in the control and stress rats. In different groups, foot-shock stress had no effect on the apical and basal dendritic length in the CA1 region of the hippocampus. These results indicate that activating adrenergic receptors diminish fear memory and anxiety-like behaviors in the foot-shock stress, which this impact is independent of CA1 long-term potentiation induction. [ABSTRACT FROM AUTHOR]

Introduction: The basolateral amygdala (BLA) is a key structure that integrated anxiety information. It is suggested that baso-lateral area of amygdala receives a dense norepinephrine innervation from the locus coeruleus nucleus. Furthermore, stress increased norepinephrine secretion in the BLA. In the present study, we examined the effects of the stimulation of β2-adrenoceptors in the BLA on anxiety-like behaviors following foot-shock stress. Materials and Methods: Foot-shock stress (10 Hz, 40 mV for 60 seconds) for 4 consecutive days applied to animals. Salbutamol (the β2-adrenoreceptor agonist; 4 µg/rat) bilaterally injected into the BLA 5 min before starting foot-shock stress for 4 consecutive days. Anxiety-like behaviors assessed 24h after the last session of stress, using elevated plus-maze (EPM) and open field test (OFT). Results: Foot-shock stress significantly decreased time spent and the number of entries into the open arms of EPM. Similarly, stress significantly decreased the time spent and the number of entries into the center area of OFT. Furthermore, foot-shock stress significantly decreased the number of grooming and rearing behaviors. Additionally, intra-BLA infusions of salbutamol before stress significantly increased time spent and the number of entries into the open arms as compared with stress group. In addition, OFT results showed that salbutamol increased the time spent in the center, number of center entries, the number of rearing and grooming behaviors, line crossing and total distance as compared with the stress group. Conclusion: It is likely that β2- adrenoceptors of the BLA mediate the induced-anxiety-behaviors by foot-shock stress. [ABSTRACT FROM AUTHOR]

It is believed that α-adrenoceptors have critical contribution in the process of pain information. Anterior cingulate of cortex (ACC) is a key area of brain associated with pain perception. Pharmacological studies demonstrated that crocin, as a potent antioxidant, has analgesic effects. The underlying analgesic mechanism of the crocin is far from clear. Therefore, the present study was design to examine the interaction of anti-nociceptive effects of crocin with α1- and α2-adrenoceptors of ACC in chronic constriction injury (CCI) model of neuropathic pain. Intra-ACC injection of crocin significantly decreased cold allodynia (using acetone test) and anxiety (using elevated plus maze test) in neuropathic rats from 2 days to 6 days' post-surgery. Co-injection of crocin and prazosin (α1-adrenoceptors antagonist, 30 μg/5μl) had no effect on the allodynia. However, co-injection of crocin and yohimbine (α2-adrenoceptors antagonist, 30 μg/5μl) significantly increased the allodynia on days 4 and 6 post-surgery as compared with CCI+crocin rats. Moreover, our data identified that neuropathy decreased open arm entries and locomotor activity. Additionally, crocin increased entries to open arms; but this increase was not significant as compared to CCI group. There was no significant difference between CCI+Crocin and CCI+crocin+prazosin groups. However, co-injection of crocin and yohimbine significantly decreased entries to open arms as compared with CCI+crocin group. Furthermore, co-injection of crocin with prazosin or yohimbine did not cause significant changes in locomotor activity. The present study suggested that the anti-nociceptive and anxiolytic effects of crocin appear to be mediated through α2-, and not α1-adrenoceptors in the ACC. [ABSTRACT FROM AUTHOR]

Gallic acid (GA) is known to be a natural phenolic compound with antioxidant and neuroprotective effects. This study aims to investigate the impact of GA against restraint stress-induced oxidative damage, anxiety-like behavior, neuronal loss, and spatial learning and memory impairment in male Wistar rats. The animals were divided into four groups (n = 8) and subjected to restraint stress for 4 h per day for 14 consecutive days or left undisturbed (control without inducing stress). In the treatment group, the animals were treated with 2 mL normal saline plus 100 mg/kg GA per day for 14 consecutive days (STR + GA group). The animals received the drug or normal saline by gavage 2 h before inducing restraint stress. ELISA assay measured oxidative stress factors. Elevated-plus maze and Morris water maze tests assessed anxiety-like behavior and spatial learning and memory, respectively. Also, neuronal density was determined using Nissl staining. Restraint stress significantly increased MDA and reduced the activities of GPX and SOD in the stressed rats, which were reserved by treatment with 100 mg/kg GA. Restraint stress markedly enhanced the anxiety-like behavior and spatial learning and memory impairment that were reserved by GA. In addition, treatment with GA reduced the neuronal loss in the stressed rats in the hippocampus and prefrontal cortex (PFC) regions. Taken together, our findings suggest that GA has the potential to be used as a good candidate to attenuate neurobehavioral disorders as well as neuronal loss in the hippocampus and PFC induced by restraint stress via reducing oxidative damage. • Gallic acid significantly reduced anxiety-like behaviors in the chronic restraint stress animals. • Gallic acid ameliorates spatial memory impairment in the stressed animals. • Gallic acid reduced the neuronal loss in the CA1 region of the hippocampus and prefrontal cortex in the stressed animals. [ABSTRACT FROM AUTHOR]

The prenatal stress during pregnancy has a wide variety of negative effects on the offspring behaviors. As such, in the present study the effect of prenatal immobilization stress was investigated on the brain BDNF level, spatial memory, anxiety and depression-like behavior in the F1 generation female NMRI mice. Twenty female pregnant mice were randomly allocated to stress and control groups (n = 10/group). The stress group was placed in PVC cylinders (2.5 cm in diameter and 20 cm in length) for one hour/day until the 15th day of pregnancy. The female F1 offspring was nursed by their mothers until reaching 25–30 g (9–10 weeks) which was tested for spatial memory, anxiety and depressive-like behavior using Barnes Maze, elevated plus-maze and forced swimming test, respectively. Also, the brain BDNF level was assessed by the ELISA method. Mice that underwent prenatal restraint stress exhibited impaired spatial memory in the Barnes Maze, which the time and distance to achieve the target hole and the number of errors in the female adult offspring increased than the control group. In the elevated plus-maze, the animals that underwent prenatal restraint stress spent less time in the open arms of the maze and reduced entering the open arms, compared to the control group. In addition, stress caused a significant decrease in swim time and a significant increase in float time for the female adult offspring compared to the control group. The brain BDNF concentration also decreased significantly in the stress group compared to the control group. This data suggests that prenatal stress may impair spatial memory and induce anxiety and depressive-like behavior in the adult offspring female mice via reducing brain BDNF. [ABSTRACT FROM AUTHOR]

Introduction: Noise pollution is an unwanted inevitable distribution of the modern and industrialized life of mankind. With the expansion of urban life, humans are daily exposed to noise pollution which can cause anxiety and disorders in cognitive activities. The present study was aimed to investigate the impact of sub-chronic urban traffic noise pollution on learning, memory and anxiety-like behavior in adult male rats. Methods: Thirty two adult male Wistar rats (weighing 275-300g) were used in the present experimental study. The animals were divided into two groups: the control and the noiseexposed. The rats in the test group were exposed to a 90dB noise recorded from a crowded street traffic for 6h/10 days. Control rats were intact. Morris water maze (MWM) and an elevated plus maze (EPM) were used to assess spatial learning and memory and anxiety-like behavior in rats. Results: The findings displayed that both control and noise-exposed group improved their maze steering over 4 days of experiment in MWM; however, noise-exposed group had more latency and traveled-distance in MWM to find the hidden platform in probe trial compared to those of control (P<0.05). Moreover, noise-exposed group showed a significant increase in weight gain compared to the control group (P<0.05). In addition, the spent time in open arm of the EPM was significantly decreased compared to controls (P<0.05). Conclusion: Urban traffic noise pollution for a short-term period causes a meaningful increase on weight gain, disorders in retrieval memory and increase in anxiety-like behavior in rats. [ABSTRACT FROM AUTHOR]