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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]

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]

Objective(s): Post-traumatic stress disorder (PTSD), one of the most devastating kinds of anxiety disorders, is the consequence of a traumatic event followed by intense fear. In rats with contextual fear conditioning (CFC), a model of PTSD caused by CFC (electrical foot shock chamber), deep brain stimulation (DBS) alleviates CFC abnormalities. Materials andMethods: Forty Male Wistar rats (220-250 g) were divided into 5 groups (n=8) and underwent stereotactic surgery to implant electrodes in the right basolateral nucleus of the amygdala (BLn). After 7 days, some animals received a foot shock, followed by another 7-day treatment schedule (DBS treatment). Next, freezing behavior was measured as a predicted response in the absence of the foot shock (re-exposure time). Blood serum corticosterone levels and amygdala c-Fos protein expression were assessed using Enzyme-linked immunosorbent assay (ELISA) and Western blot, respectively. Furthermore, freezing behaviors by re-exposure time test and general anxiety by elevated plus-maze (EPM) were evaluated. Results: PTSD decreased serum corticosterone levels and increased both amygdala c-Fos expression and freezing behaviors. Therefore, DBS treatment significantly (P<0.001) enhanced serum corticosterone levels and could significantly (P<0.001) reduce both c-Fos protein expression and freezing behaviors' duration. However, DBS treatment has no effect on the general anxiety in PTSD rats. Conclusion: We argue that these outcomes might demonstrate the mechanism of DBS treatment, a complete therapeutic strategy, in PTSD patients [ABSTRACT FROM AUTHOR]

The present study explored the effect of α1-adrenergic receptors in the basolateral amygdala (BLA) on memory formation in the hippocampus under repeated stress. Male rats received injections of the α1-adrenergic receptor agonist (phenylephrine) or antagonist (prazosin) bilaterally into the BLA five min before foot-shock stress, and emotional and spatial memory and in-vivo long-term potentiation (LTP) in the Cornu Ammonis (CA1) region of the hippocampus were examined. Foot-shock stress impaired performance in emotional and spatial memory tests. However, it had no significant effect on any of the LTP parameters in the hippocampus. Intra-BLA phenylephrine injection significantly impaired emotional and spatial memory performance in stressed animals. On the other hand, administration of intra-BLA prazosin significantly reduced emotional and spatial memory in the control (intact) animals. Neither of the two drugs had any significant effects on LTP parameters. Prazosin effectively impaired memory in the control, but not in the stressed rats. Stress appears to have suppressed the effect of prazosin, and it seems to be a significantly stronger stimulus than prazosin. Taken together, these findings provide new insights into the effects of α1-adrenergic receptors in the BLA on memory storage, during the stress experience. [ABSTRACT FROM AUTHOR]

The catastrophic effects of opioids use on public health and the economy are documented clearly in numerous studies. Repeated morphine administration can lead to either a decrease (tolerance) or an increase (sensitization) in its behavioral and rewarding effects. Morphine-induced sensitization is a major problem and plays an important role in abuse of the opioid drugs. Studies reported that morphine may exert its effects by the release of nitric oxide (NO). NO is a potent neuromodulator, which is produced by nitric oxide synthase (NOS). However, the exact role of NO in the opioid-induced sensitization is unknown. In this study, we reviewed the role of NO on opioid-induced sensitization in 2 important, rewarding regions of the brain: nucleus accumbens and ventral tegmentum. In addition, we focused on the contribution of NO on opioid-induced sensitization in the limbic system. [ABSTRACT FROM AUTHOR]

Chronic restraint stress induces cognitive abnormalities through changes in synapses and oxidant levels in the amygdala and hippocampus. Given the neuroprotective effects of fruit of Terminalia chebula (Halileh) in different experimental models, the present investigation aimed to address whether Terminalia chebula is able to reduce chronic restraint stress-induced behavioral, synaptic and oxidant markers in the rat model. Thirty-two male Wistar rats were randomly divided into four groups as follows: control (did not receive any treatment and were not exposed to stress), stress (restraint stress for 2 h a day for 14 consecutive days), Terminalia chebula (received 200 mg/kg hydroalcoholic extract of Terminalia chebula), and stress + Terminalia chebula groups (received 200 mg/kg extract of Terminalia chebula twenty minutes before stress) (n = 8 in each group). We used the shuttle box test to assess learning and memory, Golgi-Cox staining to examine dendritic spine density in the dentate gyrus region of the hippocampus and the basolateral and central nuclei of the amygdala, and total antioxidant capacity (TAC) and total oxidant status (TOS) in the brain. The shuttle box test results demonstrated that Terminalia chebula treatment had a profound positive effect on memory parameters, including step-through latency (STL) and time spent in the dark room, when compared to the stress group. Daily oral treatment with Terminalia chebula effectively suppressed the loss of neural spine density in the dentate gyrus region of the hippocampus and the basolateral and central nuclei of the amygdala caused by chronic restraint stress, as demonstrated by Golgi-Cox staining. Additionally, the results indicate that Terminalia chebula significantly reduced the TOS and increased TAC in the brain compared to the stress group. In conclusion, our results suggest that Terminalia chebula improved memory impairment and synaptic loss in the dentate gyrus of the hippocampus and the basolateral and central nuclei of the amygdala induced by restraint stress via inhibiting oxidative damage. • Administration of Terminalia chebula (Terminalia C.) improves emotional memory in the stress animals. • Terminalia C. suppressed the loss of neural spine density in the dentate gyrus region of the hippocampus in stress. • Terminalia C. suppressed the loss of neural spine density in the basolateral and central nuclei of the amygdala in stress. • Terminalia C. significantly reduced the TOS and increased TAC in the brain in the stress animals. [ABSTRACT FROM AUTHOR]