Search

The serotonin-1A receptors (5-HT1A) in the two cerebral hemispheres are differentially involved in memory. The distribution of 5-HT1A receptors in the left and right amygdala is different. Furthermore, evidence shows that the 5-HT1A receptors in the left and right amygdala work differently in memory function. The basolateral amygdala (BLA) also regulates hippocampal long-term potentiation (LTP) during stress. However, which BLA structure in each hemisphere underlies such lateralized function is unclear. The present research investigated the possible involvement of 5-HT1A lateralization in the BLA on stress-induced memory impairment. 5-HT1A receptor antagonist (Way-100-635) was injected into the left, right, or bilateral BLA twenty minutes before chronic restraint stress (CRS) for 14 consecutive days. Results indicated that suppression of 5HT1A-receptors in the BLA plays an essential role in reducing the acquisition of passive avoidance in the shuttle box test and spatial memory in the Barnes maze test in the stress animals. This decrease was significant in the CRS animals with left and bilateral suppressed 5HT1A-receptors in the BLA. Field potential recording results showed that the left, right, and bilateral injection of Way-100-635 into the BLA significantly reduced the slope and amplitude of fEPSP in the CA1 area of the hippocampus in stressed rats. No significant difference was observed in neuronal arborization in the CA1 area of the hippocampus. In conclusion, the 5-HT1A receptor in the left and right sides of BLA nuclei play a different role in memory consolidation in the hippocampus under stress. [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.

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]

Context: The involvement of unilateral and bilateral inhibition of the ventral tegmental area (VTA) in response to stress is not well understood. Objective: In the present study, the effect of unilateral and bilateral inhibition of the VTA on hormonal, metabolic, and locomotor responses to stress was assessed. Material and methods: Male rats seven days after cannulation into the VTA received electro foot-shock stress for seven consecutive days. Twenty minutes before induction of stress, 2% lidocaine hydrochloride or sterile saline (control) was injected either uni- or bi-laterally into the VTA. Results: Results showed that stress significantly increased serum corticosterone level, adrenal gland weight and anorexia, reduced weight gain, food-intake, and locomotor activity. However, bilateral inactivation of VTA prevented stress-induced these parameters changes. Conclusion: The present study demonstrated that the bilateral VTA blockade effectively relieves the symptoms of stress, while the unilateral VTA blockade does not significantly improve the changes caused by stress. [ABSTRACT FROM AUTHOR]

Introduction: The basolateral amygdala (BLA) is implicated in stress-related disorders such as anxiety-like behavior. Substantial data exist demonstrating a close relationship between anxiety and adrenergic receptor function in patients with anxiety disorders; however, little is known about the effects of the â1 adrenergic receptor in the BLA on anxiety. This experiment examined the effects of the â1 adrenergic receptor in the BLA on anxiety-like behavior. Methods: Male Wistar rats were exposed to foot-shock stress four consecutive days that were uncontrollable. The â1-adrenoreceptor agonist (dobutamine; 0.5ìl/side) or antagonist (atenolol; 0.25ìl/side) bilaterally infused into the BLA five minutes before foot-shock stress. Anxiety-like behaviors were assessed 24h after four consecutive day's uncontrollable stress using elevated plus-maze (EPM) and open field test (OFT). Results: Findings of EPM revealed that foot-shock stress leads to anxiogenic effect with reduction the time spent and the number of entries into the open arms and increased head-dipping. Intra-BLA infusions of atenolol before stress affected animal behavior differently, such that it significantly increased the time spent and the number of entries into the open arms and decreased head-dipping. Also, OFT results showed the intra-BLA infusion of atenolol increased the time periods spent in the center, number of center entries and reduced the number of rearing as compared with the stress group. Conclusion: These results suggest that the anxiety-like behavior observed after the foot-shock stress is mediated, in part, by exaggerated â1 adrenergic receptor acting at the BLA. [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]