Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure to acute stress by forced swim impairs spatial learning and memory in rats. The retrosplenial cortex plays an important role in spatial learning and memory. A cell population that expresses immature neuronal markers, including doublecortin (DCX), plays a key role in plasticity of the adult brain through formation of new neurons. Here, we aimed to determine whether rats exposed to acute stress showed changes in DCX expression in retrosplenial cortex cells. Twelve male Sprague-Dawley rats were used. Six were subjected to acute stress by forced swim (group S), and the remaining six served as controls (group C). Immunohistochemical staining was performed for DCX, neuron-specific nuclear protein, parvalbumin, calbindin, calretinin, and somatostatin. Newly generated cells were immunohistochemically detected by daily administration of 5-bromo-2'-deoxyuridine for 1 week. Fluoro-Jade B staining was performed to detect cell death. Group S showed lower number of DCX-expressing cells than group C (P<0.001). The proportion of DCX-expressing cells showing neuron-specific nuclear protein co-localization (24% in group S; 27% in group C) or parvalbumin co-localization (65% in group S; 61% in group C) remained unchanged after acute stress exposure. Neither 5-bromo-2'-deoxyuridine-positive nor Fluoro-Jade B-positive cells were found in the retrosplenial cortex of groups S and C. DCX-expressing cells in the retrosplenial cortex decreases markedly without cell death after acute stress exposure. Neuronal differentiation of these cells toward gamma aminobutyric acidergic interneurons appears to be unaltered. The decrease in DCX expression may reduce plasticity potential within the retrosplenial cortex and attenuate spatial learning and memory function.
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PMID:Decrease in doublecortin expression without neuronal cell death in rat retrosplenial cortex after stress exposure. 2219 88

Amygdala is a limbic structure involved in the stress response. The immunohistochemical and morphometric methods were used to examine whether the chronic mild psychological stress during the early postnatal period would change activation of amygdaloid nuclei in response to the same stressor in adult. In the study we focused on the role of neurons containing calbindin (CB), calretinin (CR), parvalbumin (PV) and nitric oxide synthase (NOS). The rats were divided into three groups: control non-stressed animals and two experimental: EI consisted of animals that were exposed to acute stress in the high-light, open-field test (HL-OF) at P90 (P - postnatal day) and EII consisted of rats that were exposed to chronic stress in HL-OF, daily during the first 21 postnatal days and then once at P90. The scheme of activation of amygdaloid nuclei under stress in EI and EII group was similar. The highest density of c-Fos-ir cells (c-Fos - a marker of neuronal activation) was demonstrated by the medial nucleus (Me) and bed nucleus of the accessory olfactory tract (BAOT). The amygdaloid nuclei diversity after HL-OF was determined by the high activation of the NOS-ir cells in the Me and NOS- and CR-ir cells in the BAOT. These are probably projection neurons involved in modulation of defensive, reproductive and autonomic behavior in stress response and creation/storage of aversive memory. However, in comparison with EI group, significant decrease in density of c-Fos-ir cells, in almost all amygdaloid nuclei of EII group was revealed. Particularly in BAOT and Me the strong decrease of activity of NOS- and CR-ir neurons was observed. It probably results in attenuation of stress responses what, depending on the circumstances, can be adaptive or maladaptive.
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PMID:The influence of early postnatal chronic mild stress stimulation on the activation of amygdala in adult rat. 3192 96