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)

Brain norepinephrine (NE) modulates many aspects of the stress response. The interaction between NE and neuropeptides such as galanin, with which it is closely associated and which may be released from noradrenergic terminals under conditions of high activity, has not been well studied. We therefore investigated the modulatory effects of galanin in the central nucleus of the amygdala (CeA) on behavioral responsivity to stress when activation of the noradrenergic system was amplified using the adrenergic autoreceptor antagonist yohimbine (2.5 mg/kg ip). Either immobilization stress or yohimbine alone had anxiogenic effects on rat behavior in the elevated plus maze. However, yohimbine pretreatment before stress produced a paradoxical anxiolytic response, which we hypothesized was attributable to galanin release in CeA. Microdialysis verified that yohimbine amplified NE release in CeA during immobilization stress, and also showed that whereas there was no detectable change in galanin release in CeA during stress alone, there was an increase during immobilization stress after yohimbine pretreatment. Bilateral administration of the galanin antagonist M40 into CeA before stress blocked the anxiolytic influence of yohimbine pretreatment. Exogenous galanin mimicked the anxiolytic effect of yohimbine pretreatment, and this too was blocked by M40. These results suggest that amplifying the noradrenergic response to stress can recruit galanin release in CeA, which buffers the anxiety-like behavioral response to acute stress. The balance between noradrenergic and peptidergic neurotransmission may be modified by prior stress, drug treatment or genetic variability, and may represent a novel target for treatment of stress-related neuropsychiatric disorders.
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PMID:Behavioral reactivity to stress: amplification of stress-induced noradrenergic activation elicits a galanin-mediated anxiolytic effect in central amygdala. 1183 Jan 75

The neuropeptide galanin has been identified as a possible neurotransmitter/neuromodulator within the central nervous system. In the present study, a potential role for galanin in the lateral bed nucleus of the stria terminalis (BSTL) in modulating behavioral and neuroendocrine responses to an acute stress was investigated. In the first experiment, acute immobilization stress induced anxiety-like behavioral responses in rats, measured on the social interaction and elevated plus-maze tests. Immobilization stress decreased both social interaction time and open arm exploratory behavior on the elevated plus-maze. Bilateral administration of the galanin antagonist M40 (1.0 nmole/0.2 microl) into BSTL immediately prior to stress exposure attenuated the anxiogenic-like effects of immobilization stress, restoring both social interaction time and exploration of open arms to control levels. Administration of the antagonist alone had no effect on baseline behavior of unstressed control rats in either test, suggesting that the modulatory effect of galanin elicited during stress is not exerted tonically in unstressed animals. In the second experiment, immobilization stress produced an increase in plasma adrenocorticotropic hormone (ACTH) that was also attenuated by bilateral administration of M40 into BSTL prior to stress. These results suggest that during stress, the neuropeptide galanin exerts a modulatory effect in the BSTL, facilitating behavioral and neuroendocrine components of the acute stress response.
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PMID:Modulatory effects of galanin in the lateral bed nucleus of the stria terminalis on behavioral and neuroendocrine responses to acute stress. 1206 4

Galanin (GAL) has been implicated in modulating anxiety, although a precise role remains unclear. Previous studies revealed anxiolytic effects, anxiogenic effects, or no effect, depending on the test, brain region, route of drug administration and context. We have shown previously that microinjection of the GAL antagonist M40 into central amygdala blocked an anxiolytic response to acute stress on the elevated plus maze when rats were pretreated with yohimbine, suggesting an anxiolytic effect of GAL. By contrast, we also showed that microinjection of M40 into the lateral bed nucleus of the stria terminalis attenuated anxiety-like behavioral responses to stress on the plus maze and social interaction tests, implying an anxiogenic effect for GAL. The behavioral response to stress on both these tests is a reduction of an ongoing behavior (open-arm exploration or social interaction, respectively). To better understand the anxiety-modulating role of GAL, it is also important to ascertain its effect on a response that represents an activation rather than suppression of behavior. Thus, in this study, we investigated an active behavioral response to acute stress in rats, the shock-probe defensive burying response. Bilateral microinjections of M40 into lateral septum (LS), a region important to this response and innervated by GAL, dose-dependently decreased burying without affecting immobility. No change was seen in hindpaw withdrawal latency on a thermosensitivity assay, suggesting that the reduction in burying behavior was not attributable to changes in cutaneous pain sensitivity. These results indicate that in LS, GAL facilitates the active anxiety-like behavioral response on the defensive burying test, similar to its facilitatory effect on anxiety-like stress-induced suppression of behavior in the lateral bed nucleus. These results highlight the fact that, rather than a unified system-like role in modulating anxiety, the effects of GAL can be either facilitating or attenuating, and are region-specific, context-specific and response-specific.
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PMID:Administration of the galanin antagonist M40 into lateral septum attenuates shock probe defensive burying behavior in rats. 1608 87