Chronic stress was induced by 14-day exposure to twice daily stressors in an unpredictable sequence (chronic variable stress, CVS). In the morning after the end of CVS, stressed and non-stressed controls were exposed to a novel restraint stress challenge. As previously documented, CVS caused adrenal hypertrophy, thymic involution, and attenuated body weight gain. None of these endpoints were affected by BSTpm lesions. Chronic stress Selleckchem GDC-0994 exposure facilitated plasma corticosterone responses to the novel restraint stress

and elevated CRH mRNA. Lesions of the BSTpm increased novel stressor-induced plasma ACTH and corticosterone secretion and enhanced c-fos mRNA induction in the paraventricular nucleus of the hypothalamus (PVN). In addition, lesion of the BSTpm resulted

in an additive increase in CVS-induced facilitation of corticosterone responses and PVN CRH expression. Collectively these data confirm that the BSTpm markedly inhibits HPA responses to acute stress, but do not strongly support an additional role for this region in limiting HPA axis responses to chronic drive. The data further suggest that acute versus chronic stress integration are subserved by different brain circuitry. (C) 2008 Published by Elsevier Ltd.”
“An adequate emotional response to stress is AMG510 concentration essential for survival and requires the fine-tuned regulation of several distinct neuronal circuits. Therefore, a precise control of these circuits is necessary to prevent behavioral imbalances. During the last decade, numerous investigations have evidenced that the endocannabinoid (eCB) system is able to crucially control stress coping. Its central component, Amine dehydrogenase the cannabinoid type 1 receptor (CBI receptor), is located at the presynapse, where it is able to attenuate neurotransmitter release after its activation by postsynaptically produced and released eCBs. To date, the eCB system has been found to control the neurotransmitter release from several neuron populations (e.g.

GABA, glutamate, catecholarnines and monoamines), suggesting a general mechanism for tuning neuronal activity, and thereby regulating emotion and stress responses. In this review, we aim at summarizing the anatomical and functional relation of the eCB system to an adequate response to stressful situations. Of special interest will be neuronal connections to the hypothalamic-pituitary-adrenal axis, but also circuits between cortical structures, such as prefrontal cortex, amygdala and hippocampus, and subcortical regions, such as raphe nuclei and locus coeruleus. We further like to step toward allocating eCB system functions to distinct cellular subpopulations in the brain. It has emerged that the eCB system is spatially well defined, and its detailed knowledge is a prerequisite for understanding the eCB system in the context of controlling behavior. Thus, advanced approaches combining different genetic and pharmacological tools to dissect specific eCB system functions are of particular interest.