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Stress-induced redistribution of corticotropin-releasing factor receptor subtypes in the dorsal raphe nucleus.

ABSTRACT: The stress-related neuropeptide corticotropin-releasing factor (CRF) is involved in determining behavioral strategies for responding to stressors, in part through its regulation of the dorsal raphe (DR)-serotonin (5-HT) system. CRF(1) and CRF(2) receptor subtypes have opposing effects on this system that are associated with active versus passive coping strategies, respectively.Immunoelectron microscopy and in vivo single-unit recordings were used to assess CRF receptor distribution and neuronal responses, respectively, in the DR of stressed and unstressed rats.Here we show that in unstressed rats CRF(1) and CRF(2) are differentially distributed within DR cells, with CRF(1) being prominent on the plasma membrane and CRF(2) being cytoplasmic. Stress experience reverses this distribution, such that CRF(2) is recruited to the plasma membrane and CRF(1) tends to internalize. As a consequence of this stress-induced cellular redistribution of CRF receptors, neuronal responses to CRF change from inhibition to a CRF(2)-mediated excitation.Given evidence that CRF(1) and CRF(2) activation are associated with distinct behavioral responses to stress, the stress-triggered reversal in receptor localization provides a cellular mechanism for switching behavioral strategies for coping with stressors.

SUBMITTER: Waselus M

PROVIDER: S-EPMC2728006 | biostudies-literature | 2009 Jul

REPOSITORIES: biostudies-literature

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Stress-induced redistribution of corticotropin-releasing factor receptor subtypes in the dorsal raphe nucleus.

Waselus Maria M Nazzaro Cristiano C Valentino Rita J RJ Van Bockstaele Elisabeth J EJ

Biological psychiatry 20090411 1

<h4>Background</h4>The stress-related neuropeptide corticotropin-releasing factor (CRF) is involved in determining behavioral strategies for responding to stressors, in part through its regulation of the dorsal raphe (DR)-serotonin (5-HT) system. CRF(1) and CRF(2) receptor subtypes have opposing effects on this system that are associated with active versus passive coping strategies, respectively.<h4>Methods</h4>Immunoelectron microscopy and in vivo single-unit recordings were used to assess CRF ...[more]

PMID: 19362706

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Project description:Environmental stimuli elicit drug craving and relapse in cocaine users by triggering the retrieval of strong cocainerelated contextual memories. Retrieval can also destabilize drug memories, requiring reconsolidation, a protein synthesis-dependent storage process, to maintain memory strength. Corticotropin-releasing factor (CRF) signaling in the basolateral amygdala (BLA) is necessary for cocainememory reconsolidation. We have hypothesized that a critical source of CRF in the BLA is the dorsal raphe nucleus (DR) based on its neurochemistry, anatomical connectivity, and requisite involvement in cocaine-memory reconsolidation. To test this hypothesis, male and female Sprague-Dawley rats received adeno-associated viruses to express Gi-coupled designer receptors exclusively activated by designer drugs (DREADDs) selectively in CRF neurons of the DR and injection cannulae directed at the BLA. The rats were trained to self-administer cocaine in a distinct environmental context then received extinction training in a different context. They were then briefly reexposed to the cocaine-predictive context to destabilize (reactivate) cocaine memories. Intra-BLA infusions of the DREADD agonist deschloroclozapine (DCZ; 0.1 mM, 0.5 μL/hemisphere) after memory reactivation attenuated cocaine-memory strength, relative to vehicle infusion. This was indicated by a selective, DCZ-induced and memory reactivation-dependent decrease in drug-seeking behavior in the cocaine-predictive context in DREADD-expressing males and females at test compared to respective controls. Notably, BLA-projecting DR CRF neurons that exhibited increased c-Fos expression during memory reconsolidation co-expressed glutamatergic and serotonergic neuronal markers. Together, these findings suggest that the DRCRF → BLA circuit is engaged to maintain cocaine-memory strength after memory destabilization, and this phenomenon may be mediated by DR CRF, glutamate, and/or serotonin release in the BLA.

Dataset Information

Stress-induced redistribution of corticotropin-releasing factor receptor subtypes in the dorsal raphe nucleus.

Publications

Stress-induced redistribution of corticotropin-releasing factor receptor subtypes in the dorsal raphe nucleus.

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