A role for the CRF-containing pathway from central nucleus of the amygdala to bed nucleus of the stria terminalis in the stress-induced reinstatement of cocaine seeking in rats

@article{Erb2001ARF,
  title={A role for the CRF-containing pathway from central nucleus of the amygdala to bed nucleus of the stria terminalis in the stress-induced reinstatement of cocaine seeking in rats},
  author={Suzanne M. Erb and Natalina Salmaso and Demetra Rodaros and Jane Stewart},
  journal={Psychopharmacology},
  year={2001},
  volume={158},
  pages={360-365}
}
Abstract. Rationale: We reported previously that bilateral injection of a corticotropin-releasing factor (CRF)-receptor antagonist, D-Phe CRF12–41, into the bed nucleus of the stria terminalis (BNST) blocks the reinstatement of cocaine seeking induced by footshock, whereas the injection of CRF into the same region induces reinstatement. One source of CRF in the BNST arises from a CRF-containing projection originating in the central nucleus of the amygdala (CeA). Objective: To determine whether… 
Blockade of Stress-Induced But Not Cocaine-Induced Reinstatement by Infusion of Noradrenergic Antagonists into the Bed Nucleus of the Stria Terminalis or the Central Nucleus of the Amygdala
TLDR
The data suggest that stress-induced NA activation in the BNST and in the region of the CeA is critical to relapse to drug seeking induced by stress but not to relapse induced by priming injections of cocaine, and it is hypothesized that NA activity leads to activation of corticotropin-releasing factor neurons in these regions.
Region-specific effects of brain corticotropin-releasing factor receptor type 1 blockade on footshock-stress- or drug-priming-induced reinstatement of morphine conditioned place preference in rats
TLDR
The present results demonstrate dissociable roles of CRF1 receptors in the BNST, amygdala, and NAc in footshock-stress- vs morphine-priming-induced reinstatement of drug CPP.
Beta-2 adrenergic receptors mediate stress-evoked reinstatement of cocaine-induced conditioned place preference and increases in CRF mRNA in the bed nucleus of the stria terminalis in mice
TLDR
Findings indicate that, during stress, norepinephrine, via β2-ARs, either directly or indirectly activates CRF-releasing neurons in the BNST that interface with motivational neurocircuitry to induce reinstatement of cocaine-conditioned reward.
Stress-Induced Cocaine Seeking Requires a Beta-2 Adrenergic Receptor-Regulated Pathway from the Ventral Bed Nucleus of the Stria Terminalis That Regulates CRF Actions in the Ventral Tegmental Area
TLDR
It is demonstrated that, in the vBNST, corticotropin releasing factor is expressed in neurons that innervate the ventral tegmental area (VTA), a site where the CRF receptor antagonist antalarmin prevents the reinstatement of cocaine seeking by a stressor, intermittent footshock, following intravenous self-administration in rats.
Effects of lidocaine-induced inactivation of the bed nucleus of the stria terminalis, the central or the basolateral nucleus of the amygdala on the opponent-process actions of self-administered cocaine in rats
TLDR
These data suggest that the BNST and to a lesser extent the CeA, but not the BLA, play a role in mediating the opponent-process actions of self-administered cocaine.
A Study of Corticotropin-releasing Factor-catecholamine Interactions in the Reinstatement of Cocaine Seeking in Rats
TLDR
Findings suggest a functional interaction between NA and CRF systems in mediating stress-induced reinstatement of cocaine seeking, whereby activation of CRF receptors occurs subsequent to, and downstream of, the sites of action of NA.
Differential involvement of the core and shell subregions of the nucleus accumbens in conditioned cue-induced reinstatement of cocaine seeking in rats
TLDR
The functional integrity of the Nacc, but not the NACs, is necessary for conditioned cue-induced reinstatement of cocaine seeking behavior.
Involvement of central amygdalar and bed nucleus of the stria terminalis corticotropin-releasing factor in behavioral responses to social defeat.
TLDR
Data suggest that CRF acts within a neural circuit that includes the amygdala and the BNST to modulate agonistic behavior following social defeat, and is a critical component of the neural circuitry mediating conditioned defeat.
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References

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A Role for the Bed Nucleus of the Stria Terminalis, But Not the Amygdala, in the Effects of Corticotropin-Releasing Factor on Stress-Induced Reinstatement of Cocaine Seeking
TLDR
It is reported that D-Phe acts in the bed nucleus of the stria terminalis (BNST), and not in the amygdala, to block footshock-induced reinstatement of cocaine seeking in cocaine-trained rats.
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TLDR
It is strongly suggested that CRH in the CSF can activate the BNST, which could lead to activation of brainstem and hypothalamic BN ST target areas involved in anxiety and stress responses.
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TLDR
The data suggest that brain CRF plays a critical role in stress- induced, but only a modulatory role in cocaine-induced, reinstatement of cocaine seeking in rats, and shows that although reinstatementof cocaine seeking by footshock stress requires minimal, basal, levels of corticosterone, stress-induced increases in cortic testosterone do not play a role in this effect.
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TLDR
It is suggested that CRF, a major brain peptide involved in stress, contributes to relapse to heroin-seeking induced by stressors.
In vivo CRF release in rat amygdala is increased during cocaine withdrawal in self‐administering rats
TLDR
Evidence is provided that cocaine withdrawal activates CRF neurons in the amygdala, a site that has been implicated in emotional and anxiogenic effects of stress and drug withdrawal syndromes.
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TLDR
A role for the medial septum is thought to be involved in neuronal processes underlying behavioural inhibition, thus it is speculated that stressors provoke relapse by interfering with these processes.
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TLDR
The present data suggest that CRF contributes to stress-induced relapse to alcohol seeking via its actions on extra-hypothalamic sites, and point to a general role of CRF in relapse to drugs induced by stressors.
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