Quantification of extracellular levels of corticosterone in the basolateral amygdaloid complex of freely-moving rats: A dialysis study of circadian variation and stress-induced modulation

Bouchez, Gaëlle; Millan, Mark J.; Rivet, Jean‐Michel; Billiras, Rodolphe; Boulanger, Raphaël; Gobert, Alain P.

doi:10.1016/j.brainres.2012.01.010

Cited by 23 publications

(11 citation statements)

References 99 publications

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“…The serotonin content of the BLA was increased by fear conditioning (Conditioning: F (1,36) = 4.381, P < 0.05, n = 4–8/group; Fisher’s PLSD comparing all Stress and No Stress groups with control groups, P < 0.05, Figure 2), but not exposure to the novel context (Fisher’s PLSD comparing Context Only and Home Cage groups, P = n.s., Figure 2), consistent with other studies showing that fear conditioning and other stressors increase extracellular serotonin in the amygdala [14,37]. Within the groups that received fear conditioning, there was no effect of pairing on serotonin levels (Pairing: F (1,27) = 0.46, P = n.s., Figure 2), and, most critically, serotonin was similarly elevated in Stress and No Stress mice (Pairing X Stress: F (1,27) = 0.002, P = n.s., n = 7–8/group, Figure 2).…”

Section: Resultssupporting

confidence: 90%

Stress Enables Reinforcement-Elicited Serotonergic Consolidation of Fear Memory

Baratta

Kodandaramaiah

Monahan

et al. 2016

Biological Psychiatry

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Background Prior exposure to stress is a risk factor for developing post-traumatic stress disorder (PTSD) in response to trauma, yet the mechanisms by which this occurs are unclear. Using a rodent model of stress-based susceptibility to PTSD, we investigated the role of serotonin in this phenomenon. Methods Adult mice were exposed to repeated immobilization stress or handling, and the role of serotonin in subsequent fear learning was assessed using pharmacological manipulation and western blot detection of serotonin receptors, measurements of serotonin, high-speed optogenetic silencing, and behavior. Results Both dorsal raphe serotonergic activity during aversive reinforcement and amygdala serotonin 2c receptor (5-HT2CR) activity during memory consolidation are necessary for stress enhancement of fear memory, but neither process affects fear memory in unstressed mice. Additionally, prior stress increases amygdala sensitivity to serotonin by promoting surface expression of 5-HT2CR without affecting tissue levels of serotonin in the amygdala. We also show that the serotonin that drives stress enhancement of associative cued fear memory can arise from paired or unpaired footshock, an effect not predicted by theoretical models of associative learning. Conclusion Stress bolsters the consequences of aversive reinforcement, not by simply enhancing the neurobiological signals used to encode fear in unstressed animals, but rather by engaging distinct mechanistic pathways. These results reveal that predictions from classical associative learning models do not always hold for stressed animals, and suggest that 5-HT2CR blockade may represent a promising therapeutic target for psychiatric disorders characterized by excessive fear responses such as that observed in PTSD.

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Section: Resultssupporting

confidence: 90%

Stress Enables Reinforcement-Elicited Serotonergic Consolidation of Fear Memory

Baratta

Kodandaramaiah

Monahan

et al. 2016

Biological Psychiatry

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“…In vivo microdialysis has previously been used to determine stress-induced changes in extracellular levels of CORT in limbic regions such as the hippocampus (Droste et al, 2008(Droste et al, , 2009) and amygdala (Bouchez et al, 2012). The results of the current study are consistent with these previous reports in that acute stress exposure to a naive rat elicited a significant increase in CORT levels in the CBL.…”

Section: Stress Antidepressant Treatment and Amygdalar Glutamatergicsupporting

confidence: 93%

Repeated restraint stress-induced atrophy of glutamatergic pyramidal neurons and decreases in glutamatergic efflux in the rat amygdala are prevented by the antidepressant agomelatine

et al. 2015

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“…Yohimbine, an α2-adrenergic receptor antagonist, is a pharmacological stressor that activates the HPA axis (Bouchez et al, 2012; Marinelli et al, 2007) and also induced cocaine-seeking behavior in both squirrel monkeys and rats. Yohimbine is commonly used as a pharmacological stressor to model the stress-induced reinstatement of drug-seeking behavior (Buffalari and See, 2011; Kupferschmidt et al, 2009; Lee et al, 2004).…”

Section: 4 - Discussionmentioning

confidence: 99%

Antagonism of the neuropeptide S receptor with RTI-118 decreases cocaine self-administration and cocaine-seeking behavior in rats

Schmoutz

Zhang

Runyon

et al. 2012

Pharmacology Biochemistry and Behavior

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Neuropeptide S (NPS) is a neuromodulatory peptide, acting via a G-protein-coupled receptor to regulate sleep, anxiety and behavioral arousal. Recent research has found that intracerebroventricular NPS can increase cocaine and alcohol self-administration in rodents, suggesting a key role in reward-related neurocircuitry. It is hypothesized that antagonism of the NPS system might represent a novel strategy for the pharmacological treatment of cocaine abuse. To this end, a small-molecule NPSR antagonist (RTI-118) was developed and tested in animal models of cocaine seeking and cocaine taking. Male Wistar rats (n=54) trained to self-administer cocaine and food under a concurrent alternating FR4 schedule exhibited specific dose-dependent decreases in cocaine intake when administered RTI-118. RTI-118 also decreased the reinstatement of extinguished cocaine-seeking behavior induced by conditioned cues, yohimbine and a priming dose of cocaine. These data support the hypothesis that antagonism of the neuropeptide S receptor may ultimately show efficacy in reducing cocaine use and relapse.

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Quantification of extracellular levels of corticosterone in the basolateral amygdaloid complex of freely-moving rats: A dialysis study of circadian variation and stress-induced modulation

Cited by 23 publications

References 99 publications

Stress Enables Reinforcement-Elicited Serotonergic Consolidation of Fear Memory

Stress Enables Reinforcement-Elicited Serotonergic Consolidation of Fear Memory

Repeated restraint stress-induced atrophy of glutamatergic pyramidal neurons and decreases in glutamatergic efflux in the rat amygdala are prevented by the antidepressant agomelatine

Antagonism of the neuropeptide S receptor with RTI-118 decreases cocaine self-administration and cocaine-seeking behavior in rats

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