Restraint stress increases serotonin release in the central nucleus of the amygdala via activation of corticotropin-releasing factor receptors

Abstract

Decreases in serotonergic activity in the central nucleus of the amygdala reduce responses to stressors, suggesting an important role for serotonin in this region of the amygdala in stress reactivity. However, it is not known whether exposure to stressors actually increases serotonin release in the central nucleus of the amygdala. The current experiment tested the hypothesis that restraint stress increases extracellular serotonin within the central nucleus of the amygdala and adjacent medial amygdala using in vivo microdialysis in awake male rats during the dark phase of the light-dark cycle. Serotonin release in the central nucleus increased immediately in response to restraint stress. In contrast, there was no change in serotonin release within the adjacent medial amygdala during or following restraint. Since corticotropin-releasing factor is an important mediator of both responses to stressors and serotonergic activity, subsequent experiments tested the hypothesis that central nucleus serotonergic response to restraint stress is mediated by central corticotropin-releasing factor receptors. Administration of the corticotropin-releasing factor type 1 and 2 receptor antagonist DPhe-CRF (icv, 10 μg/5 μl) prior to restraint stress suppressed restraint-induced serotonin release in the central nucleus. The results suggest that restraint stress rapidly and selectively increases serotonin release in the central nucleus of the amygdala by the activation of central corticotropin-releasing factor receptors. Furthermore, the results imply that corticotropin-releasing factor mediated serotonergic activity in central nucleus of the amygdala may be an important component of a stress response.

Voluntary exercise and increased food intake after mild chronic stress improve social avoidance behavior in mice

“…This latter finding suggests that DA metabolic ratio in the hippocampus is not involved in the exercise-induced improvement in social interaction. Serotonin is thought to be an important molecule in emotional stability [1,36], and there are some reports concerning the effect of exercise on changing 5-HT transporter expression [37]. Our present experiments showed that the 5-HT metabolite, 5-HIAA, was significantly decreased in the amygdala following SDS + exercise.…”

Neurobiology of Stress-Induced Reproductive Dysfunction in Female Macaques

“…Restraint stress, or activation of the corticotropin releasing hormone (CRH) receptor type 2 with intracerebroventricular urocortin, suppressed luteinizing hormone (LH) pulses in ovariectomized rats (Li et al , 2005). These effects may be mediated via the raphe serotonin system (Ruggiero et al , 1999; Pernar et al , 2004; Clark et al , 2007; Mo et al , 2008) or brainstem noradrenergic systems (Mitchell et al , 2005; Dunn and Swiergiel, 2008), as well as via hypothalamic circuits (MacLusky et al , 1988; Dobson et al , 2003). …”

Metabotropic Glutamate Receptor Subtype 8 in the Amygdala Modulates Thermal Threshold, Neurotransmitter Release, and Rostral Ventromedial Medulla Cell Activity in Inflammatory Pain

“…It has been shown that ( S)-3,4-DCPG increases glutamate and decreases GABA release consis-tently with PAG-antinociceptive descending system activation and consequent antinociception. Apart from GABA and glutamate, serotonin (5-hydroxytryptamine, 5-HT) also plays a role in controlling behavioral responses to unpleasant stimuli such as pain at CeA level (Mo et al, 2008). Reciprocal interactions between serotonin, glutamate, and GABA, which have been reported in the limbic system and pain matrix areas (Maione et al, 1998;Ciranna, 2006), have relevant meaning in both pain and pain-related anxiety as well as depression establishment and maintenance (Curzon, 1988;Wang and Nakai, 1994;Kalia, 2005;Phelps and LeDoux, 2005).…”