The behavioral phenotype of pituitary adenylate-cyclase activating polypeptide-deficient mice in anxiety and depression tests is accompanied by blunted c-Fos expression in the bed nucleus of the stria terminalis, central projecting Edinger–Westphal nucleus, ventral lateral septum, and dorsal raphe nucleus

Gaszner, Balázs; Kormos, Viktória; Kozicz, Tamás; Hashimoto, Hitoshi; Reglődi, Dóra; Helyes, Zsuzsanna

doi:10.1016/j.neuroscience.2011.11.046

Cited by 92 publications

(75 citation statements)

References 74 publications

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“…This observation is in agreement with earlier findings [33][34][35]. When the animals were pretreated with different receptor antagonists, some antagonists proved to eliminate the anxiogenic action of PACAP-38.…”

Section: Discussionsupporting

confidence: 93%

Neurotransmitter-mediated anxiogenic action of PACAP-38 in rats

Telegdy

Adamik

2015

Behavioural Brain Research

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Section: Discussionsupporting

confidence: 93%

Neurotransmitter-mediated anxiogenic action of PACAP-38 in rats

Telegdy

Adamik

2015

Behavioural Brain Research

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“…PACAPergic synapses are also found on CRH-expressing neurons in the BNST of the rat (Kozicz et al, 1997), an area in which PACAP expression is up-regulated by both stress and CORT (Lezak et al, 2014), and in which PACAP infusion causes anxious behavior (Hammack et al, 2009), and infusion of the PAC1 receptor antagonist PACAP(6-38) antagonizes both anorexia and CORT elevation in response to chronic stress (Roman et al, 2014). The BNST is also a site of PACAP-dependent regulation of both c-fos and fos-B expression as a result of chronic stress (Gaszner et al, 2012; Lehmann et al, 2013). PACAP infusion into the central amygdala decreases active coping in response to stress (Legradi et al, 2007), consistent with PACAPergic innervation patterns of this brain area (Piggins et al, 1996; Schafer et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Activation of the HPA axis and depression of feeding behavior induced by restraint stress are separately regulated by PACAPergic neurotransmission in the mouse

Jiang

Eiden

2016

Stress

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We measured serum CORT elevation in wild-type and PACAP-deficient C57Bl/6N male mice after acute (1 hr) or prolonged (2–3 hr) daily restraint stress for seven days. The PACAP-dependence of CORT elevation was compared to that of stress-induced hypophagia. Daily restraint induced unhabituated peak CORT elevation, and hypophagia/weight loss, of similar magnitude for 1, 2 and 3 hr of daily restraint, in wild-type mice. Peak CORT elevation, and hypophagia, were both attenuated in PACAP-deficient mice for 2 and 3 hrs daily restraint. Hypophagia induced by 1-hr daily restraint was also greatly reduced in PACAP-deficient mice, however CORT elevation, both peak and during recovery from stress, was unaffected. Thus, hypothalamic PACAPergic neurotransmission appears to affect CRH gene transcription and peptide production, but not CRH release, in response to psychogenic stress. A single exposure to restraint sufficed to trigger hypophagia over the following 24 hours. PACAP deficiency attenuated HPA axis response (CORT elevation) to prolonged (3 hr) but not acute (1 hr) single-exposure restraint stress, while hypophagia induced by either a single 1 hr or a single 3 hr restraint were both abolished in PACAP-deficient mice. These results suggest that PACAP’s actions to promote suppression of food intake following an episode of psychogenic stress is unrelated to the release of CRH into the portal circulation to activate the pituitary-adrenal axis. Furthermore, demonstration of suppressed food intake after a single 1-hr restraint stress provides a convenient assay for investigating the location of the synapses and circuits mediating the effects of PACAP on the behavioral sequelae of psychogenic stress.

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“…PACAP and PAC1 receptors are selectively upregulated in the BNST following chronic variate stress, and BNST PACAP activation is anxiogenic (Hammack et al, 2009). PACAP and PAC1 receptor null mice also demonstrate reduced anxiety-like behavior (Hashimoto et al, 2001; Otto et al, 2001; Gaszner et al, 2012; Hattori et al, 2012), and the glucocorticoid response in PACAP null animals is altered after stressor exposure (Morita et al, 2006; Hatanaka et al, 2008; Stroth and Eiden, 2010; Tsukiyama et al, 2011; Lehmann et al, 2013). In humans, PACAP dysregulation has recently been associated with a number of psychopathologies including post-traumatic stress disorder (PTSD).…”

Section: Introductionmentioning

confidence: 99%

PAC1 receptor antagonism in the bed nucleus of the stria terminalis (BNST) attenuates the endocrine and behavioral consequences of chronic stress

Roman¹,

Lezak²,

Hartsock³

et al. 2014

Psychoneuroendocrinology

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Summary Chronic or repeated stressor exposure can induce a number of maladaptive behavioral and physiological consequences and among limbic structures, the bed nucleus of the stria terminalis (BNST) has been implicated in the integration and interpretation of stress responses. Previous work has demonstrated that chronic variate stress (CVS) exposure in rodents increases BNST pituitary adenylate cyclase activating polypeptide (PACAP, Adcyap1) and PAC1 receptor (Adcyap1r1) transcript expression, and that acute BNST PACAP injections can stimulate anxiety-like behavior. Here we show that chronic stress increases PACAP expression selectively in the oval nucleus of the dorsolateral BNST in patterns distinct from those for corticotropin releasing hormone (CRH). Among receptor subtypes, BNST PACAP signaling through PAC1 receptors not only heightened anxiety responses as measured by different behavioral parameters but also induced anorexic-like behavior to mimic the consequences of stress. Conversely, chronic inhibition of BNST PACAP signaling by continuous infusion with the PAC1 receptor antagonist PACAP(6-38) during the week of CVS attenuated these stress-induced behavioral responses and changes in weight gain. BNST PACAP signaling stimulated the hypothalamic-pituitary-adrenal (HPA) axis and heightened corticosterone release; further, BNST PACAP(6-38) administration blocked corticosterone release in a sensitized stress model. In aggregate with recent associations of PACAP/PAC1 receptor dysregulation with altered stress responses including post-traumatic stress disorder, these data suggest that BNST PACAP/PAC1 receptor signaling mechanisms may coordinate the behavioral and endocrine consequences of stress.

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Cited by 92 publications

References 74 publications

Neurotransmitter-mediated anxiogenic action of PACAP-38 in rats

Neurotransmitter-mediated anxiogenic action of PACAP-38 in rats

Activation of the HPA axis and depression of feeding behavior induced by restraint stress are separately regulated by PACAPergic neurotransmission in the mouse

PAC1 receptor antagonism in the bed nucleus of the stria terminalis (BNST) attenuates the endocrine and behavioral consequences of chronic stress

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