CRF type 1 receptors in the dorsal periaqueductal gray modulate anxiety-induced defensive behaviors

Litvin, Yoav; Pentkowski, Nathan S.; Blanchard, D. Caroline; Blanchard, Robert J.

doi:10.1016/j.yhbeh.2007.04.012

Cited by 34 publications

(20 citation statements)

References 57 publications

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“…To the best of our knowledge, the present studies are the first to specifically characterize and quantify the burying response to i.c.v. CRF administration, though this response has been previously reported in mice (Litvin et al 2007) and rats (Korte et al 1993;Price et al 1998;Wiersma et al 1995) and could only be seen if bedding material were present. Although the burying response evoked by CRF appeared almost identical to behaviors directed towards the electrified probe in the defensive burying response, the occurrence of burying in the absence of a specific aversive stimulus made the behavior appear spontaneous as reported following muscimol injected into the nucleus accumbens (Reynolds and Berridge, 2001).…”

Section: Characterization Of Crf-evoked Behaviorsmentioning

confidence: 70%

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

et al. 2008

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Rationale-Central administration of corticotropin-releasing factor (CRF) elicits a specific pattern of behavioral responses resembling a stress-like state, and is anxiogenic in rodent models of anxiety.Objectives-Specific behaviors evoked by the administration of CRF were measured. The roles of CRF receptor subtypes and that of serotonergic and noradrenergic systems in mediating these responses were studied.Methods-Burying, grooming and head shakes were quantified in rats following intracerebroventricular administration of CRF and urocortin II and after pretreatment with antagonists. The role of forebrain norepinephrine in the behavioral responses to CRF (0.3 μg) was examined following pretreatment with the neurotoxin DSP-4 and that of serotonin after depletion using systemic administration of para-chlorophenylalanine (p-CPA).Results-CRF at 0.3 and 3.0 μg caused robust increases in burying, grooming and head shakes, but urocortin II was ineffective. Pretreatment with either antalarmin or propranolol significantly attenuated the CRF-evoked behaviors. Destruction of forebrain NE pathways blocked spontaneous burying behavior elicited by CRF and conditioned burying directed towards an electrified shock probe. In contrast, depletion of 5-HT selectively attenuated CRF-evoked grooming.Conclusions-Overt behavioral responses produced by CRF, burying, grooming, and head shakes, appeared to be mediated through the CRF 1 receptor. Spontaneous burying behavior evoked by CRF or conditioned burying directed towards a shock probe were disrupted by lesion of the dorsal noradrenergic bundle and may represent anxiety-like behavior caused by CRF activation of the LC. In contrast, CRF-evoked increases in grooming were dependent on serotonin.

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Section: Characterization Of Crf-evoked Behaviorsmentioning

confidence: 70%

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

et al. 2008

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“…The PAG is a well-known brain center processing pain signals and other functions (Behbehani, 1995). For instance, some studies showed that CRF acts in the PAG via CRF 1 receptors to induce defensive behavior (Borelli and Brandao, 2008; Litvin et al, 2007). The newly identified CRF-ir neurons in the ventral median PAG provide additional anatomical evidence that CRF plays a role in functions involving PAG pathways.…”

Section: Discussionmentioning

confidence: 99%

Comparison of CRF-immunoreactive neurons distribution in mouse and rat brains and selective induction of Fos in rat hypothalamic CRF neurons by abdominal surgery

et al. 2011

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Mice and rats are widely used in stress-related behavioral studies while little is known about the distribution of the stress hormone, corticotropin-releasing factor (CRF) in the mouse brain. We developed and characterized a novel rat/mouse CRF polyclonal antibody (CURE ab 200101) that was used to detect and compare the brain distributions of CRF immunoreactivity in naïve and colchicine-treated rats and mice. We also assessed whether the visceral stressor of abdominal surgery activated brain CRF neurons using double labeling of Fos/CRF in naïve rats. CRF-ir neurons were visualized in the cortex, bed nucleus of the stria terminalis, central amygdala, hypothalamic paraventricular nucleus (PVN), Barrington’s nucleus and dorsolateral tegmental area in naïve rats. CRF-immunoreactive (ir) neurons in the mouse brain were detected only after colchicine. The pattern shows fundamental similarity compared to the colchicine-treated rat brain, however, there were differences with a lesser distribution in both areas and density except in the lateral septum and external subnucleus of the lateral parabrachial nucleus which contained more CRF-ir neurons in mice, and CRF-ir neurons in the dorsal motor nucleus of the vagus were found only in mice. Abdominal surgery in naïve rats induced Fos-ir in 30% of total CRF-ir neurons in the PVN compared with control (anesthesia alone) while Fos was not co-localized with CRF in other brain nuclei. These data indicate that CRF-ir distribution in the brain displays similarity as well as distinct features in mice compared to rats that may underlie some differential stress responses. Abdominal surgery activates CRF-ir neurons selectively in the PVN of rats without colchicine treatment.

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“…For example, direct injections of corticotrophin-releasing hormone (CRH), substance P or cholecystokinin (CCK) into the dPAG produce anxiogeniclike effects (22-24). …”

Section: Classical Neurotransmitters the Pag And Defensive Behaviorsmentioning

confidence: 99%

Fine-tuning of defensive behaviors in the dorsal periaqueductal gray by atypical neurotransmitters

Fogaça

Lisboa

Aguiar

et al. 2012

Braz J Med Biol Res

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This paper presents an up-to-date review of the evidence indicating that atypical neurotransmitters such as nitric oxide (NO) and endocannabinoids (eCBs) play an important role in the regulation of aversive responses in the periaqueductal gray (PAG). Among the results supporting this role, several studies have shown that inhibitors of neuronal NO synthase or cannabinoid type 1 (CB1) receptor agonists cause clear anxiolytic responses when injected into this region. The nitrergic and eCB systems can regulate the activity of classical neurotransmitters such as glutamate and γ-aminobutyric acid (GABA) that control PAG activity. We propose that they exert a ‘fine-tuning’ regulatory control of defensive responses in this area. This control, however, is probably complex, which may explain the usually bell-shaped dose-response curves observed with drugs that act on NO- or CB1-mediated neurotransmission. Even if the mechanisms responsible for this complex interaction are still poorly understood, they are beginning to be recognized. For example, activation of transient receptor potential vanilloid type-1 channel (TRPV1) receptors by anandamide seems to counteract the anxiolytic effects induced by CB1 receptor activation caused by this compound. Further studies, however, are needed to identify other mechanisms responsible for this fine-tuning effect.

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CRF type 1 receptors in the dorsal periaqueductal gray modulate anxiety-induced defensive behaviors

Cited by 34 publications

References 57 publications

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

Comparison of CRF-immunoreactive neurons distribution in mouse and rat brains and selective induction of Fos in rat hypothalamic CRF neurons by abdominal surgery

Fine-tuning of defensive behaviors in the dorsal periaqueductal gray by atypical neurotransmitters

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