Role of dopamine D1 and D2 receptors in CRF-induced disruption of sensorimotor gating

Vinkers, Christiaan H.; Risbrough, Victoria B.; Geyer, Mark A.; Caldwell, Sorana; Low, Malcolm J.; Hauger, Richard L.

doi:10.1016/j.pbb.2007.01.018

Cited by 19 publications

(19 citation statements)

References 90 publications

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“…This is noteworthy because dopamine receptor agonists can decrease PPI at some intervals and increase PPI at others [13, 55, 56, 59]. The present findings, along with those of Vinkers et al [36], showing that CRF decreases PPI in both D 1 and D 2 receptor knockout mice, suggests that CRF does not decrease PPI via an indirect effect on dopamine. However, there are data that suggest otherwise.…”

Section: Discussionsupporting

confidence: 77%

“…For example, Meloni et al, [62] found that a selective D 1 receptor antagonist blocks the CRF-induced increase in startle amplitude. However, this is not so in mice, and both D 1 and D 2 receptor knockout mice show a CRF-induced increase in startle amplitude [36]. We have found that the effect of CRF on startle, but not PPI, is blocked by ketanserin, a 5-HT 2A/C antagonist [57].…”

Section: Discussionmentioning

confidence: 99%

“…CRF cell bodies and fibers are found in a number of brain regions [26], and CRF receptors are expressed in brain regions which mediate PPI such as the cortex, the hippocampus, the nucleus accumbens, and the basolateral nucleus of the amygdala [27,28,29,30,31]. We, and others, have shown that exogenously administered CRF diminishes PPI in rats [32,33,34] and mice [35,36], and CRF over-expressing mice show reduced PPI [37,38]. Further, the effect of CRF on PPI is mediated by the CRF 1 receptor, not by glucocorticoid receptors [39].…”

Section: Introductionmentioning

confidence: 99%

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Interaction between the effects of corticotropin-releasing factor and prepulse parameters on prepulse inhibition in two inbred rat strains and the F1 generation of a cross between them

Conti

Sutherland

Muhlhauser

2009

Behavioural Brain Research

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Levels of prepulse inhibition (PPI) depend on the interval between the startling and prepulse stimuli. Brown Norway rats show less PPI of the acoustic startle response than Wistar-Kyoto (WKY) rats when the interval between the prepulse and startling stimulus is 100 msec. Central administration of corticotropin-releasing factor (CRF) decreases PPI at this inter-stimulus interval. Here, the effect of CRF on PPI over a range of inter-stimulus intervals was examined in WKY and BN rats, and in the F1 generation of a cross between them. Rats received an intracerebroventricular infusion of either saline or CRF 30 min prior to testing PPI. Test trials included startle stimulus alone trials, and trials on which a prepulse stimulus of either 6, 12, or 15 dB above background preceded the startling stimulus by either 20, 75, 100, 500 or 2000 msec. CRF decreased PPI in WKY rats at all inter-stimulus intervals and all prepulse intensities, while the effect of CRF on PPI in BN rats only occurred at intermediate intervals. BN and WKY rats showed different levels of PPI only at the intermediate intervals. Baseline PPI in the F1 rats resembled the WKY phenotype. The CRF-induced change in PPI in the F1 generation has some qualities of the effects in each of the progenitor strains. These results suggest that both the effect of rats strain and of CRF on PPI depend on the inter-stimulus interval, and that there is an interaction between prepulse stimulus intensity and the inter-stimulus interval.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Interaction between the effects of corticotropin-releasing factor and prepulse parameters on prepulse inhibition in two inbred rat strains and the F1 generation of a cross between them

Conti

Sutherland

Muhlhauser

2009

Behavioural Brain Research

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“…For instance, increased dopamine transmission has been shown to increase startle responses (Davis and Aghajanian 1976; Davis 1980; Davis et al 1986) and dopamine D1 receptor activation mediates CRF effects on startle in rats (Meloni et al 2006). However, in mice CRF-induced startle is unaffected by the genetic disruption and pharmacological blockade of D1 or D2 receptors suggesting species differences in the signaling transduction pathways mediating CRF effects on startle (Vinkers et al 2007). In mice, we have found that noradrenergic transmission via α1 receptor activation plays a permissive role in CRFinduced startle hyperreactivity (Gresack and Risbrough 2011).…”

Section: Discussionmentioning

confidence: 99%

The role of PKC signaling in CRF-induced modulation of startle

et al. 2013

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Rationale Hypersignaling of corticotropin releasing factor (CRF) has been implicated in stress disorders, however many of its downstream mechanisms of action remain unclear. In vitro, CRF1 receptor activation initiates multiple cell signaling cascades, including protein kinase A (PKA), protein kinase C (PKC) and mitogen-activated protein kinase kinase MEK1/2 signaling. It is unclear however, which of these signaling cascades mediate CRF-induced behaviors during stress. Objectives We examined the role of PKA, PKC and MEK1/2 signaling pathways in CRF-induced anxiety as measured by startle hyperreactivity. Methods Mice treated with intracerbroventricular (ICV) ovine CRF (oCRF) were pretreated with the PKA inhibitor Rp-cAMPS, PKC inhibitor BIM (bisindolylmaleimide) or MEK1/2 inhibitor PD98059 (ICV) and assessed for acoustic startle reactivity. Results The PKC inhibitor BIM significantly attenuated CRF-induced increases in startle. BIM was also able to block startle increases induced by oCRF when both compounds were infused directly into the bed nucleus of stria terminalis (BNST). PKA and MEK1/2 inhibition had no significant effects on CRF-induced changes in startle at the dose ranges tested. CRF-induced disruption of PPI was not significantly reversed by any of the 3 pretreatments at the dose ranges tested. Conclusions PKC signaling is required for CRF-induced increases in startle, and this effect is mediated at least in part at the BNST. These findings suggest PKC signaling cascades: 1) may be important for the acute effects of CRF to induce startle hyperreactivity, and 2) support further research of the role of PKC signaling in startle abnormalities relevant to disorders such as posttraumatic stress disorder.

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“…In fact, Meloni et al (2006a) reported that CRF-enhanced startle, in rats, is blocked by systemic injections of the D1 receptor antagonist SCH 23390. Vinkers et al (2007) were unable to replicate this in mice however, and also reported normal CRF-enhanced startle in D1-receptor knockouts. They suggested that species or dosage differences (including non-selectivity at the doses used by Meloni and colleagues) may have accounted for the different outcomes of those two studies.…”

Section: A Specific Neural Circuit For Sustained Fearmentioning

confidence: 92%

Selective participation of the bed nucleus of the stria terminalis and CRF in sustained anxiety-like versus phasic fear-like responses

Walker

Miles

Davis

2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

293

272

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The medial division of the central nucleus of the amygdala (CeA M ) and the lateral division of the bed nucleus of the stria terminalis (BNST L ) are closely related. Both receive projections from the basolateral amygdala (BLA) and both project to brain areas that mediate fear-influenced behaviors. In contrast to CeA M however, initial attempts to implicate the BNST in conditioned fear responses were largely unsuccessful. More recent studies have shown that the BNST does participate in some types of anxiety and stress responses. Here, we review evidence suggesting that the CeA M and BNST L are functionally complementary, with CeA M mediating short-but not long-duration threat responses (i.e., phasic fear) and BNST L mediating long-but not short-duration responses (sustained fear or 'anxiety'). We also review findings implicating the stress-related peptide corticotropin-releasing factor (CRF) in sustained but not phasic threat responses, and attempt to integrate these findings into a neural circuit model which accounts for these and related observations. Keywords anxiety; startle; amygdala; bed nucleus of the stria terminalis; corticotropin releasing factor A now-familiar and widely-adopted neural circuit model of fear places the amygdala in center stage and assigns different functions to different amygdala subdivisions (Fig. 1). Thus, the basolateral group (BLA) screens incoming sensory information for threat cues and, if such cues are detected, passes this information on to the central nucleus of the amygdala's medial subdivision (CeA M ), which mediates threat responses by way of its many projections to areas that mediate specific fear-influenced behaviors (c.f., Davis, 1992;Fanselow and LeDoux, 1999;Maren, 2001;Pare et al., 2004).In the following pages, we review evidence suggesting that this model is incomplete, and should be expanded to include the bed nucleus of the stria terminalis (specifically, it's lateral subdivision -BNST L ). In fact, by many criteria, the CeA and BNST are closely related (Alheid © 2009 Elsevier Inc. All rights reserved.Correspondence should be addressed to: David L. Walker, Emory University School of Medicine, 954 Gatewood Road NE, Yerkes Neurosci Bldg -Rm 5214, Atlanta, GA 30329, Ph: (404) Fax: (404) 727-8070, dlwalke@emory.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptProg Neuropsychopharmacol Biol Psychiatry. Author manuscript; available in PMC 2010 November 13. Published in final edited form as:Prog Neuropsychopharmacol Biol Psychiatry. Alheid and Heimer, 1988;Johnston, 1923). Of par...

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Role of dopamine D1 and D2 receptors in CRF-induced disruption of sensorimotor gating

Cited by 19 publications

References 90 publications

Interaction between the effects of corticotropin-releasing factor and prepulse parameters on prepulse inhibition in two inbred rat strains and the F1 generation of a cross between them

Interaction between the effects of corticotropin-releasing factor and prepulse parameters on prepulse inhibition in two inbred rat strains and the F1 generation of a cross between them

The role of PKC signaling in CRF-induced modulation of startle

Selective participation of the bed nucleus of the stria terminalis and CRF in sustained anxiety-like versus phasic fear-like responses

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