Corticotropin-releasing factor modulates defensive-withdrawal and exploratory behavior in rats.

Takahashi, Lorey K.; Kalin, Ned H.; Burgt, Jennifer A. Vanden; Sherman, Jack E.

doi:10.1037/0735-7044.103.3.648

Cited by 176 publications

(99 citation statements)

References 47 publications

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“…The DW test (Takahashi et al, 1989) used a modified setup of the open field activity box. This open field (100 x 100 cm with 50 cm side walls) contained a dark grey PVC tube (diameter 10 × 21 cm), dividing the total area into two compartments: an illuminated area and a dark area.…”

Section: 1 Defensive Withdrawalmentioning

confidence: 99%

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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Short title:Stress-related behavior in Brattleboro rat after DDAVP treatment You created this PDF from an application that is not licensed to print to novaPDF printer (http://www.novapdf.com) Balázsfi et al. 2Highlights  The effect of AVP on affective and memory symptoms is due to its central role  DDAVP treatment compensated the peripheral effects of congenital AVP absence  DDAVP did not significantly alter the behavior of KO animals in the paradigms tested  AVP signaling in the medial amygdala contributes to the behavioral effect measured in FS AbstractBeside its hormonal function in salt and water homeostasis, vasopressin -released into distinct brain areas -plays a crucial role in stress-related behavior resulting in the enhancement of an anxious/depressive-like state.We aimed to investigate whether correction of the peripheral symptoms of congenital absence of AVP also corrects the behavioral alterations in AVP-deficient Brattleboro rats. Wild type (WT) and vasopressin-deficient (KO) male Brattleboro rats were tested.Half of the KO animals were treated by desmopressin (V2-receptor agonist) via osmotic minipump (subcutaneous) to eliminate the peripheral symptoms of vasopressin-deficiency. Anxiety was studied by elevated plus maze (EPM), defensive withdrawal (DW) and marble burying (MB) tests, while depressive-like changes were monitored in forced swimming (FS) and anhedonia by sucrose preference test. Cell activity was examined in septum and amygdala by c-Fos immunohistochemistry after 10min FS.

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Section: 1 Defensive Withdrawalmentioning

confidence: 99%

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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“…The emergence test was conducted as described previously (Holmes et al, 2003b;Smith et al, 1998;Takahashi et al, 1989). The apparatus consisted of an opaque black Plexiglas cube (16 Â 16 Â 19 cm 3 ) with an exit (6 Â 4 cm 2 ) on one side at floor level.…”

Section: Emergence Testmentioning

confidence: 99%

Reduced Anxiety and Depression-Like Behaviors in Mice Lacking GABA Transporter Subtype 1

Liu

Cai

et al. 2006

Neuropsychopharmacol

117

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g-Aminobutyric acid (GABA) transporter subtype 1 (GAT1), which transports extracellular GABA into presynaptic neurons, plays an important regulatory role in the function of GABAergic systems. However, the contributions of the GAT1 in regulating mental status are not fully understood. In this paper, we observed the behavioral alterations of GAT1 knockout (GAT1 À/À ) mice using several depressionand anxiety-related models (eg, the forced-swimming test and the tail-suspension test for testing depression-related behaviors; the openfield test, the dark-light exploration test, the emergence test, and the elevated plus maze (EPM) test for anxiety-related behaviors). Here we found that GAT1 À/À mice showed a lower level of depression-and anxiety-like behaviors in comparison to wild-type mice. Furthermore, GAT1 À/À mice exhibited measurable insensitivity to selected antidepressants and anxiolytics such as fluoxetine, amitriptyline, buspirone, diazepam, and tiagabine in the tail-suspension test and/or the EPM test. Moreover, the basal level of corticosterone was found to be significantly lower in GAT1 À/À mice. These results showed that the absence of GAT1 affects mental status through enhancing the GABAergic system, as well as modifying the serotonergic system and the hypothalamic-pituitary-adrenal (HPA) activity in mice.

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“…Thus, CRF given centrally induces anxiogenic behaviors in various animal models, such as open field (Britton et al, 1982;Liang and Lee, 1988;Takahashi et al, 1989), EPM (Baldwin et al, 1991), conflict test (Britton et al, 1985), social interaction (SI) (Dunn and File, 1987), acoustic startle (Swerdlow et al, 1986;Liang et al, 1992), and conditioned fear response (Cole and Koob, 1988). So far, two CRF receptor subtypes, CRF 1 and CRF 2 , have been identified (De Souza et al, 1985;Chalmers et al, 1995;Perrin and Vale, 1999;Dautzenberg and Hauger, 2002).…”

Section: Introductionmentioning

confidence: 99%

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

Lee

Fitz

Johnson

et al. 2008

Neuropsychopharmacol

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Increased extra-hypothalamic corticotrophin-releasing factor (CRF) neurotransmission has been suggested as one putative factor in the pathophysiology of anxiety disorders. We have previously reported that administering repeated subanxiogenic doses (termed 'priming') of the CRF receptor agonist urocortin 1 (Ucn1) into the basolateral amygdala (BLA) of rats elicited long-lasting behavioral changes in social interaction (SI) and elevated plus maze (EPM) tests of anxiety. Although substantial similarity exists, the bed nucleus of the stria terminals (BNST) and the amygdala are thought to play distinct roles in anxiety responses. Rats primed with Ucn1 in the BLA not only demonstrated increased anxiety-like behaviors, but also physiological sensitivity to intravenous sodium lactate infusions, which is seen in subjects with panic or posttraumatic stress disorders, but not social or generalized anxiety disorders. In the present study, we tested if similar priming with subanxiogenic doses of Ucn1 in the BNST of rats will induce either chronic anxiety or sensitivity to sodium lactate. After determining the dose of Ucn1 that is subanxiogenic when injected into the BNST, repeated intra-BNST injections of this subanxiogenic dose of Ucn1 (6 fmol/100 nl) elicited persistent (present even after 4 weeks) anxiety-like responses in the SI but not EPM test. Prior local injection of a CRF receptor antagonist, astressin, into the BNST blocked this effect. Unlike Ucn1 priming in the BLA, rats primed in the BNST showed no cardiovascular changes following lactate infusion. Thus, BNST priming appears to selectively model the pathophysiology of subjects with anxiety syndromes like social anxiety, which are not lactate sensitive.

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Corticotropin-releasing factor modulates defensive-withdrawal and exploratory behavior in rats.

Cited by 176 publications

References 47 publications

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Reduced Anxiety and Depression-Like Behaviors in Mice Lacking GABA Transporter Subtype 1

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

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