Temporary Inactivation of the Bed Nucleus of the Stria Terminalis But Not of the Amygdala Blocks Freezing Induced by Trimethylthiazoline, a Component of Fox Feces

Fendt, Markus; Endres, Thomas; Apfelbach, Raimund

doi:10.1523/jneurosci.23-01-00023.2003

Cited by 257 publications

(207 citation statements)

References 39 publications

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“…The present study demonstrates that rats exposed to a ferret engage in anxiety-related BI which is consistent with previous reports demonstrating that rats exposed to cat or cat odors display an increase in fear-related behavioral responses such as freezing, avoidance and riskassessment (Blanchard et al, 1989;McGregor et al, 2002). Results with fox odor have been less consistent with some reports of increased freezing when a rat is presented with the synthetic compound 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) derived from the fox anal gland (Wallace and Rosen, 2000;Fendt et al, 2003), whereas other reports fail to demonstrate any fear-related behavioral responses to TMT (McGregor et al, 2002). It is possible that the differences between cat and fox odor result from the type of odor used (odor from fur/skin for cat versus odor from synthetic compound TMT for fox) and variations in the intensity of the odor stimulus that was employed (Takahashi et al, 2005).…”

Section: Discussionsupporting

confidence: 86%

“…Some studies suggest that the CeA is not involved in unconditioned fear responses as indicated by a lack of an effect of CeA lesions on rat freezing behavior elicited by cat or fox odor (Fendt et al, 2003;Li et al, 2004;Rosen, 2004). In terms of c-fos expression, studies have demonstrated no increase in cfos expression in the CeA following exposure to cat odor (Dielenberg et al, 2001) or ferret odor (Masini et al, 2005); whereas, another study reported a significant increase in the number of Fos-positive cells in the CeA in rats following fox odor exposure .…”

Section: Discussionmentioning

confidence: 99%

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Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Roseboom

Nanda

Bakshi

et al. 2007

Psychoneuroendocrinology

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SummaryBehavioral inhibition (BI) is an adaptive defensive response to threat; however, extreme BI is associated with anxiety-related psychopathology. When rats are exposed to a natural predator they display stress-and anxiety-related behavioral alterations and physiological activation. To develop a preclinical rodent model to study mechanisms underlying human BI and anxiety, we examined the extent to which ferret exposure elicits anxiety-related BI and HPA and amygdala activation of the CRF system. In the first experiment, BI and other behaviors were assessed in the presence or absence of a ferret. In the second experiment, ferret-induced corticosterone release and changes in brain cfos expression were assessed. In the final experiment, gene chip and quantitative real time-PCR analyses were performed on amygdala tissue from control and ferret-exposed rats. Ferret exposure increased BI and submissive posturing, as well as plasma corticosterone and the number of Fospositive cells in several brain regions including the amygdala. Gene expression analysis revealed increased amygdalar mRNA for CRF-binding protein, but not the CRF 1 receptor, CRF 2 receptor or CRF. In rodents, ferret exposure can be used to elicit anxiety-related BI, which is associated with HPA and amygdala activation. Since the amygdala and the CRF system have been implicated in adaptive and maladaptive anxiety responses in humans, these data support use of our rodent model to further investigate mechanisms underlying anxiety-related psychopathology in humans.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Roseboom

Nanda

Bakshi

et al. 2007

Psychoneuroendocrinology

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“…Besides the fact that subnuclei of the amygdala may be differently involved in the mediation of associative and nonassociative fear responses (see Fendt et al, 2003), a large body of evidence agrees with the idea that the BLA is involved in emotional pavlovian learning, neural plasticity, and storage of emotional memory. In turn, this learned information critically influences the coordination of emotional responses mediated by a number of brain structures (Maren, 2001).…”

Section: Discussionsupporting

confidence: 55%

Increased Fear Learning Coincides with Neuronal Dysinhibition and Facilitated LTP in the Basolateral Amygdala following Benzodiazepine Withdrawal in Rats

Isoardi

Martijena

Carrer

et al. 2004

Neuropsychopharmacol

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Animals chronically administered with diazepam (DZM -2 mg/kg/day i.p.) or vehicle (VEH) for 21 days were tested in a fear-conditioning paradigm 4 days after the last administration. Increased freezing was observed in DZM withdrawn rats as compared to VEH injected control rats in both associative and nonassociative context and this increase was greatest for the DZM withdrawal group in the paired context. In animals anesthetized with urethane, single pulses in the medial prefrontal cortex evoked a field potential including a population spike (PS) in the basolateral complex of the amygdala (BLA) of control animals, whereas in DZM withdrawn animals multiple PSs were evoked. In brain slices from control rats, stimulation of the external capsule evoked a field potential including a PS in the BLA, whereas in DZM withdrawn rats multiple PSs were evoked. The amplitude of the PS was smaller in slices obtained from DZM withdrawn rats than from control rats, and paired pulse inhibition was significantly less in the former. Perfusion with DZM 2 mM of slices obtained from DZM withdrawn rats eliminated repetitive spiking. GABAergic blockade with 50 mM picrotoxin in control rats resulted in the appearance of multiple secondary PSs. In slices from DZM withdrawn rats high-frequency stimulation induced a highly significant potentiation that lasted at least 2 h (LTP), whereas in control rats the same stimulation did not induce LTP. Neuronal hyperexcitability leading to facilitated LTP observed in BLA of DZM withdrawn rats could be due to depressed GABAergic activity (dysinhibition). The increased synaptic plasticity may be at the root of the increased fear learning observed in withdrawn animals.

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“…The bed nucleus of the stria terminalis (BNST) is thought to be a key structure for mediating anxiety-like responses elicited by unconditioned or ethologically valid threats (Lee and Davis, 1997;Walker and Davis, 1997;Davis and Shi, 1999;Fendt et al, 2003), and is a key structure that relays and integrates limbic and autonomic information related to stress responses (Cullinan et al, 1993;Forray and Gysling, 2004;Herman et al, 2004). The BNST has also been identified as an area critical for stress-induced reinstatement of drug-seeking behaviors, and for the increased anxiety associated with protracted withdrawal (Erb and Stewart, 1999;Leri et al, 2002;Aston-Jones and Harris, 2004).…”

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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Temporary Inactivation of the Bed Nucleus of the Stria Terminalis But Not of the Amygdala Blocks Freezing Induced by Trimethylthiazoline, a Component of Fox Feces

Cited by 257 publications

References 39 publications

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Increased Fear Learning Coincides with Neuronal Dysinhibition and Facilitated LTP in the Basolateral Amygdala following Benzodiazepine Withdrawal in Rats

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

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