Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ganglionic blocking agents, chlorisondamine (CL) and hexamethonium (HEX) were used to examine the role of altered autonomic function in the behavioral response to i.c.v.-administered corticotropin-releasing factor (CRF). Animals were tested in either a novel modified open field or in their home cages. CRF-induced alterations in locomotion, grooming and eating were assessed in both environments in the presence or absence of CL or HEX. In the home cage the ability of CRF to increase grooming was attenuated by pretreatment with either CL or HEX. In the modified open field only HEX significantly suppressed grooming. In the familiar environment CRF-induced increases in locomotion were significantly inhibited by CL. However, in a novel environment, where CRF suppresses locomotion, CL was inactive. The competitive ganglionic nicotinic blocking agent, HEX, on the other hand, inhibited both the increased locomotion produced by CRF in the home cage and also the decreased locomotion induced by CRF in the modified open field. CRF suppression of food consumption was attenuated by CL. These results indicate that while centrally-mediated activation of the sympathetic nervous system cannot account for the full magnitude of the behavioral effects of i.c.v. CRF, such activation may play a part in both the locomotor activating components of the CRF response seen in the familiar environment as well as the suppressive effects seen in the novel environment.
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PMID:Effects of ganglionic blocking agents on behavioral responses to centrally administered CRF. 256 99

A series of experiments examined the effects of systemic administration of the beta adrenergic antagonist propranolol on the enhanced conditioned fear and the locomotor hyperactivity induced by central administration of corticotropin releasing factor (CRF). In Experiment 1, CRF (0.5 microgram) was shown to reduce responding in both the conditioned stimulus (cs) and the pre-cs components of an on-the-base-line conditioned suppression schedule. The effects of CRF on cs, but not pre-cs responding were antagonized by propranolol, at doses (2.5, 5.0 and 10.0 mg/kg) that did not affect responding themselves. This reversal of the anxiogenic effects of CRF by propranolol was specific to l- and not d-propranolol, showing that it did not result from nonspecific membrane stabilization. Propranolol also failed to reverse the reduced responding induced by the benzodiazepine inverse agonist FG 7142 in this schedule. In Experiment 2, propranolol was shown to potentiate the locomotor hyperactivity induced by CRF in a familiar photocell cage. These results suggest that activation of beta adrenoceptors may be an important mechanism in the behavioral inhibition induced by CRF, and that the neurochemical mechanisms that underlie the "anxiogenic" and the "activating" behavioral effects of CRF are neuropharmacologically distinct.
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PMID:Propranolol antagonizes the enhanced conditioned fear produced by corticotropin releasing factor. 284 75

Corticotropin-releasing factor (CRF) has behavioral activating effects when injected intracerebroventricularly in rats. CRF dose-dependently increased activity in a familiar photocell cage environment. This activation persisted after hypophysectomy, opiate receptor blockade, and low-dose dopamine receptor blockade, which suggests a unique mechanism of action. CRF also improved acquisition of a visual discrimination task. In aversive situations such as an open field test CRF produced behavioral changes consistent with increased emotionality. These results suggest that CRF liberated directly into the central nervous system may have a neurotropic action important for mobilizing behavioral responses to stress.
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PMID:Corticotropin-releasing factor and behavior. 387 12

Corticotropin-releasing factor injected intracerebroventricularly in a dose of 1 microgram produced a prolonged locomotor activation (3 h) in rats previously habituated to the test cage environment. This activation was reversed by alpha-flupenthixol (intraperitoneally), a dopamine receptor antagonist, only at cataleptic doses and not at all by naloxone (subcutaneously) in doses of 0.02-5.0 mg/kg. The effective dose 50% (ED50) for the alpha-flupenthixol reversal of locomotor activity induced by corticotropin-releasing factor was 0.13 mg/kg; similar to the 0.14 mg/kg ED50 needed to reverse the locomotor activation produced by caffeine (10 mg/kg s.c.). The ED50 necessary to reverse amphetamine (0.75 mg/kg s.c.) locomotion with this drug was 0.07 mg/kg. The results suggest that the corticotropin-releasing factor acts independently of direct activation of the dopamine or opioid peptide systems.
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PMID:Effects of alpha-flupenthixol and naloxone on CRF-induced locomotor activation. 609 52

Corticotropin-releasing factor was administered into the lateral cerebral ventricles of rats. Sixty minutes later, animals were tested in an open field conflict test or in their home cages for a variety of behaviors which have been shown to be related to the degree of responsiveness to novelty. CRF, in a dose related fashion, altered the frequency of those behaviors which are normally expressed in response to the novel environment. Specifically, CRF caused an increase in grooming and decreases in the amount of rearing, the number of approaches to a food pellet placed in the center of the open field, the amount of food eaten in both the open field and the home cage and a decrease in the mean amount of food eaten per approach to the food pedestal.
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PMID:Intraventricular corticotropin-releasing factor enhances behavioral effects of novelty. 698 18

The effect of corticotropin-releasing factor (CRF) on ultrasonic vocalizations (USVs) and other behaviors of isolated rat pups was examined at 5/6-, 9/10-, and 13/14-days. The hypothesis tested was that central CRF affects USV rate biphasically: as endogenous CRF increases from low basal levels it initiates USV production, but at higher levels CRF diminishes USV production. As predicted, the largest doses of CRF (0.1 and 1 microgram) and of its antagonist alpha-helical CRF9-41 (aH-CRF; 20 micrograms) administered intracerebroventricularly (ICV) reduced USV rate compared to saline treatment during a 2-min isolation at ambient temperature in pups of all ages. Other behaviors were either unaffected or increased by drug treatment. Effects were not attributable to sedation or to a change in core temperature. Peripheral administration of 1 microgram CRF or 20 micrograms aH-CRF had no effect. When isolation occurred in a heated chamber containing soiled bedding from the home cage to minimize baseline USV rate, ICV-CRF (0.001, 0.01, 0.1, or 1 microgram) did not enhance the rate. The quieting ability of aH-CRF is evidence that central endogenous CRF enhances the rate of ongoing USVs during brief isolation; the quieting ability of CRF suggests that this peptide may also be responsible for the reduction in USV rate that normally occurs during more protracted isolation. However, CRF alone is not sufficient to induce vocalizing in quiet pups.
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PMID:Corticotropin-releasing factor modulation of the ultrasonic vocalization rate of isolated rat pups. 758 94

Intracerebroventricular (i.c.v.) injection of corticotropin-releasing factor (CRF) and emotional stress (ES) induce stimulation of colonic motility in rats, an effect blocked by i.c.v. injection of CCK-8s. This study examined in rats the contribution of the central nucleus of the amygdala (CA) in the blocking effect of CCK-8s on ES and CRF-induced colonic hypermotility. CRF (500 ng/kg, i.c.v.) induced a 73.5% increase in colonic spike burst frequency. Bilateral infusions of 1, 5, 10 and 20 ng/kg of CCK-8s in the CA region 10 min prior to CRF i.c.v. injection reduced, in a dose related manner, the CRF-induced stimulation of colonic motility. A 109% increase in colonic spike burst frequency was observed in rats placed in a test cage in which they had previously received electric footshocks (ES). CCK-8s and A-71623, a selective CCK-A receptor agonist, (10, 25 and 50 ng/kg) infused bilaterally into the CA, 30 min before ES, significantly reduced this stimulatory effect, while CCK-4 and A-63387, a selective CCK-B receptor agonist (10, 25 and 50 ng/kg), had no effect on such a response. CA lesions by ibotenic acid did not affect ES-induced increase in colonic spike activity. However, CCK-8s (50 ng/kg) microinfused into CA lesioned rats was unable to block the ES-induced stimulation of colonic motility, while CCK-8s i.c.v. injected (100 ng/kg) is still active on the colonic response to ES. These results suggest that CA is a site of interaction of CCK-8s with CRF to block the colonic response to stress and that these effects involve the CCK-A receptor subtype.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholecystokinin blockade of emotional stress- and CRF-induced colonic motor alterations in rats: role of the amygdala. 783 46

Colchicine blockade of axonal transport from the paraventricular nucleus to the median eminence was used to indirectly infer ACTH secretagog release in response to the psychological stressors of social interactions and various degrees of novelty. Placing a rat in a new cage with either the smell or presence of a novel conspecific decreased arginine vasopressin and oxytocin (OT) contents, but not corticotropin-releasing factor content. Secretagog contents were unchanged in rats in their home cages faced with a novel conspecific. Secretagog release during social stress is thus primarily a function of being in a novel setting. For different degrees of novelty, rats were placed in either a novel cage, a novel bucket, or a novel bucket smelling of another rat. Whereas secretagog contents were unchanged with a novel cage, OT content alone decreased in response to both the bucket and the unclean bucket. Despite a graded corticosterone response, there was no distinction in the OT response, suggesting that the colchicine technique cannot accurately reflect gradations of stressors.
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PMID:Patterns of adrenocorticotropin secretagog release in response to social interactions and various degrees of novelty. 789 37

Defensive burying behavior is a coping strategy in rodents in response to an aversive stimulus where fear will facilitate burying and treatment with anxiolytics will result in less burying. To test the hypothesis that endogenous corticotropin-releasing factor (CRF) is involved in the defensive burying response, the effects of an ICV CRF antagonist were tested on defensive burying behaviors as well as the plasma adrenocorticotropic hormone (ACTH) and plasma corticosterone response. Rats were allowed to self-administer one mild electric shock (1.0 mA) through a probe mounted on the wall of the home cage by briefly touching it. Following this shock, control rats typically display burying behavior, as defined as moving the bedding material toward and/or over the shock probe. A CRF antagonist, alpha-hel CRF9-41, was administered ICV (1, 5, and 25 micrograms) 1 min after they received the shock. The 5 micrograms dose of the CRF antagonist significantly attenuated the time spent in defensive burying compared to vehicle-treated controls. The 5 and 25 micrograms doses of alpha-hel CRF9-41 increased the latency to display defensive burying. However, the enhanced release of plasma ACTH and plasma corticosterone concentrations in the stressed animals was not significantly modified over the 15-min period by either of the three doses of CRF antagonist. The results suggest that endogenous CRF is involved in the expression of defensive burying behavior and that the brain CRF receptors modulating the behavioral response may be different from the CRF receptors modulating the hormonal response of defensive burying.
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PMID:Effect of corticotropin-releasing factor antagonist on behavioral and neuroendocrine responses during exposure to defensive burying paradigm in rats. 808 89

We investigated the role of central corticotropin-releasing factor (CRF) in the development of cardiovascular and thermal responses induced by stress or by interleukin-1 beta (IL-1 beta) in free-moving rats. Intracerebroventricular (icv) injection of alpha-helical CRF9-41 (10 micrograms), a CRF receptor antagonist, significantly attenuated hypertension, tachycardia, and a rise in body temperature induced by cage-switch stress, a mild stress. However, icv injection of alpha-helical CRF9-41 (10 micrograms) had no effect on hypertension, tachycardia, or fever induced by intraperitoneal (ip) injection of IL-1 beta (2 micrograms/kg) or icv prostaglandin E2 (PGE2, 100 ng). In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). The present results suggest that central CRF has an important role in the development of the cage-switch stress-induced responses, but it does not seem to contribute to the hypertension, tachycardia, and fever induced by ip IL-1 beta or by central PGE2. However, it is possible that when IL-1 beta directly acts on the central nervous system, some of its actions are mediated by central CRF.
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PMID:Effect of a central CRF antagonist on cardiovascular and thermoregulatory responses induced by stress or IL-1 beta. 823 54


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