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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present work examined the generalizability of the anhedonia phenomenon (extinction-like responding with repeated neuroleptic treatment) by examining the effects of pimozide (PIM) on nondeprived rats lever pressing for a sucrose solution reward (32%) in an eight day dosing regime. The procedures used replicated the essential features of a previous study (Gramling et al. [10]) wherein the effects of PIM on rats licking directly a sucrose solution were assessed. Thirty nondeprived rats were trained to lever press on a CRF schedule for a 32% sucrose solution reward and then assigned to one of five treatment groups (N = 6). The treatment conditions included a no-reward group (EXT; vehicle injections), two pimozide (PIM) with reward conditions (either PIM 0.25 mg/kg + RWD or PIM 0.5 mg/kg + RWD), and a vehicle control group (RWD; vehicle injections). These four groups each received their respective injections and operant exposure for eight consecutive days. The fifth group was a home cage (HC) control condition wherein the rats were injected with 0.5 mg/kg PIM each test day but did not receive operant exposure until the fourth test day. The PIM treated rats exhibited a significant curvilinear pattern of responding on the rate measure across eight days of testing, whereas rats in the no-reward condition exhibited a significant downward linear trend across eight days of testing. Within-session analysis revealed that rats in the EXT group responded at significantly higher rates during the first five minutes of testing on the first test day compared to rats in the PIM 0.5 + RWD condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Some effects of pimozide on nondeprived rats' lever pressing maintained by a sucrose reward in an anhedonia paradigm. 361 48

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

An inhibitory effect of stress on reproductive function is well established. This inhibition involves activation of the hypothalamic-pituitary-adrenal (HPA) axis, which leads to a suppression of LH secretion. It has been proposed that this suppression is mediated by a direct effect of CRF that is independent of glucocorticoid actions. We tested this proposition by examining plasma LH levels in adult rats that were both ovariectomized (OVX) and adrenalectomized (ADX). Each animal was surgically implanted with an indwelling atrial cannula and exposed to intermittent foot shock for 100 min. Blood samples were drawn just prior to putting the animals into the test cage and then at 20-min intervals. Results revealed normal castrate levels of plasma LH in both ADX and ADX/OVX animals prior to shock. A significant shock-induced suppression of LH was observed in OVX animals within 20 min after the onset of shock and remained throughout the duration of the session. In contrast, no evidence was obtained for a suppression of LH in OVX/ADX animals at any time point. Additional studies demonstrated a marked suppression of LH in experimentally naive OVX/ADX females implanted with corticosterone capsules for 2 weeks prior to blood sampling. Overall, these results support a primary role for glucocorticoid actions in the stress-induced inhibition of reproductive function.
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PMID:Adrenalectomy reverses stress-induced suppression of luteinizing hormone secretion in long-term ovariectomized rats. 804 84

These experiments investigated the effect of either systemic opiate blockade by naloxone (5 mg/kg) or intracerebroventricular CRF (250 pmol), or the two treatments combined, on physiological and endocrine responses of male rats to two types of stress: restraint by itself (representing a psychological stress), and restraint combined with a tail clip (representing an additional mild physical nociceptive stress). Rats were restrained in a plastic container for 15 min, with or without a tail clip. Heart rate, body temperature, and serum corticosterone were measured. The first experiment showed that restraint induced marked tachycardia, maximal at 5 min, and declining thereafter. There was also a pronounced hypothermia, maximal at 10 min, and serum corticosterone was elevated 10 min after the end of the period of restraint. The presence of a tail clip increased the cardioaccelerator response, but had no effect on hypothermia. Naloxone had no effect on heart rate during restraint or on postrestraint corticosterone, but accentuated hypothermia. The effects of naloxone occurred independently of the presence of a tail clip. A subsidiary experiment showed that rats transferred to an unfamiliar cage showed a marked hyperthermic response, as described by others. The second experiment showed that CRF (250 pmol ICV) did not modify the tachycardiac response to restraint, but reduced hypothermia. This also occurred irrespective of the presence of a tail clip. The third experiment investigated the interaction between naloxone and CRF, and showed that the ameliorative effects of ICV CRF on restraint-induced hypothermia were prevented by systemic naloxone, but that neither tachycardia nor corticosterone responses were altered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interactions between corticotropin-releasing factor and endogenous opiates on the cardioaccelerator, hypothermic, and corticoid responses to restraint in the rat. 848 94

1. We investigated the central role of corticotrophin-releasing factor (CRF-41) in psychological stress-induced responses, including cardiovascular, thermoregulatory and locomotive activity in free-moving rats. 2. Psychological stress was induced by cage-switch stress. After rats were placed in the novel environment, blood pressure, heart rate, body temperature and locomotive activity significantly increased. The intracerebroventricular (I.C.V.) injection of alpha-helical CRF(9-41), a CRF-41 receptor antagonist, significantly attenuated the stress-induced hypertension, tachycardia, hyperthermia and increase in locomotive activity. However, in unstressed rats, the I.C.V. injection of alpha-helical CRF(9-41) had no effect on physiological parameters measured in this study. 3. In unstressed rats, the I.C.V. injection of CRF-41 (1 microgram and 10 micrograms) increased blood pressure, heart rate, body temperature and locomotive activity in a dose-dependent manner. The changes in these responses were quite similar to those observed during cage-switch stress. 4. The results suggest that central CRF-41 plays an important role in psychological stress-induced hypertension, hyperthermia, tachycardia and increase in locomotive activity. However, it is likely that central CRF-41 does not contribute to normal cardiovascular and body temperature regulation when rats are free from stress.
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PMID:The central role of corticotrophin-releasing factor (CRF-41) in psychological stress in rats. 848 93

In order to examine the involvement of corticotropin-releasing hormone (CRF) receptor in the formation of anxiety, we investigated whether CRF receptor antagonist CP-154,526 suppressed conditioned fear stress. First, rats were individually subjected to 30 min of footshock. Twenty-four hours after footshock, the rats were again placed in the chamber and observed for 5 min without shock. CP-154,526 was administered 30 min before placing the rats in the chamber again. After that, CP-154,526 was once more administered 30 min before applying footshock. Administration of CP-154,526 30 min both before conditioned fear stress (placing the rats inside the cage but not applying footshock) and before actual footshock significantly reduced freezing behavior. These results show that CP-154,526 blocked both the acquisition and expression of conditioned fear, thus suggesting that the CRF receptor might be related to anxiety.
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PMID:Suppression of conditioned fear by administration of CRF receptor antagonist CP-154,526. 1107 Oct 21

The effects of tripeptide corticoliberin fragment CRF4-6 (icv; 6, 30, and 150 nmol/head) on behaviour of rats were investigated under non-stressing and stressing conditions. CRF4-6 activated rat behaviour under non-stressing conditions (home cage): the duration of locomotion and exploratory behaviour was increased whereas the duration of passive behaviour and sleep was decreased. On the other hand, CRF4-6 suppressed the rat exploratory behaviour under stressing conditions (elevated plus-maze): the duration of non-exploratory behaviour was increased; numbers of rearings and leanings out to open arms were reduced. All observed effects of the tripeptide CRF4-6 were dose-dependent. Behavioural effects of the tripeptide were similar to the well-known action of the whole corticoliberin molecule. Therefore we suggest that CRF4-6 is located in the active part of CRF or it can be a physiologically active corticoliberin derivative.
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PMID:[Corticoliberin fragment CRF4-6 modifies rat behavior in opposite ways under stressing and non-stressing conditions]. 1603 39

The involvement of nociceptin (N/OFQ) and the nociceptin/orphanin FQ peptide (NOP) receptor in behavior associated with stress and anxiety has been established but their role in the regulation of the hypothalamo-pituitary-adrenal (HPA) axis under conditions of stress has not been fully investigated. We used the selective NOP receptor antagonist UFP-101 to examine the contribution of endogenous N/OFQ to HPA axis control under conditions of restraint stress in the morning and the evening. We found that in the morning during the HPA axis circadian nadir rats exposed to restraint stress in both the presence and absence of UFP-101 exhibited significantly elevated plasma corticosterone at 30 min post-i.c.v. injection compared to the home cage control group. Additionally, rats treated with UFP-101 and exposed to restraint had significantly elevated corticosterone levels at 60 min post-i.c.v. injection compared to all other treatment groups. Interestingly, while there was a significant increase in the expression of CRF mRNA in the paraventricular nucleus (PVN) of rats exposed to restraint stress only, there was no comparable increase in those co-treated with UFP-101. There was no change in the expression of AVP or POMC mRNA in any of the treatment groups. In contrast, when carried out in the evening we observed significantly elevated plasma corticosterone in the vehicle-treated restraint group only at 30 min post-i.c.v. injection. There was no significant difference between the UFP-101-treated restraint group and either of the home cage control groups or the vehicle-treated restraint group. Additionally, in contrast to the morning study, UFP-101 did not prolong glucocorticoid release at the 60 min time-point. These results demonstrate for the first time a differential effect of UFP-101 on restraint stress-induced HPA axis activity characterized by significant prolongation of stress-induced activity in the morning but no significant effect on the response to restraint in the evening.
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PMID:The nociceptin/orphanin FQ antagonist UFP-101 differentially modulates the glucocorticoid response to restraint stress in rats during the peak and nadir phases of the hypothalamo-pituitary-adrenal axis circadian rhythm. 1757 67

In the hippocampus, a brain structure critically important in the stress response, GABA controls neuronal activity not only via synaptic inhibition, but also via tonic inhibition through stimulation of extrasynaptic GABA receptors. The extracellular level of GABA may represent a major determinant for tonic inhibition and, therefore, it is surprising that its responsiveness to stress has hardly been investigated. To clarify whether hippocampal extracellular GABA levels change in response to acute stress, we conducted an in vivo microdialysis study in rats. We found that dialysate GABA levels respond to various neuropharmacological manipulations such as reuptake inhibition, elevated concentrations of K(+), tetrodotoxin and baclofen, indicating that a large proportion of hippocampal extracellular GABA depends on neuronal release and that GABA re-uptake plays a role in determining the extracellular levels of this neurotransmitter. Next, rats were exposed to a novel cage or to forced swimming in 25 degrees C water. Interestingly, these two stressors resulted in opposite effects. Novelty caused a fast increase in GABA (120% of baseline), whereas forced swimming resulted in a profound decrease (70% of baseline). To discriminate between the psychological and physical aspects (i.e. the effects on body temperature) of forced swimming, another group of animals was forced to swim at 35 degrees C. This stressor, like novelty, caused an increase in hippocampal GABA, suggesting a stimulatory effect of psychological stress. The effects of novelty could not be blocked by the corticotropin-releasing factor receptor antagonist D-Phe-CRF(12-41). These results are the first to demonstrate stressor-dependent changes in hippocampal extracellular GABA; an observation which may be of particular significance for GABAergic tonic inhibition of hippocampal neurons.
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PMID:Exposure to novelty and forced swimming evoke stressor-dependent changes in extracellular GABA in the rat hippocampus. 1769 36

Defeat is a social stressor involving subordination by a threatening conspecific. Type 2 corticotropin-releasing factor receptors (CRF(2)) are abundant in brain regions implicated in defeat responses and are putative stress-related molecules. The present study sought to determine whether neuroactivation and CRF(2) expression co-occurred at brain region or cellular levels following acute defeat. Male "intruder" Wistar rats were placed into the cage of an aggressive "resident" Long-Evans rat (n=6). Upon defeat, intruders (n=6) were placed in a wire-mesh chamber and were returned to the resident's cage for an additional 75 min. Controls (n=6) were handled and returned to their home cage for the same duration. Coronal brain sections were stained for an immediate early gene product, Fos, as a neuronal activation marker. Combined immunohistochemistry with in situ hybridization was performed on a subset of brain sections from defeated intruders to visualize Fos immunoreactivity and CRF(2) mRNA jointly. Defeated rats had fivefold, sevenfold, and 10-fold more Fos-positive cells than controls in the arcuate, ventromedial nucleus of the hypothalamus, and medial amygdala post-defeat. Significant colocalization of CRF(2) mRNA and Fos-positive cells was observed in the posterior medial amygdala but not in the arcuate nucleus or ventromedial hypothalamus. The results indicate CRF(2) receptor-positive neurons in the posterior medial amygdala are involved in the neural response to social defeat.
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PMID:Social defeat stress activates medial amygdala cells that express type 2 corticotropin-releasing factor receptor mRNA. 1935 76


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