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

Investigations were made of the action of ACTH and LH-RH on a number of behavioural paradigms and the possible involvement of neurotransmitters or opiates by pretreatment of receptor blockers in rats and mice. ACTH delayed the extinction of active avoidance behaviour. Atropine and haloperidol blocked this action, whereas phenoxybenzamine and propranolol were ineffective. LH-RH or a highly potent analogue of LH-RH (D-Trp6-LH-RH) decreased the rate of disappearance of dopamine in the hypothalamus following alpha-methyl- paratyrosine inhibition of catecholamine synthesis, and blocked the accumulation of serotonin following MAO inhibition. LH-RH or the analogue attenuated the consolidation of passive avoidance learning. Apomorphine-induced cage-climbing was also inhibited by the LH-RH analogue, but this action was not influenced by naloxone. Open-field activity (ambulation, rearing and grooming) was decreased by the analogue peptide. Naloxone blocked the action on ambulation and rearing, but was ineffective on grooming. The LH-RH analogue caused a dose-dependent increase in cataleptogenic activity. This action could not be blocked with naloxone. The LH-RH analogue suppressed picrotoxin-induced seizures. Naloxone restored the situation to the control level. The data suggested that the effects of some neurohormones are mediated by transmitters or endogenous opiates, and that both peptide-transmitter and peptide-peptide interactions have to be considered in the action of neurohormones.
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PMID:Involvement of neurotransmitter and neuropeptides in behavioural action of some neurohormones. 198 90

Ejaculation-induced reward in the male rat was evaluated by the conditioned place-preference paradigm. It was supposed that ejaculation induces a reward state such that it can be conditioned to environmental stimuli. Males were allowed to ejaculate once and were then immediately transferred to a place-preference cage. One ejaculation produced place preference. Naloxone (16 mg/kg) not only blocked this place preference but also induced a place aversion. Naloxone by itself had no effect on place preference. It is suggested that release of endogenous opioids renders ejaculation rewarding. Pimozide, in a dose of 1 mg/kg, had no effect on ejaculation-induced reward. Dopamine thus seems to be of slight importance for that effect of copulation. Perhaps compulsive sexual activity obeys the same mechanisms as compulsive drug use in opiate addicts.
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PMID:Reinforcing properties of ejaculation in the male rat: role of opioids and dopamine. 215 20

These experiments tested the hypothesis that the suppressing and facilitating effects of morphine on intracranial self-stimulation (ICS) (measured 1 h and 3 h post-injection, respectively) are influenced by associative, non-pharmacological factors. Experiment 1 confirmed previous demonstrations that the facilitation of ICS by morphine (10 mg/kg) develops with repeated drug exposures. Once ICS facilitation had developed, the effect was mimicked by saline injection in most subjects. In a separate group of animals, previous exposure to morphine in the home cage prevented drug-induced facilitation of ICS. Tolerance to ICS suppression developed after repeated pairings of the drug and the ICS chambers, but not when the drug had previously been received in the home cage. Experiment 2 examined the effect of low (0.3, 1, 3 mg/kg) doses of chronic morphine on ICS. Facilitation was observed with 1 and 3 mg/kg, but only after repeated testing. Naloxone (0.1 and 1 mg/kg) failed to reverse facilitation in a number of these subjects. In Experiment 3, animals receiving their daily injections of morphine were allowed to self-stimulate only at 3 h post-injection (when ICS facilitation is usually maximal), rather than at 1 h and 3 h post-injection. ICS facilitation was not observed, even with repeated testing. These data indicate that the facilitation of ICS by morphine is the outcome of a learned association between drug administration and the ICS procedure, rather than the invariable result of opiate receptor activation. Repeated exposure to morphine is required for the initial establishment of ICS enhancement, but the subsequent expression of this behavior is not directly related to opiate receptor activity.
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PMID:Associative factors in the effects of morphine on self-stimulation. 308 35

Blood samples were taken from conscious, chronically-catheterized rats during parturition for measurement of oxytocin by specific radioimmunoassay. After the birth of the 3rd pup, rats were allowed to remain in their nesting cage (undisturbed rats) or were transferred for 45 min to a glass bowl (disturbed rats); at the time of transfer, rats were given an i.v. injection of the opioid antagonist naloxone or saline vehicle. Subsequent parturition was prolonged in saline-treated disturbed rats, but not in naloxone-treated disturbed rats. Parturition was significantly hastened in naloxone-treated undisturbed rats. Naloxone injections were followed by a large rise in plasma oxytocin concentrations in disturbed and undisturbed rats. We conclude, from a statistical analysis of the relationship within experimental groups between plasma oxytocin concentration and speed of parturition, that the effects of disturbance and of naloxone upon parturition may be accounted for, at least in part, by their effects upon oxytocin release. However, the effects of disturbance on parturition may not be mediated entirely by activation of opioid pathways. Naloxone did not potentiate oxytocin release in non-pregnant rats, or on Day 1 post partum, but did potentiate oxytocin release on Day 22 of pregnancy even in rats before the onset of parturition. Endogenous opioid pathways regulating oxytocin release therefore appear to be active during late pregnancy and during parturition itself.
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PMID:Endogenous opioid actions and effects of environmental disturbance on parturition and oxytocin secretion in rats. 318 53

An increasing amount of anatomical, physiological, and pharmacological evidence suggest that pain inhibitory circuitry is linked with cardiovascular regulatory systems in man and laboratory animals. Induction of hypertension in rats by different methods (mineralocorticoid treatment, stenosis of renal artery, or social deprivation) is associated with reduced responsiveness to noxious thermal stimuli (hot-plate) or to noxious mechanical stimuli (paw pressure). Genetically hypertension-prone rats derived from the SABRA strain and spontaneously hypertensive rats derived from Wistar/Kyoto strain also display a similar hypoalgesia. Acute increases in blood pressure are associated with reduced sensitivity to painful stimuli. Additionally, the interaction between blood pressure and pain perception has also been supported by the demonstration that various experimental interventions that diminish the magnitude of hypertension also attenuate the hypoalgesia. Recent clinical findings are also in agreement with the laboratory animal findings since sensory and pain thresholds have been shown to be significantly higher in unmedicated essential hypertensive subjects compared to normotensive controls. Thus, the human data corroborate animal data and suggest that a relation between blood pressure and pain sensitivity is likely to be a general phenomenon. It is unlikely that damage to peripheral pain fibers caused by a change in blood pressure contributes to the observed hypoalgesia. Naloxone, which has no effect on blood pressure, returns the pain sensitivity to normal levels. Behavioral tests (open field and motor activity cage) of normotensive and of renal and genetically (SBH and SHR) hypertensive rats exclude the possibility of a general motor deficit in hypertensive rats. Endogenous opioid peptides in central and peripheral nervous systems as well as in endocrine organs are implicated, although non-opioid mechanisms are also evident. Activation of baroreceptor afferents by acute or chronic increases in arterial or venous blood pressure may play an important role in the somatosensory responses associated with the increase in blood pressure. Coordinated cardiovascular-pain regulatory responses may be part of an adaptive mechanism that helps the body to face stressful events.
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PMID:The relationship between cardiovascular and pain regulatory systems. 352 85

In the present study tail-flick latency (TFL) and squeak threshold (ST) were investigated in different environmental conditions in normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The TFL did not vary significantly during the testing period (120 min). The ST increased gradually and significantly with time when measured in rats restrained in the TFL test tube. Freely moving rats transferred to the TFL test tube showed a marked decrease of the ST. During the stay in the TFL test tube, the ST value increased gradually. Also after transfer from the test tube to the home cage the threshold increased to the same level as freely moving rats. There were no significant differences in these effects between WKY and SHR. Naloxone (1 mg kg-1 i.v.) decreased the ST in both freely moving and restrained animals of either strain. Intravenous injection of morphine (mg kg-1) gave a pronounced threshold increase of ST in both groups. It is suggested that animals restrained in the TFL test tube become hyperalgesic. The adaptation to stress is reflected in the ST but not in the TFL. Squeak threshold appears to be influenced by a tonically active endorphin system.
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PMID:Differential stress effects on responses to noxious stimuli as measured by tail-flick latency and squeak threshold in rats. 357 23

Naloxone induces behavioural changes in rodents exposed to novel environments, indicating the involvement of endogenous opioid mechanisms in these situations. The present study investigated whether soiled sawdust substrate from the cage of an unfamiliar, isolated, male conspecific modifies the effect of naloxone (0.5 or 12.5 mg/kg) upon behaviour of mice in an open field test situation. There was little difference between the effects of naloxone upon the frequency of acts or postures shown in the soiled and unsoiled environments. Cluster analysis of the activities according to their position and frequency in behavioural sequences, revealed variations in behavioural organisation in these two situations in control animals, and differential responses to naloxone administration. The data are discussed in terms of an involvement in behaviour of opioid mechanisms which can be modified by non-painful, biologically-relevant, aversive stimuli such as unfamiliar, conspecific-soiled substrates.
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PMID:Substrate soiled by an unfamiliar conspecific modifies opioid activity in mice placed in novel environments. 407 Apr 16

Naloxone (1 mg/Kg s.c.), in the light phase of the daily light-dark cycles during the 30 and 60 min of the test, shows an antidipsogenic effect of the same intensity in chronically water-deprived rats which drink more (+ 176% and + 162%) than the acutely water-deprived animals. In chronically water-deprived rats, the time interval from the drug introduction (5, 30, 60 and 90 min) is not critical for the intensity of the antidipsogenic action of naloxone. When water intake is controlled by a 20% variable ratio schedule that does not allow the animals to satisfy, during the session, more than 50% of their thirst, the time interval from the introduction of naloxone is critical. When the rats can drink freely for 30 min in their home-cage after they satisfied their thirst partially by means of bar-pressing, naloxone, paradoxically shows a weaker and not significant antidipsogenic action. The results and the usefulness of the behavioural test are briefly discussed.
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PMID:Antidipsogenic action of naloxone under different water deprivation conditions. 668 15

The opiate antagonist naloxone reduced the food intake induced in rats by acute injection of insulin. The suppression was most marked in the first hour after insulin injection. Insulin provoked less food intake when rats were tested in a novel environment compared with those tested in their home cage, but naloxone again significantly suppressed the intake in the first hour. Naloxone had no effect upon insulin-induced hypoglycemia.
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PMID:Naloxone suppresses insulin-induced food intake in novel and familiar environments, but does not affect hypoglycemia. 705 Oct 49

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


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