Pharmacology, biochemistry, and behavior
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Pharmacol. Biochem. Behav. · Jul 1986
Comparative StudyCentrally-administered opioid selective agonists inhibit drinking in the rat.
The effects of intracerebroventricular injection of mu (morphine), kappa (dynorphin-(1-13), ethylketocyclazocine, and U50,488H), and delta ([D-Pen2, D-Pen5]enkephalin) opioid agonists on water intake of 14 hr water deprived rats was studied. All agonists caused a dose related decrease in time spent drinking, with a rank order potency of dynorphin-(1-13) greater than morphine greater than ethylketocyclazocine greater than [D-Pen2, D-Pen5]enkephalin = U50, 488H. ⋯ The potent inhibition of drinking following centrally-given dynorphin-(1-13), at doses that did not affect the latency to begin drinking, supports a role for endogenous dynorphin in the homeostatic control of water balance. This function may not be primarily mediated through activation of a kappa opioid receptor since dynorphin-(1-13) was 80-230 times more potent than the selective kappa agonist, U50,488H or ethylketocyclazocine.
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Pharmacol. Biochem. Behav. · Jun 1986
Antagonism of morphine analgesia by intracerebroventricular naloxonazine.
Intravenous pretreatment with naloxonazine, an irreversible and selective antagonist of mu-1 sites for over 24 hr, reduces analgesia induced by morphine as well as a series of opiates and enkephalins. The present study evaluated whether intracerebroventricular (ICV) administration of naloxonazine produces similar long-term (24 hr) reductions in morphine analgesia on the tail-flick and jump tests. Naloxonazine failed to alter baseline tail-flick latencies or jump thresholds, but antagonized in a dose-dependent manner morphine analgesia for 24 hr. ⋯ Naloxonazine also shifted full morphine dose-response curves to the right. Again, naloxonazine antagonized morphine in the jump test more effectively than in the tail-flick assay. These data provide support for the involvement of the mu-1 opioid binding site in the central mediation of morphine analgesia and point out the differing sensitivities of two analgesiometric assay systems to naloxonazine.
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Pharmacol. Biochem. Behav. · Jan 1986
Effects of preshock experience on enhancement of rat brain noradrenaline turnover induced by psychological stress.
The present study examined alterations of brain noradrenaline (NA) turnover as a function of preshock and psychological stress treatments, by measuring contents of NA metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), in discrete brain regions of male Wistar rats. Psychological stress induced by exposing to the sight, sound and odor of other rats being shocked produced higher levels of MHPG-SO4 in the hypothalamus, amygdala and locus coeruleus (LC) region, as well as higher levels of plasma corticosterone. ⋯ These results suggest that: a purely psychological stressor caused acutely enhanced NA turnover in specific brain regions; regional NA activity appeared to be reinstated simply by reexposure to the environment previously associated with shock; preshock experience further intensified the enhancement of amygdaloid NA turnover evoked by psychological stress. An additional experiment, studying the aftereffects of preshock experience, clearly showed that these findings result from sensitization or conditioning to the environment previously paired with shock, and not merely from the aftereffects of the shock per se.
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Pharmacol. Biochem. Behav. · Sep 1985
Comparative StudyThe effect of opiates and naloxone on food intake in virgin and lactating rats.
Lactation provides an excellent model of non-obese hyperphagia. There is accumulating evidence that endogenous opioids play a role in the modulation of the hormonal changes that occur during lactation. Because endogenous opioids appear also to play a role in the regulation of feeding, we studied the effects of the opiate agonist, butorphanol tartrate, and an opiate antagonist, naloxone, on food intake in virgin female rats and in rats during early, mid and late lactation and during post-weaning. ⋯ We found that female rats were relatively insensitive to the food suppressant effects of naloxone following 24 hour food deprivation, while male rats tested under similar conditions had a decreased intake in response to naloxone. Despite the marked hyperphagia that occurred during lactation, there were minimal alterations in the response to opiate agonists and antagonists during this time period. Our data suggest that endogenous opioids may not play a pivotal role in the hyperphagia of lactation.
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Pharmacol. Biochem. Behav. · Jan 1985
Involvement of a GABAergic mechanism in the anticonvulsant effect of pentobarbital against maximal electroshock-induced seizures in rats.
The interaction between pentobarbital and other modulators of GABAergic transmission (diazepam, ethanol and progabide) was investigated on maximal electroshock seizures and on the loss of righting reflexes in rats. Pentobarbital, diazepam and ethanol produced a dose-dependent protection against electroshock seizures, with pentobarbital being more potent (3- and 50-times) than diazepam and ethanol. Progabide neither provided protection nor caused loss of righting reflex. ⋯ The protective effect of diazepam was antagonized by RO15-1788, picrotoxin and bicuculline pretreatments. The antagonism of pentobarbital protection by a specific GABA receptor antagonist, bicuculline suggests involvement of the GABAergic system in the anticonvulsant effect of pentobarbital. These results indicate that, like diazepam, the anticonvulsant effect of pentobarbital appears to be mediated through a GABAergic mechanism.