PubMed Health⌕ Search

Biomedical subjects

Z Amit

Publications and source records attributed to Z Amit.

At least 127 records · Page 7Linked to original sources
PubMed1982

Actions of drugs of abuse on brain reward systems: a reconsideration with specific attention to alcohol.

Research in the areas of intracranial self-stimulation and drug self-administration has provided a substantial data base that has contributed to our understanding of brain reward mechanisms. In a recent article, Wise [83] argued that dopamine is the catecholamine critically involved in the central mediation of reward. The present paper attempts to examine the available data with particular reference to alcohol, but also with reference to opiates, and argues that the reinforcing effects of at least these drugs are primarily and directly mediated by noradrenergic rather than dopaminergic systems in the brain. It also argues, in direct contrast to Wise, that in the context of these drugs, dopamine seems to play a minor if not negligible role.

Alcohol Drinking↗
PubMed1981

An examination of possible interactions between zimelidine, a serotonin uptake inhibitor, and ethanol ingested conjointly in human subjects.

Non-alcoholic male subjects were given either a placebo or zimelidine (100, 200 or 300 mg, p.o.) 2 h prior to consumption of alcohol (1 g/kg) or a non-alcoholic mixer. Slight increases in heart rate and diastolic blood pressure induced by alcohol were unaffected by pretreatment with zimelidine. Alcohol, zimelidine, and the combination of the two, did not affect any of the hematologic measures except for serum potassium levels. The latter were reduced slightly but not in any discernible pattern. Blood alcohol concentrations were not changed by zimelidine pretreatment. Conversely, blood concentrations of zimelidine and its metabolite norzimelidine were also relatively unaffected by alcohol consumption. In general, the results indicate that the simultaneous administration of zimelidine and alcohol to human subjects does not produce any observable adverse effects.

Adolescent↗
PubMed1981

Pre-exposure effects of morphine, diazepam and delta 9-THC on the formation of conditioned taste aversions.

Prior to taste aversion conditioning with morphine, diazepam or delta 9-tetrahydrocannabinol (delta 9-THC), rats received pre-exposures to the vehicle or one of the three drugs. Morphine pre-exposures blocked the aversion normally induced by morphine, but not by delta 9-THC or diazepam. Diazepam pre-exposures attenuated both the morphine- and diazepam-induced taste aversions to a significantly greater degree than the taste aversion induced by delta 9-THC. As a result of delta 9-THC pre-exposures, the aversions induced by diazepam and delta 9-THC were attenuated as well as the morphine-induced aversion, which was the most greatly attenuated. These results demonstrate that pre-exposure effects are not necessarily bi-directional and, moreover, they are inconsistent with current hypotheses which attempt to account for the attenuating effect of drug pre-exposures on taste-aversion conditioning.

Animals↗
PubMed1981

Heroin and morphine: aversive and analgesic effects in rats.

Although a number of studies demonstrate morphine-induced taste aversions, no such reports exist for heroin. In a conventional taste aversion paradigm, rats were injected with one of six heroin doses (0.5-12.0 mg/kg) after consuming a novel saccharin solution (Experiment 1). When the saccharin was reintroduced a second time no significant reduction in consumption occurred at any of the doses tested. It was therefore concluded that heroin does not readily induce a taste aversion. In Experiment 2, morphine was tested in an identical taste aversion paradigm and, as expected, a significant taste aversion did result at two of the doses tested. Experiment 3 demonstrated that heroin produced analgesia equal to or greater than morphine when comparing dosages of heroin which failed to induce a CTA with CTA-inducing morphine dosages. Thus, whereas heroin is more potent than morphine as an analgesic, heroin is less potent than morphine as a CTA-inducing agent.

Analgesics↗
PubMed1981

Morphine conditioned taste aversion reversed by periaqueductal gray lesions.

The role of the periaqueductal gray (PAG) in morphine conditioned taste aversion (CTA) was studied using male Wistar rats as subjects. Following the presentation of a novel saccharin solution, animals with or without a lesion of the PAG were intraperitoneally injected with either morphine, lithium, ethanol or fenfluramine. As evident by the amount of saccharin solution consumed on a subsequent presentation, a PAG lesion reversed a morphine CTA but not CTAs produced by the other drugs used. The results suggest that the PAG may in part mediate morphine CTA.

Animals↗
PubMed1980

Opiate receptors may mediate the suppressive but not the excitatory action of ACTH on motor activity in rats.

Subcutaneous injections of adrenocorticotropin (ACTH) or of the opiate antagonist naltrexone produced a one (2.0 mg/kg) dpressed, whereas smaller doses of ACTH (50 micrograms/kg) and of naltrexone (0.125 and 0.25 mg/kg) stimulated motor activity in the open field test. Furthermore, naltrexone at a dose level that had no effect on motor activity blocked the suppressive effect of the high doses of ACTH but had no effect on the stimulating effect of the intermediate dose of ACTH. Finally, chronic naltrexone administration resulted in enhanced sensitivity to the suppressive but not to the stimulating effect of ACTH on motor activity. It is argued that opiate receptors may play a selective role in the effect of ACTH on motor activity. Such receptors may mediate the supressive effect of high doses of ACTH whereas other, naltrexone insensitive receptor systems may mediate the stimulating effect of ACTH on activity functions.

Adrenocorticotropic Hormone↗
PubMed1980

Heroin, but not levorphanol, produces explosive motor behavior in naloxone-treated rats.

Intraventricular infusions of heroin (an opiate) or levorphanol (an opioid) in rats produced rigidity but not explosive motor behavior (EMB). When preceded by an IP injection of naloxone, infusions of heroin but not levorphanol produced EMB. The results suggest that naloxone-antagonized effects of opiates mask EMB and that certain opioids do not induce EMB.

Animals↗