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Biomedical subjects

G E Rockman

Publications and source records attributed to G E Rockman.

6 recordsLinked to original sources
PubMed1979

Intraventricular self-administration of acetaldehyde, but not ethanol, in naive laboratory rats.

For 11 consecutive days, naive rats were maintained in operant chambers where they were given the opportunity to self-administer acetaldehyde (1,2, or 5% v/v), ethanol (2 or 10% v/v), or pH control solutions directly into the cerebral ventricles. Only the animals that had access to the 2 and 5% acetaldehyde solutions showed rates of lever pressing significantly higher than controls. It is suggested that acetaldehyde rather than ethanol itself may mediate the positive reinforcing effects of ethanol in the brain.

Acetaldehyde↗
PubMed1979

Attenuation of ethanol intake by 5-hydroxytryptamine uptake blockade in laboratory rats. I. Involvement of brain 5-hydroxytryptamine in the mediation of the positive reinforcing properties of ethanol.

The role of 5-hydroxytryptamine (5-HT) uptake blockade in the mediation of the positive reinforcing peroperties of ethanol in male wistar rats was investigated. It was demonstrated that treatment with zimelidine (H102/09) a 5-HT uptake inhibitor, specifically attenuated ethanol consumption. In an attempt to extinguish the ethanol drinking response, ethanol preferring animals in a second experiment, were provided with ethanol as the only source of fluid in combination with zimelidine treatment. Animals treated in such a manner subsequently reduced their ethanol consumption when presented with a free-choice between ethanol and water. These results were attributed to an increased availability of central 5-HT, suggesting that central 5-HT mechanisms may in some way be involved in the mediation of the positive reinforcing properties of ethanol.

Alcohol Drinking↗
PubMed1979

Attenuation of ethanol intake by 5-hydroxytryptamine uptake blockade in laboratory rats: II. Possible interaction with brain norepinephrine.

This experiment was undertaken to examine whether the attenuation of ethanol consumption following treatment with zimelidine (H102/09) could be due to an invasion of surplus serotonin into norepinephrine neurons. In an attempt to prevent this proposed invasion by serotonin, ethanol preferring animals were pre-treated with desmethylimipramine (DMI), a norepinephrine reuptake inhibitor, prior to treatment with zimelidine. The results demonstrated that those animals treated in such a manner consumed significantly more ethanol than those animals treated with zimelidine alone. Based on these results it is suggested that the observed attenuation of ethanol consumption following zimelidine treatment, could be partially due to a serotonin-induced functional depletion of norepinephrine.

Alcohol Drinking↗
PubMed1978

Suppression of voluntary ingestion of morphine by inhibition of dopamine-beta-hydroxylase.

Male Wistar rats were exposed to a free choice between water and a morphine-sucrose solution. Following stabilization of baseline levels of consumption of morphine, the animals were injected for 5 consecutive days with either FLA-57 (45 or 60 mg/kg i.p.), a non-toxic dopamine-beta-hydroxylase inhibitor or its vehicle. The FLA-57 treated animals significantly attenuated their preference for morphine during the injection and post-injection periods although there were no significant differences related to the dosages used. These treatments produced a concomitant reduction in central norepinephrine levels suggesting that norepinephrine may be involved in the mediation of the reinforcing properties of morphine consumed by laboratory rats. The possibility of common neural mechanisms regulating the pharmacological actions of both morphine and ethanol are discussed.

Animals↗
PubMedDate not supplied

Possible involvement of acetaldehyde, norepinephrine and their tetrahydroisoquinoline derivatives in the regulation of ethanol seld-administration.

In this study, we examined the possible role of acetaldehyde in the mediation of the reinforcing properties of ethanol. We also examined the possible interaction of acetaldehyde and brain norepinephrine in this mediation. We found that rats will self-administer acetaldehyde delivered into the cerebral ventricles, and that this operant behaviour can be attenuated by injections of a dopamine-beta-hydroxylase inhibitor. The results are discussed in terms of a role for tetrahydroisoquinoline alkaloids in alcoholism.

Acetaldehyde↗