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Biomedical subjects

D A Gorelick

Publications and source records attributed to D A Gorelick.

12 recordsLinked to original sources
PubMed1992

Hypothalamic-pituitary function during alcohol exposure and withdrawal and cocaine exposure.

This chapter examines the neuroendocrine effects of acute exposure to and withdrawal from alcohol and cocaine, with special emphasis on the hypothalamic-pituitary-adrenal (HPA) axis. We present the results from two preliminary controlled inpatient studies that document HPA dysfunction during acute exposure to alcohol and cocaine and during withdrawal from alcohol. We discuss the methodological approach of these studies in comparison to related attempts in the literature to use measures of thyroid and prolactin regulation to predict risk of relapse to alcohol and cocaine use, respectively. Our data and the results of related studies are presented in the context of a proposed index of HPA axis dysfunction that may provide a useful clinical measure of susceptibility to relapse during protracted abstinence from alcohol or cocaine.

Adrenocorticotropic Hormone↗
PubMed1992

Effect of fluoxetine on alcohol consumption in male alcoholics.

To test the effect of inhibiting serotonin uptake on voluntary alcohol intake, 20 alcohol-dependent males were housed on a locked hospital ward with 60-ml drinks of 97.5 proof alcohol available in a fixed interval drinking decision paradigm 13 times each day. After a 3-day, single-blind placebo baseline period, 10 subjects each received the serotonin uptake blocker fluoxetine (up to 80 mg po daily) or placebo double-blind for 28 days. The fluoxetine group had a 14% lower alcohol intake during the 1st week only, associated with a lower proportion of requests for alcohol and less craving for alcohol (as rated by research staff). There were no significant effects in later weeks, nor any differences in scores on the Hamilton Depression and Anxiety Scales or the Hopkins Symptom Checklist.

Adult↗
PubMed1992

Progression of dependence in male cocaine addicts.

We studied the self-reported temporal sequence of cocaine-related problems in 45 male predominantly Black (85%), lower SES cocaine addicts undergoing inpatient treatment at a large urban VA psychiatric hospital. Subjects reported recent average use of 2.5 g of cocaine per day for 14 days each month and experiencing a mean of 14 cocaine-related problems. The temporal sequence of cocaine-related problems was roughly consistent with the sequence of alcohol-related problems reported for alcoholics, with the earliest problems being interpersonal (e.g., arguments with others) and the most recent problems the severest (e.g., job loss, marital separation). The cocaine addicts showed a faster progression from first cocaine use to first cocaine-related problems (mean of 3.75 years) than that reported for alcoholics from first drink to first heavy drinking (8-10 years). Cocaine smokers had a faster course (3.4 years) than intranasal users (5.3 years).

Adult↗
PubMed1992

Alcohol and cocaine. Clinical and pharmacological interactions.

Both clinical experience and epidemiological studies in community and specialized (e.g., treatment) populations indicate that the prevalence of co-use of alcohol and cocaine, and the comorbidity of alcoholism and cocaine addiction, are greater than would be expected from the chance occurrence of two independent conditions. Alcohol and cocaine have pharmacokinetic and pharmacodynamic interactions that may account for some of this co-use. While their reinforcing properties have neuropharmacological and behavioral differences, a unified theory of reinforcement by alcohol and cocaine has been proposed, involving dopamine activity in the ventral tegmental area-nucleus accumbens circuit. Regardless of their pharmacology, the prevalent co-use of alcohol and cocaine has important implications for drug abuse treatment and indicates the need for future research on this topic.

Alcoholism↗
PubMed1979

Severe aggression in rats induced by mescaline but not other hallucinogens.

Pairs of male Sprague-Dawley rats were administered mescaline, lysergic acid diethylamide (LSD), psilocin, N,N-dimethyltryptamine (DMT), 3,4-dimethoxyphenylethylamine (DMPEA), or 5-hydroxydopamine (5-OHDA) IP prior to being placed in a shock-elicited aggression situation. When foot shock was delivered, controls struck each other with their forepaws, but never engaged in either biting or injurious fighting. Mescaline-treated rats (50 or 250 mg) rarely struck each other, but engaged in nearly lethal biting. While LSD (25--400 micrograms/kg), psilocin (2.0 mg/kg), and DMT (5 mg/kg) produced some biting, this did not significantly differ from controls and never resulted in injuries. At higher doses, psilocin, DMT, and DMPEA decreased the amount and intensity of fighting. Rats treated with 5-OHDA (8--200 mg/kg) or LSD (25--400 micrograms/kg) did not differ from controls. These results suggest that mescaline's ability to induce pathological aggression in rats exposed to foot shock is not shared by other hallucinogens or nonhallucinogenic mescaline analogues.

Aggression↗
PubMed1978

Beta-endorphin is behaviorally active in rats after chronic intravenous administration.

Male Sprague-Dawley rats received 14 daily intravenous injections of saline or human beta-endorphin (2.5 mg/kg). Animals were given one-way active avoidance training on the eleventh day, and analgesia testing on the twelfth (tail-flick) and thirteenth (hot-plate) days. Beta-endorphin had no effect on the number of trials needed to reach the avoidance criterion, but significantly lengthened response latencies. Beta-endorphin had no analgesic effect in either test procedure.

Animals↗
PubMed1978

Paranoid delusions and auditory hallucinations associated with digoxin intoxication.

The 83-year-old woman in this case report developed paranoid delusions and auditory hallucinations in association with toxic serum levels of digoxin, while remaining alert, unagitated, and coherent in thinking. No cardiovascular or metabolic abnormalities were discovered to account for her psychiatric symptoms. Her mental status rapidly returned to normal as serum digoxin declined to therapeutic levels.

Aged↗
PubMed1977

Facilitation and disruption by mescaline and 3,4-dimethoxyphenylethylamine of shock avoidance in rats.

The effects of mescaline hydrochloride (4.95-79.2 mg/kg i.p.) and its non-hallucinogenic analogue 3,4-dimethoxyphenylethylamine hydrochloride (DMPEA) (12.5-100 mg/kg i.p.) on shock avoidance in a shuttlebox were studied in male Long-Evans rats trained to high (above 88%, good performers) or low (below 6%, poor performers) stable base-line avoidance rates. In good performers, mescaline and DMPEA caused a dose-dependent decrease in avoidance rate (ED 50's 44.6 and 39.2 mg/kg, respectively) without affecting presession (5-min adaptation period) or intertrial shuttlebox crossings. In poor performers, mescaline caused a dose-dependent increase in avoidance rate (ED 50 = 24.8 mg/kg) and intertrial crossings, without affecting presession crossings. The results suggest that mescaline, but not DMPEA, has dual facilitative and disruptive effects on avoidance behavior at similar dose ranges. The facilitative, but not the disruptive, effect may be related to changes in motor activity.

Animals↗
PubMed1975

Does increasing stress change the behavioral action of mescaline from disruption to facilitation?

This experiment is related to the hypothesis of Bridger and of Wray that hallucinogens have facilitatory effects on animal behavior when stress is part of the experiment and have disruptive effects otherwise. Male Long-Evans rats were trained to high (above 89%), stable base line rates of shuttlebox avoidance, then given each of four treatments at 6-day intervals after returning to base line avoidance rates: 1. saline (1 ml i.p.), 2. saline+stressor, 3. mescaline hydrochloride (36.6 mg/kg i.p.), 4. mescaline (39.6 mg/kg i.p.)+stressor. Stress treatment was 1.0 mA footshock (1 sec duration) every 20-30 sec for 15 min between injection and session. Sessions (100 trials) began 20 min after injection. Treatments 1 and 2 had no effect on avoidance rate. Treatments 3 and 4 significantly decreased avoidance rate, with the latter causing significantly more decrease than the former. None of the treatments affected presession (5 min adaptation period) or intertrial crossings of the shuttlebox or latency on escape trials. These results suggest that exposure to a stressor, per se, is not the crucial factor causing hallucinogens to have facilitatory effects on animal behavior.

Adaptation, Psychological↗