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Biomedical subjects

S M Antelman

Publications and source records attributed to S M Antelman.

At least 55 records · Page 3Linked to original sources
PubMed1982

Differences among 'serotonergic' anorectics in a cross-tolerance paradigm: do they all act on serotonin systems?

Rats on a 4 hr/day feeding schedule showed anorexia after i.p. injections of several 'serotonergic' agents. Tolerance developed within a few days of daily administration of all drugs except fluoxetine. The tolerant animals were then given a cross-tolerance test with a different agent, either the next day or after a drug free washout period. Rats which were tolerant to quipazine or MK 212 showed no cross-tolerance to fenfluramine or norfenfluramine. In contrast, rats which were tolerant to fenfluramine showed good cross-tolerance to quipazine or MK 212. However, after a washout period between the end of the chronic fenfluramine regimen and the cross-tolerance test, quipazine regained its full anorectic potency. The development of tolerance to fenfluramine was dependent upon the number of injections, not on their spacing. Fenfluramine-tolerant animals showed a partial decay of tolerance after a 3 day washout, but still retained some tolerance after 12 days. These findings imply that the mechanisms underlying the development of tolerance may differ from those which mediate its maintenance. Our data further suggest that not all of the agents act on the same neural system(s), and raise the possibility that non-serotonergic and/or non-cerebral systems may be involved in the mode of action of these agents.

Animals↗
PubMed1980

Electroconvulsive shock: progressive dopamine autoreceptor subsensitivity independent of repeated treatment.

Repeated electroconvulsive shock, applied to rats, induces a subsensitivity of dopamine autoreceptors located in the substantia nigra as indexed by single-unit electrophysiological techniques. This reduced sensitivity is time-dependent, since effects similar to those seen with repeated treatment were also observed when single electroconvulsive shock was followed by an appropriate treatment-free interval. These data, coupled with identical results after the repeated administration of tricyclic antidepressants, raise the possibility that a reduction of dopamine autoreceptor sensitivity could underlie both electroconvulsive shock and pharmacological treatment of depression.

Animals↗
PubMed1980

Repeated tricyclics induce a progressive dopamine autoreceptor subsensitivity independent of daily drug treatment.

Dopamine (DA) has largely been ignored in considering possible mechanisms underlying the therapeutic effects of tricyclic anti-depressants (TCA). Most previous work done has focused on the ability of some TCAs to block the in vitro re-uptake of DA--an effect which unfortunately requires very high doses. Recently, however, Serra et al. proposed that TCAs may exert their therapeutic effects by inducing a subsensitivity of presynaptic receptors located on the dendrites and soma of DA neurones (DA autoreceptors). This hypothesis was directly tested by examining the influence of TCAs on the demonstrated ability of the DA agonist, apomorphine, to depress selectively the spontaneous activity of single DA cells. We now report that repeated administration of both typical and atypical TCAs induces a progressive subsensitivity of DA autoreceptors, and that this gradual augmentation of DA autoreceptor subsensitivity depends on the passage of time rather than daily TCA administration. The latter finding suggests that daily drug administration may not be therapeutically necessary.

Action Potentials↗
PubMed1980

Interchangeability of stress and amphetamine in sensitization.

In view of similarities between the behavioral, biochemical, and electrophysiological effects of amphetamine and stress, we tested the hypothesis that presentation of a stressor, mild tail pressure, can sensitize an animal to the later effects of amphetamine, and vice versa. Our findings supported this hypothesis and suggest that amphetamine and at least some stressors may be interchangeable in their ability to induce a sensitization. The data raise the possibility that stress might be a common variable contributing to both amphetamine psychosis and some forms of schizophrenia.

Animals↗
PubMed1980

Amphetamine stereotypy is not a homogeneous phenomenon: sniffing and licking show distinct profiles of sensitization and tolerance.

Sniffing and licking components of amphetamine-induced stereotypy were studied separately during chronic drug treatment. Sniffing showed a gradual increase, or sensitization, in intensity and duration. By contrast, licking developed tolerance for approximately the first 21 days, followed by a progressive increase. Stereotypy is therefore not a homogeneous phenomenon, and sniffing and licking are probably subserved by distinct neuroanatomic substrates. The sensitization of sniffing behavior may be related to the induction of amphetamine-induced paranoid psychosis in humans.

Animals↗
PubMed1980

Orbital or medial frontal cortical lesions have different effects on tail pressure-elicited oral behaviors in rats.

Three groups of rats were tested with daily tail pressure (TP) tests until reliable and stable baseline eating, gnawing or licking was observed. One group then received bilateral aspiration of the medial frontal cortex, a second group received orbital frontal cortical lesions, and a third group received control lesions of the motor cortex. Daily TP tests were continued postoperatively. There was no disruption of TP-elicited oral behaviors after medial frontal or motro cortex lesions. In contrast, orbital frontal lesions abolished TP behaviors on the first day postoperatively, and there was a slow recovery of TP until day 5 when the elicited behaviors were about 80% of preoperative levels. The time course of recovery of TP-elicited oral behavior closely paralleled the recovery of elective eating after orbital frontal lesions, both in the group given TP and in another group given orbital lesions but not TP. These data demonstrate a marked difference between the medial and orbital divisions of the prefrontal cortex in the mediation of stress-induced oral behavior, and we discuss our data in terms of the possible role of dopamine terminals in these regions.

Animals↗