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Biomedical subjects

D E Clody

Publications and source records attributed to D E Clody.

14 recordsLinked to original sources
PubMed1987

Low doses of cis-flupentixol attenuate motor performance.

We evaluated the effects of cis-flupentixol on reinforced responding. The experimental subjects were rats and the reinforced response was a lever press. The procedure was a five-component multiple schedule that provided five different reinforcement rates. Cis-flupentixol produced dose-dependent decreases in reinforced responding. An equation, the matching law, was fitted to the results. One parameter of this equation represents the estimated response rate asymptote. Cis-flupentixol produced dose-dependent decreases in the asymptotes. A second parameter of the equation represents the rate of reinforcement that maintains a one-half asymptotic response rate. Cis-flupentixol did not appear to affect this measure. There is evidence that the response rate asymptote measures motor components of response rate and that the reinforcement parameter measures the efficacy of the reinforcement maintaining the response. According to these results, cis-flupentixol systematically affected the motor-component of reinforced responding-it slowed down lever pressing-without affecting the subject's sensitivity to the reinforcer maintaining the response. In contrast, other neuroleptics have decreased the subjects' sensitivity to reinforcement, according to the matching law measures.

Animals↗
PubMed1985

Effect of chronic desmethylimipramine or electroconvulsive shock on selected brain and platelet neurotransmitter recognition sites.

Rats were treated with electroconvulsive shock (ECS), desmethylimipramine (DMI), ECS plus DMI, or diazepam. In vitro analyses showed that chronic ECS produced an elevated density of recognition sites for [3H]imipramine (IMI) in platelet membranes, but had no effect on membrane preparations derived from cortical tissue. A similar elevation in receptor binding was seen exclusively in platelets after chronic ECS plus DMI, whereas no effect was observed with DMI alone. Equilibrium dissociation constant (KD) values for [3H]IMI were also increased in platelet membranes from rats given chronic ECS or ECS plus DMI treatment. Chronic ECS or DMI administration produced a decreased density of beta-adrenergic recognition sites in frontal cortex and cerebellum as assessed by [3H]dihydroalprenolol (DHA) binding. The combination of ECS plus DMI produced a similar decrease. In addition, chronic diazepam administration produced a down-regulation of the beta-adrenergic receptor only in the cerebellum. These data provide evidence for the differential regulation of brain and peripheral neurotransmitter recognition sites.

Animals↗
PubMed1985

Hippocampal muscarinic receptor loss following trimethyl tin administration.

The effects of trimethyl tin on passive and active avoidance behavior, hippocampal muscarinic receptors and hippocampal cell destruction were examined in male rats. The animals were intubated with 18 mumoles/kg (3.5 mg/kg) of TMT hydrochloride or vehicle. When tested two weeks later treated animals exhibited marked deficits in retention of passive avoidance and extinction of active avoidance tasks. Receptor binding analysis, using 3H-QNB, revealed a significant decrease (21%) in muscarinic receptor density in the hippocampus. Histological examination of the hippocampus revealed a concomitant loss in pyramidal cells in these animals. These results suggest that muscarinic receptors reside on the hippocampal pyramidal cells and that these cells and receptors may be involved in retention of passive avoidance behavior.

Animals↗
PubMed1982

Role of serotonin in the blockade of muricidal behavior by tricyclic antidepressants.

Dose-response curves for the ability of three tricyclic antidepressants, imipramine, desmethylimipramine and amitriptyline to inhibit muricidal behavior were measured after treatment with a tryptophan-free diet and after administration of p-chloroamphetamine. Both treatments, which have been reported to specifically reduce central levels of serotonin, decreased the ability of the drugs to inhibit muricide. The results suggest that all three antidepressants block muricide in part through their effects on serotonin.

Aggression↗
PubMed1980

Stimulus efficacy, chlorpromazine, and schizophrenia.

Stimulus efficacy can be defined in terms of rat least two variables: Proximity of a stimulus to reinforcement and the association of a stimulus with reinforcements of different magnitudes. The behavioral effects of chlorpromazine were found to be significantly modulated by stimulus efficacy and increases in efficacy attenuated drug effect. The relevance of this finding to various conjectures about the deficits seen in schizophrenia is discussed.

Animals↗
PubMed1973

Effects of dibutyryl cyclic AMP on restoration of function of damaged sciatic nerve in rats.

In two experiments, the sciatic nerve of rats was either crushed or hemisected, and N(6),O(2)-dibutyryl adenosine 3',5'-monophosphate or saline was injected intramuscularly near the site of the lesion. In both types of nerve damage, the sensorimotor functions of animals treated with N(6),O(2)-dibutyryl adenosine 3',5'-monophosphate returned earlier than did those of saline-treated control animals.

Animals↗
PubMed1972

Cyclic adenosine monophosphate phosphodiesterase in brain: effect on anxiety.

Drugs that reduce anxiety may be mediated by cyclic adenosine monophosphate in the brain because (i) potent anxiety-reducing drugs are also potent inhibitors of brain phosphodiesterase activity; (ii) dibutyryl cyclic adenosine monophosphate has the ability to reduce anxiety; (iii) the methylxanthines show significant anxiety-reducing effects; (iv) theophylline and chlordiazepoxide produce additive anxiety-reducing activity; and (v) there is a significant correlation between the anxiety-reducing property of drugs and their ability to inhibit phosphodiesterase activity in the brain.

Animals↗