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Biomedical subjects

S Gershon

Publications and source records attributed to S Gershon.

At least 217 records · Page 12Linked to original sources
PubMed1976

Reaction time as a diagnostic measure in senility.

Both simple and disjunctive reaction times (RT) are known to slow with aging but there is a paucity of information on RT changes in senility. Since disjunctive RT involves cognition in addition to the sensory-motor speed and attentional components of simple RT, it was hypothesized that disjunctive RT would be a reliable index of age-related mental decline. To test this prediction, simple and disjunctive RT were measured in matched groups of 20 normal and 20 cognitively impaired elderly. Simple RT was slower in the senile patients than in the normal subjects, but this difference was accounted for by differences in disjunctive RT. The senile patients showed a much larger performance decrement with respect to disjunctive RT than did the normal subjects--a difference which was not accounted for by differences in simple RT. In a discriminant function analysis, disjunctive RT alone correctly identified the senile patients and the normal subjects with 86% accuracy. Thus, this measure proved to be a reliable index of age-related mental decline. Preliminary data indicate that disjunctive RT slowing is correlated with non-memory mental decline, and that poor performance is related to the need for care and supervision.

Adult↗
PubMed1976

Genetics of affective disorders. I. Familial incidence study of bipolar, unipolar and schizo-affective illnesses.

47 affectively ill psychiatric patients and their first-, second- and third-degree relatives were investigated by means of an interview and pedigree analysis to determine the incidence of psychiatric illness in their families. The percentage of psychiatric illness appeared greatest in families of bipolar and schizo-affective probands and least in families of unipolar depressives. In addition, we observed that often within a particular family constellation, more than one type of psychiatric illness (i.e., bipolar manic-depression, schizophrenia, alcoholism, etc.) was present. Morbidity risks varied from one affected family to another, indicating that the genetic risk components for some families are greater than for others. These findings are suggestive of multifactorial genetic disease but other genetic models are considered.

Affective Symptoms↗
PubMed1976

Genetics of affective disorders. II. Morbidity risk and genetic transmission.

Morbidity risk and genetic transmission data on a small population of bipolar, unipolar and schizo-affective outpatients suggest a possible genetic overlap between bipolar and schizo-affective patients. There is a conspicuous absence of a homologous illness in the relatives of schizo-affective probands, although the incidence of schizophrenia was higher in these relatives as compared to the relatives of either bipolar or unipolar probands. The data, although tentative because of the relatively small numbers involved, suggest a multifactorial mode of transmission in some affective illnesses. These disease entities appear familial rather than 'genetically transmitted'. There are select families who show the heritable genetic penetrance previously recorded for these mental disorders.

Adult↗
PubMed1976

Exploration of affective illness.

This report deals with a series of experimental approaches carried out in clinical studies to attempt to examine the role of amines in relationship to affective state and the mode of action of thymoleptic agents. Attempts have been made to examine enzymes, amines and other metabolites in biological fluids to assess the role of catecholamines and indoleamines in these disorders. Synthesis inhibitors were employed in studies where antidepressant drug-induced remission was initiated and the effect of two inhibitors was assessed on the clinical state. The results are presented and discussed in regard to the significance of the role of serotonin in depressive states and the action of thymoleptic agents.

Adult↗
PubMed1976

Effect of tetrahydrocannabinols on 3H-acetylcholine biosynthesis in various rat brain slices.

The effects of delta8- and delta9-tetrahydrocannabinol on the biosynthesis of 3H-acetylcholine (ACh) from 3H-choline in cortical, hypothalamic and striatal rat brain slices were examined. The two cannabinols were found to inhibit the synthesis of 3H-ACh in the three brain regions. Treatment with cannabidiol did not alter ACh synthesis. Delta8-tetrahydrocannabinol was approximately twice as effective as the delta9-isomer. This effect was not associated with alterations in striatal and cortical choline acetyltransferase or with an impaired high-affinity uptake system for choline in the striatum. Treatment with delta8- and delta9-cannabinols, likewise, did not change striatal choline and ACh levels. Antagonism of the ACh biosynthesis inhibition occurred when slices from treated animals were incubated in depolarizing concentration of K+ ion. These results suggest that the inhibition of ACh synthesis observed in tetrahydrocannabinol-treated rats may be related to interference with the propagated action potential or with the depolarization process in cholinergic neurons.

Animals↗
PubMed1976

Effects of tranylcypromine on 5-HT uptake and its interaction with PCPA on rat brain 5-HT.

The effect of p-chlorophenylalanine-treatment in rats receiving chronic treatment with tranylcypromine on brain serotonin and 5-hydroxyindoleacetic acid levels was examined. This treatment schedule was similar to that followed in depressed patients undergoing treatment with the monoamine oxidase inhibitor. PCPA completely obviated the elevation in serotonin and further reduced 5-HIAA levels of animals treated chronically with tranylcypromine. These effects correlated with PCPA-induced reversal in the clinical improvement achieved by tranylcypromine. In in vitro studies, tranylcypromine was found to inhibit 5-HT uptake into synaptosomes with a minimal action on the spontaneous release of the amine.

Animals↗
PubMed1975

Clinical studies with dopamine-receptor stimulants.

Oral administration of ET-495 was found to cause worsening of psychiatric status in 4 out of 7 schizophrenic patients, and to induce a paranoid state and a syndrome of auditory hallucinosis in 2 non-schizophrenics. These observations were compatible with the hypothesized role of dopamine in schizophrenia. However, these psychotogenic effects were far less dramatic than those noted in other studies with amphetamine, methylphenidate or L-Dopa. Possible explanations for this differing psychotogenic potency of receptor stimulators versus presynaptic agonists are presented. Intravenous ET-495 and apomorphine did not show psychotogenic effects.

Adult↗
PubMed1975

Involvement of biogenic amines in drug-induced aggressive pecking in chicks.

Pairs of neonate chicks were administered psychoactive agents and pecks against each other were recorded during 4-hr test sessions. The first experiment assessed where drug-induced aggressive pecking could serve as a useful anti-depressant screening model. Although pecking was induced by tricyclics, d-amphetamine, and L-Dopa, ineffective agents included a MAO inhibitor (pargline) and a tricyclic indole antidepressant (iprindole). These data cast doubt on the validity of the chick pecking model as a specific antidepressant tests. A second experiment attempted to determine where different amines were involved in pecking induced by an antidepressant and a CNS stimulant. Pairs of chicks were pretreated with various doses of amine antagonists, and a standard dose of imipramine (IMI) or d-amphetamine (AMP) was administered. Haloperidol completely antagonized AMP but not IMI pecking, while phentolamine and propranolol did not modify AMP pecking, suggesting involvement of dopamine. Pecking induced by IMI was partially antagonized by a dose of methysergide ineffective in modifying AMP pecking. Neither phentolamine nor propranolol blocked IMI pecking. Serotonin was further implicated in IMI pecking in a third experiment, whether chronic PCPA pretreatment significantly decreased IMI, but not AMP pecking. These data suggest that aggressive pecking induced by AMP and IMI may be mediated by different amine systems.

Aggression↗
PubMed1975

Dose effects of smoked marihuana on human cognitive and motor functions.

Graded doses of marihuana were administered to five adults in a longitudinal repeated-measurements design. Speed of response was the basic parameter measured accross tests of increasing cognitive involvement. Marihuana produced significant dose-response effects of impaired performance in all test scores. However, single automatic motor abilities demonstrated greater sensitivity than tests of greater complexity. Evidence is presented for tolerance development.

Adult↗
PubMed1975

Morphine-dependent rats: blockade of precipitated abstinence by tetrahydrocannabinol.

Male rats were implanted subcutaneously with a pellet containg 75 milligrams of morphine base or placebo, and naloxone hydrochloride (4 milligrams per kilogram of body weight) was administered 72 hours later. Treatment with delta-9-tetrahydrocannabinol (2, 5, or 10 milligrams per kilogram) 1 hour before maloxone administration significantly reduced the intensity of abstinence; the two higher doses blocked the appearance of wet shakes and escapes, diarrhea, and increased defecation. delta-9-Tetrahydrocannabinol did not induce abstinence itself, and prior treatment with cannabidiol was ineffective in reducing naloxoneprecipitated abstinence in animals with morphine pellets. These data suggest that delta-9-tetrahydrocannabinol may be of value in facilitating narcotic detoxification.

Animals↗