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Biomedical subjects

R Raisman

Publications and source records attributed to R Raisman.

At least 55 records · Page 3Linked to original sources
PubMed1981

Regional distribution of [3H]imipramine binding in rat brain.

[3H]imipramine binding was measured in 23 microdissected areas of the rat brain and compared to published values for the endogenous levels of serotonin, noradrenaline and dopamine in the same areas. The density of [3H]imipramine binding sites appears to be highly correlated with the distribution of endogenous serotonin especially where the serotonin is located mainly in nerve terminals. A weak but still significant correlation also exists with the distribution of endogenous noradrenaline whereas no such correlation could be detected for endogenous dopamine.

Animals↗
PubMed1981

High-affinity 3H-imipramine binding in platelets from untreated and treated depressed patients compared to healthy volunteers.

Specific high-affinity binding of 3H-imipramine to human platelets possesses very similar characteristics to the sites previously described in animal and human brains. In a study comparing the binding of 3H-imipramine in platelets obtained from 39 control volunteers with 37 hospitalized, untreated, severely depressed patients, the maximal binding of 3H-imipramine was found to be significantly lower in the depressed population. There were no differences in the KD values. After 7-15 days of treatment with tricyclic anti-depressant drugs, there was an improvement in the degree of the depression but no significant change in the maximal 3H-imipramine binding. After an average of 50 days treatment, Hamilton ratings had returned to normal, but the 3H-imipramine binding values remained unchanged.

Adult↗
PubMed1981

Distribution of specific high-affinity binding sites for [3H]imipramine in human brain.

[3H]Imipramine binds with high affinity to membranes from different regions of the human brain. The highest density of binding sites was observed in the hypothalamus and substantia nigra and the lowest density in the white matter and cerebellum. As found in rat brain, tricyclic antidepressant drugs are potent inhibitors of [3H]imipramine binding. Atypical antidepressants are, however, much weaker at inhibiting the specific binding. The [3H]imipramine binding site in human cortex is apparently identical to the site already described in the rat brain and in human platelets.

Aged↗
PubMed1981

Localisation of tricyclic antidepressant binding sites on serotonin nerve terminals.

High-affinity specific [3H]imipramine binding has been demonstrated in the brain and platelets of various species including man. Electrolytic lesions of the rat dorsal raphe, which resulted in a significant decrease in the endogenous levels of serotonin produced a reduction in the density of [3H]imipramine binding sites in the hypothalamus and cortex. The affinity constants were unchanged. These results suggest that [3H]imipramine binding sites are located on serotonin nerve terminals.

Animals↗
PubMed1980

High-affinity [3H]imipramine binding in rat hypothalamus: association with uptake of serotonin but not of norepinephrine.

Inhibition of the binding of [3H]imipramine and inhibition of the uptake of [3H]serotonin and [3H]norepinephrine by a series of antidepressants and other drugs were studied in the rat hypothalamus. No correlation was found between the potencies of these drugs for the inhibition of [3H]imipramine binding and the inhibition of [3H]norepinephrine uptake. There was, however, a highly significant correlation between the potencies of these drugs for the inhibition of [3H]serotonin uptake. These results suggest that high-affinity [3H]imipramine binding might be associated with the mechanism of serotonin uptake in the brain.

Animals↗
PubMed1980

Tritiated imipramine binding sites are decreased in platelets of untreated depressed patients.

The high-affinity binding of triatiated imipramine to platelet membranes was compared in samples from 16 untreated depressed women and 21 age-matched controls of the same sex. The maximal binding in the depressed group was significantly lower than that of the controls, although the affinity constants were similar. These results suggest that binding of tritiated imipramine in human platelets may represent a biochemical index of depression, possibly reflecting similar changes in the brain.

Adult↗
PubMed1980

Specific 3H-imipramine binding in human platelets. Influence of age and sex.

Human platelets have been shown to possess high-affinity binding sites for 3H-imipramine. These binding sites have a similar affinity and drug specificity to those already described in rat brain. The platelets from healthy volunteers show no difference in 3H-imipramine binding between the sexes but there is a decrease in maximal 3H-imipramine binding with increasing age of the donor.

Adolescent↗
PubMed1980

Specific tricyclic antidepressant binding sites in rat brain characterised by high-affinity 3H-imipramine binding.

The specific binding of 3H-imipramine to various brain regions of the rat is of high affinity (Kd = 4.0 nM), rapid and reversible. It was inhibited by tricyclic antidepressants at nanomolar concentrations and by atypical antidepressants at micromolar concentrations. The binding does not seem to be directly related to known neurotransmitter receptor systems. Specific 3H-imipramine binding sites were unequally distributed between the various brain regions and undetectable in the heart and vas deferens. Rats chronically treated with desipramine for three weeks had significantly less specific 3H-imipramine binding sites in the cortex than did control animals. It is concluded that these 3H-imipramine binding sites may be important in the study of depression and of the mechanism of action of antidepressant drugs.

Animals↗
PubMed1979

Specific tricyclic antidepressant binding sites in rat brain.

The discovery of high-affinity binding sites for psychoactive drugs such as benzodiazepines, opiates and neuroleptics has opened up new approaches to the study of these drugs and their mechanisms of action. Although most tricyclic antidepressants inhibit neuronal uptake of noradrenaline and serotonin, their mechanism of action remains unclear. Changes in the sensitivity of the beta-receptor after chronic tricyclic antidepressant treatment suggest that they modulate noradrenergic neurotransmission. Tricyclic antidepressants also act directly on cholinergic, histaminergic, alpha-adrenergic and serotonergic receptors. It is not clear, however, which, if any, of these effects are related to the primary antidepressant effect or whether they are simply responsible for some of the side effects. We have thus investigated the possibility that specific binding sites for tricyclic antidepressants exist in the central nervous system. So far, binding studies using 3H-labelled tricyclic antidepressant drugs have only detected binding to histaminergic H2 and cholinergic muscarinic receptors and low-affinity binding. We demonstrate here a population of specific high-affinity binding sites for 3H-imipramine on brain membranes which may be responsible for the antidepressant effects of these drugs.

Animals↗
PubMed1979

Specific labelling of postsynaptic alpha 1 adrenoceptors in rat heart ventricle by 3H-WB 4101.

The alpha-adrenoceptor ligand, 3H-WB 4101 binds to a single population of independent sites in the rat heart ventricle. These sites are not affected by chemical sympathectomy with 6-hydroxydopamine and thus appear to be located postsynaptically. The relative order of potencies for displacement of 3H-WB 4101 binding:prazosin greater than phentolamine greater than yohimbine, is characteristic of that of the alpha 1 type of adrenoceptors. In heart ventricle 3H WB-4101 thus seems to label specifically postsynaptically located alpha 1-adrenoceptors. The significance of the specificity of this ligand is discussed with relevance to its use in the central nervous system.

Adrenergic alpha-Antagonists↗