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Biomedical subjects

H Ladinsky

Publications and source records attributed to H Ladinsky.

At least 91 records · Page 5Linked to original sources
PubMed1977

Apparent lack of a dopaminergic-cholinergic link in the rat nucleus accumbens septi-tuberculum olfactorium.

The nucleus accumbens septi and tuberculum olfactorium (NAS-TO), which from part of the mesolimbic dopaminergic system, and the striatum, which is part of the nigrostriatal dopamingeric system, contain high levels of both dopamine (DA) and acetylcholine and resemble each other in some other biochemical properties. We determined whether blockade or stimulation of DA receptors by agonists or antagonists affects the cholinergic neurons in this brain structure. The DA receptor antagonists haloperidol, pimozide, chlorpromazine and clozapine had no effect on the acetylcholine level in the NAS-TO even at 2-8 times the minimum dose required to maximally decrease striatal acetylcholine. Similarly, D-amphetamine and bromocriptine (CB 154), DA receptor stimulating drugs, had no effect on the acetylcholine level in this brain area at doses up to 3 times higher than those that produced a maximum increase in the striatum. Piribedil (15-120 mg/kg) and apomorphine (4 mg/kg) did increase acetylcholine in the NAS-TO but the action was not blocked by pimozide and is therefore not attributable to DA receptor action. The data thus indicate an apparent lack of a dopaminergic-cholinergic link in the NAS-TO.

Acetylcholine↗
PubMed1977

The cerebrospinal fluid choline levels in patients with Huntington's chorea. Negative effect of haloperidol treatment.

Lumbar cerebrospinal fluid (CSF) choline (CH) levels were measured in patients with Huntington's chorea (n = 14). This group was found not to differ significantly from normal controls (n = 13). The values for lumbar CSF Ch levels in the normal subjects were comparable with previously reported values. Of the choreic patients, seven were put on haloperidol treatment (4--6 mg daily). The CSF choline level remained unchanged with this treatment after 20 days. CSF cholinesterase activity was measured in the control and choreic group. The results were not significantly different.

Adult↗
PubMed1976

Increase in striatal acetylcholine by picrotoxin in the rat: evidence for a gabergic-dopaminergic-cholinergic link.

Picrotoxin, 2 mg/kg i.p., a GABA receptor blocking agent, increased rat striatal acetylcholine content by approximately 70% without altering the levels of this amine in the cerebral hemispheres, mesencephalon, diencephalon, hippocampus and cerebellum. Striatal choline levels were concomitantly decreased by about 25%. This dose of picrotoxin also increased striatal homovanillic acid levels by about 30%, an effect which was not antagonized by pretreatment with the dopamine receptor stimulating agent, piribedil. Picrotoxin did not affect striatal choline-O-acetyltransferase or cholinesterase activity after in vitro incubation. The action of picrotoxin on striatal acetylcholine levels was partially antagonized by pimozide and completely blocked by alpha-methyl-para-tyrosine pretreatment while the intraventricular injection of 6-hydroxydopamine was without effect. Convulsions were not prevented by any of these treatments. The results are interpreted as follows: picrotoxin released dopamine through disinhibition of the dopaminergic neurons as a result of blockade of gabergic receptors. The increased dopaminergic activity inhibited cholinergic neurons and lead to an increase in acetylcholine content. The data thus provide evidence for a possible gabergic (inhibitory)--dopaminergic (inhibitory)-cholinergic link terminating in the striatum.

Acetylcholine↗
PubMed1976

Effect of nomifensine on acetylcholine and choline in the rat striatum and brainstem.

Nomifensine, at a dose of 40 mg/kg, slightly but significantly increased rat striatal acetylcholine 60 min after i.p. administration without affecting choline levels or choline O-acetyltransferase and cholinesterase activities. This drug had no effect on brainstem acetylcholine. In contrast, d-amphetamine and desipramine both produced a small but significant increase in brainstem acetylcholine. It is suggested that nomifensine increased striatal acetylcholine indirectly through blockade of dopamine uptake.

Acetylcholine↗
PubMed1976

Lack of influence of the phase of estrus cycle or treatment with steroid contraceptive drugs on cholinergic parameters in mouse and rat brain.

Acetylcholine and choline levels were found not to fluctuate with the phase of the estrus cycle in the cerebral hemispheres, deincephalon and mesencephalon in the rat and mouse. Choline acetyltransferase activity was not altered in these brain areas in the mouse while in the rat there was a small but significant decrease in the cerebral hemispheres during proestrus (p less than 0.01), and in the mesencephalon during estrus (p less than 0.05), both with respect to diestrus. Chronic 30-day treatment with steroid contraceptive drug combinations (lynestrenol, 5 mg/kg+ mestranol, 0.3 mg/kg; lynestrenol, 2.5 mg/kg+ mestranol, 0.15 mg/kg; norethindrone, 4 mg/kg+ mestranol, 0.2 mg/kg; norethynodrel, 4 mg/kg+ mestranol, 0.06 mg/kg) did not alter cholinergic parameters in the brain areas of these two species except for minor changes in rare instances.

Acetylcholine↗
PubMed1975

Cholinergic-dopaminergic interaction in the striatum: the effect of 6-hydroxydopamine or pimozide treatment on the increased striatal acetylcholine levels induced by apomorphine, piribedil and d-amphetamine.

Apomorphine (1 and 2 mg/kg), piribedil (15 and 60 mg/kg) and d-amphetamine (5 and 10 mg/kg) increased rat striatal acetylcholine levels without affecting choline. Pretreatment with pimozide (0.5 mg/kg) completely antagonized the effect of apomorphine and piribedil and by itself markedly decreased striatal acetylcholine levels. d-Amphetamine signigicantly antagonized the effect of pimozide. Nine days after pretreatment with 6-hydroxydopamine plus pargyline, striatal dopamine was decreased by 78% while acetylcholine and choline levels remained unaltered. Under these conditions, the effect of d-amphetamine was completely abolished while apomorphine and piribedil were just as active as in the vehicle-treated group. The results suggest that d-amphetamine acted indirectly to increase striatal acetylcholine levels probably through the release of dopamine and/or noradrenaline, while apomorphine and piribedil acted directly at dopamine receptor sites.

Acetylcholine↗