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R L Borison

Publications and source records attributed to R L Borison.

At least 55 records · Page 3Linked to original sources
PubMed1980

Estrogen in experimental tardive dyskinesia.

Postmenopausal women have the highest incidence of tardive dyskinesia, suggesting that loss of ovarian function may predispose to this condition. Moreover, reports have indicated that estrogens could reduce abnormal movements in tardive dyskinesia. To test the effects of estrogen in tardive dyskinesia, ovariectomized rats were treated daily for 16 days with haloperidol alone (0.5 mg per kilogram) or haloperidol plus estradiol benzoate (EB; 8 microgram per kilogram). Rats were then challenged with apomorphine (0.25 mg per kilogram) 4 and 10 days after cessation of the chronic treatments. Chronic treatment with haloperidol alone enhanced the response to apomorphine, whereas the combined treatment produced a synergistic response. Rats treated chronically with haloperidol and then treated daily with EB after the haloperidol treatment showed an attenuation of drug-induced stereotypy. These data indicate that estrogen may mask development of tardive dyskinesia.

Animals↗
PubMed1980

Modulation of dopamine receptor sensitivity by estrogen.

Postmenopausal females have the highest incidence of tardive dyskinesia, suggesting that loss of ovarian function may predispose them to this condition. Moreover, reports have indicated that estrogens could reduce abnormal movements in tardive dyskinesia. To test the effects of estrogen in an animal model of tardive dyskinesia, ovariectomized rats were treated daily for 16 days with haloperidol (Haldol, 0.5 mg/kg) or Haldol + estradiol benzoate (EB, 10 micrograms/kg). Rats were then challenged with d-amphetamine or apomorphine 1 week following cessation of the chronic treatments. Chronic treatments with either Haldol or EB alone produced an enhanced response to both d-amphetamine and apomorphine, while the combined treatment produced a synergistic response. Rats treated chronically with Holdol, and treated daily with EB following the Haldol treatment, showed an attenuation of drug-induced stereotypy. These preliminary data indicate that estrogen can attenuate the development or mask the display of the supersensitive dopamine receptor.

Animals↗
PubMed1978

Lithium prevention of amphetamine-induced 'manic' excitement and of reserpine-induced 'depression' in mice: possible role of 2-phenylethylamine.

Repeated treatment of mice with lithium chloride (45 mg/kg, i.p., daily for 8 days) reduced the jumping, fighting, stereotypies, and hyperactivity induced by d-amphetamine (5 mg/kg, i.p.). Lithium also reduced the hypoactivity observed 1--3 h after reserpine (0.75 mg/kg, i.p.). In biochemical studies we found that 8-day treatment with lithium markedly reduced (to 45% of control) the recovery from brain of labelled 2-phenylethylamine (PEA) following i.p. injection of labelled L-phenylalanine, while decreasing recovery from brain of labelled PEA following its i.p. injection of 63% of control. In saline-treated mice, d-amphetamine appeared to increase PEA synthesis and to accelerate its disposition, whereas reserpine enhanced PEA synthesis and reduced disposition; all of these effects were antagonized by lithium pretreatments. Since PEA appears to be one of the most powerful behavioral stimulants among endogenous neuroamines, and because its deaminated metabolites are behavioral depressants, such antagonism of brain PEA metabolism may significantly contribute to the prophylactic action of lithium against both manic and depressive behavior.

Animals↗
PubMed1978

Dopamine binding following prolonged haloperidol pretreatment.

The number of binding sites for tritiated dopamine as well as the affinity of 3H-dopamine for dopamine receptors was studied in rats chronically pretreated with the neuroleptic haloperidol. The rats were given haloperidol for 14 or 21 days and were killed on day 21. It was found that 14 days of haloperidol pretreatment followed by drug withdrawal resulted in a 67% increase in the number of 3H-dopamine binding sites in the striatum and ninefold increase in the affinity constant in the striatum. The same pretreatment regimen had no effect on either the number of receptor sites or the affinity constant in the nucleus accumbens. These results are consistent with the hypothesis that chronic neuroleptic pretreatment results in receptor site hypersensitivity in the striatum, which may be a major factor in the production of tardive dyskinesia.

Animals↗
PubMed1978

A new putative neuroregulator of the extrapyramidal system.

A putative neurotransmitter, 2-phenylethylamine, which is most highly concentrated in the extrapyramidal system of human brain, is able to reverse reserpine-induced parkinsonism in animals and elicit stereotypy. This action is only partially antagonized after catecholamine depletion by pretreatment with a-methyl-para-tyrosine, and fully blocked by pretreatment with haloperidol, a dopamine receptor blocker. Therefore, via direct and/or indirect actions, 2-phenylethylamine may serve a neuroregulatory role in the extrapyramidal system.

Animals↗
PubMed1978

Enkephalins and nigrostriatal function.

Unilateral lesions of the substantia nigra were made with 6-hydroxydopamine in rats. In this model, drugs such as naloxone, which block endogenous enkephalin receptors, potentiated agents with postsynaptic dopaminergic actions, while antagonizing agents with presynaptic dopaminergic actions. Drugs which increase brain enkephalin content (d-phenylalanine or methionine-enkephalin) antagonized postsynaptically active agents and potentiated presynaptic agents. Naloxone also reversed reserpine-induced parkinsonism in rats. Separate pre- and postsynaptic enkephalinergic neurons thus seem to modulate nigrostriatal function.

Animals↗
PubMed1978

A new animal model for schizophrenia: interactions with adrenergic mechanisms.

Amphetamine-induced stereotyped behavior in animals is proposed as a model for schizophrenia. Chronic amphetamine administration produces stereotyped behavior and a paranoid schizophreniform syndrome in man, whereas in animals a behavioral sensitization to stereotypy is evoked. We now show that phenylethylamine (PEA), an amphetamine-like stimulant concentrated in the limbic system of human brain, produces stereotypy in rats with a behavioral sensitization when chronically administered. In comparing amphetamine-induced stereotypy with PEA-induced stereotypy, we found that the alpha-adrenergic blocking agents phentolamine and phenoxybenzamine selectively antagonize PEA stereotypy, whereas the beta-adrenergic blocking agent propranolol fails to alter significantly stereotypies evoked by PEA or amphetamine administration. Catecholamine depletion by alpha-methyl-p-tyrosine administration blocks stereotypies induced by both PEA amphetamine, whereas selective norepinephrine depletion antagonizes only PEA stereotypy; the amino acid precursors of both norepinephrine and dopamine potentiate stereotypies. Therefore, PEA-elicited stereotypy, but not amphetamine-elicited stereotypy, is dependent upon norepinephrine; the significance of this for the PEA animal model of schizophrenia is discussed.

Animals↗
PubMed1978

Metabolism of an amino acid with antidepressant properties.

The amino acid D-phenylalanine exerts antidepressant properties which are believed to be due to its metabolism to brain phenylethylamine. We now show that in mice, the increase in brain phenylethylamine levels induced by L-phenylalanine, but not D-phenylalanine, is antagonized by drugs which block the stereospecific decarboxylase enzyme. Our results show that D-phenylalanine metabolism to phenylethylamine is independent of pathways involving L-phenylalanine.

Animals↗