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Dopamine binding following prolonged haloperidol pretreatment.

A Hitri, W J Weiner, R L Borison

Annals of Neurology

|February 1, 1978

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Chronic haloperidol treatment in rats increased dopamine receptor binding sites and affinity in the striatum. This suggests neuroleptic-induced receptor hypersensitivity may contribute to tardive dyskinesia.

Area of Science:

Neuroscience
Pharmacology
Neurobiology

Background:

Neuroleptic medications like haloperidol are used to treat psychosis.
Tardive dyskinesia is a potential side effect of long-term neuroleptic use.

Purpose of the Study:

To investigate the effects of chronic haloperidol pretreatment on dopamine receptor characteristics in rats.
To explore the link between neuroleptic treatment and potential receptor changes contributing to tardive dyskinesia.

Main Methods:

Rats were chronically administered haloperidol for 14 or 21 days.
Dopamine receptor binding assays using tritiated dopamine (3H-dopamine) were performed on striatal and nucleus accumbens tissue.
Analysis of binding site number and affinity constant was conducted.

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Main Results:

A 14-day haloperidol pretreatment followed by withdrawal significantly increased the number (67%) and affinity of 3H-dopamine binding sites in the striatum.
No significant changes in receptor site number or affinity were observed in the nucleus accumbens.
These findings indicate region-specific alterations in dopamine receptor sensitivity.

Conclusions:

Chronic haloperidol exposure leads to dopamine receptor hypersensitivity in the rat striatum.
Striatal receptor hypersensitivity may be a key mechanism underlying the development of tardive dyskinesia.