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Enhancement of Hypophysectomy‐Induced Dopamine Receptor Hypersensitivity in Male Rats by Chronic Haloperidol Administration
Author(s) -
Gordon John H.,
Diamond Bruce I.
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb02709.x
Subject(s) - dopamine , dopamine receptor , medicine , endocrinology , prolactin , haloperidol , hypophysectomy , dopamine receptor d2 , dopamine receptor d1 , receptor , apomorphine , chemistry , pharmacology , dopaminergic , hormone
It has been reported that hypophysectomy (HYPOX) would antagonize the development of a neuroleptic‐induced dopamine receptor hypersensitivity, and suggested that the neuroleptic‐induced dopamine receptor hypersensitivity may be mediated by the neuroleptic‐induced hyperprolactinemia. Conversely, we and others have reported on the ability of HYPOX animals to develop a neuroleptic‐induced dopamine receptor hypersensitivity. The present study was undertaken to define the possible role(s) of prolactin in the modulation of striatal dopamine receptor sensitivity. The data from these studies indicate: that HYPOX alone will result in the development of a striatal dopamine receptor hypersensitivity; that the HYPOX‐induced dopamine receptor hypersensitivity could be increased by the chronic administration and withdrawal of haloperidol; that administration of prolactin to HYPOX rats would partially antagonize the development of the neuroleptic‐induced dopamine receptor hypersensitivity; and that the administration of prolactin alone had minimal effects on the apomorphine‐induced behavior or neurochemistry of the HYPOX animals. These results suggest that the neuroleptics do not require the presence of a pituitary secretion (specifically, prolactin) to induce a striatal dopamine receptor hypersensitivity; however, they do indicate that a pituitary secretion, perhaps prolactin, may have the ability to modulate striatal dopamine sensitivity.