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Effects of haloperidol, quinelorane, and lithium on regional neurotensin/neuromedin N concentrations: Further evidence for neurotensin/neuromedin N‐Dopamine interactions
Author(s) -
Clement Rita,
Griff Dan,
Banks Beth,
Nemeroff Charles,
Kitabgi Patrick,
Bissette Garth
Publication year - 1994
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890170405
Subject(s) - haloperidol , chemistry , nucleus accumbens , neurotensin , dopamine receptor d2 , agonist , pharmacology , medicine , endocrinology , dopamine , receptor , neuropeptide , biochemistry
In order to further characterize the pharmacologic mechanisms that mediate the antipsychotic drug‐induced increase in neurotensin (NT) in nucleus accumbens and striatum, the effects of three weeks treatment with psychotherapeutic levels of lithium alone or in conjunction with haloperidol were compared to the ability of haloperidol alone to alter NT and neuromedin N (NMN) regional brain concentrations in rats. A separate experiment examined the ability of a selective dopamine D2 receptor agonist, quinelorane, to alter NT/NMN regional concentrations after three weeks of treatment as compared to haloperidol, a D 2 receptor antagonist. Haloperidol (1 mg/kg) increased both NT and NMN concentrations in several brain regions and these parallel peptide increases were highly correlated. Lithium chloride (0.4 mM) had no effect, either alone or with haloperidol, on NT/NMN concentrations. Quinelorane (1 mg/kg), however, effectively increased both NT and NMN concentrations in the caudate nucleus and nucleus accumbens, as did haloperidol (2 mg/kg). These data indicate that the induction of NT and NMN, whose adjacent sequences are contained in a pro‐hormone product of a single gene, occurs in tandem and remains proportional, as well as demonstrating that putative D 2 receptor agonists can produce effects on NT/NMN systems that are similar to D 2 receptor antagonists. © 1994 Wiley‐Liss, Inc.