Abstract
A single injection of 17 β-estradiol valerate produces, 6-7 days later, potentiation of neuroleptic catalepsy. Multiple behavioral measures demonstrate that this effect occurs with an acute dose of haloperidol of 0.25 mg/kg IP. An even lower dose of haloperidol (0.10 mg/kg), which fails to make control rats cataleptic, produces catalepsy in estrogen-treated animals. Thus, estrogen lowers the threshold of haloperidol-induced catalepsy. Repeated testing alone induces cataleptic reactions in control rats. Estrogen suppresses such handling-related catalepsy in animals that subsequently show potentiation of catalepsy at a dose of haloperidol (0.10 mg/kg), which has virtually no effect on control rats. Thus, in these behavioral paradigms, estrogen by itself does not produce cataleptic effects, and estrogen-induced potentiation of haloperidol catalepsy is not merely additive to an antecedent, neuroleptic-like effect of this hormone. We interpret our results in terms of (1) the relationship of cataleptic reactions in normal rats to drug-induced cataleptic states; (2) the possible relevance of our behavioral results to basal ganglia disorders; and (3) the relationship of neuroleptic catalepsy to striatal DA receptors, and their modulation by estrogen.
Original language | English (US) |
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Pages (from-to) | 1027-1035 |
Number of pages | 9 |
Journal | Pharmacology, Biochemistry and Behavior |
Volume | 17 |
Issue number | 5 |
DOIs | |
State | Published - Nov 1982 |
Externally published | Yes |
Keywords
- Catalepsy
- Estrogen
- Haloperidol
- Neuroleptics
ASJC Scopus subject areas
- Biochemistry
- Toxicology
- Pharmacology
- Clinical Biochemistry
- Biological Psychiatry
- Behavioral Neuroscience