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Neuroleptic-induced catalepsy: a D2 blockade phenomenon?
Pharmacology, Biochemistry, and Behavior
|December 1, 1985
Summary
Molindone, a D2-blocking drug, induced catalepsy in mice, suggesting D1 receptor blockade is not essential. Haloperidol showed a training effect and potentiation with apomorphine, unlike molindone.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Typical neuroleptics like haloperidol cause catalepsy by blocking dopamine D1 and D2 receptors.
- The specific role of D1 versus D2 receptor blockade in catalepsy remains unclear.
Purpose of the Study:
- To investigate the role of dopamine D1 receptors in catalepsy using molindone, a selective D2 receptor antagonist.
- To compare the cataleptogenic effects of molindone with haloperidol.
Main Methods:
- A mouse model of catalepsy was used.
- Mice were treated with haloperidol, molindone, saline, or apomorphine.
- Catalepsy was assessed, and drug effects were compared.
Main Results:
- Molindone induced catalepsy, though less potent than haloperidol, indicating D1 receptor blockade is not strictly necessary.
- Haloperidol exhibited a 'training effect' with repeated testing, which molindone did not.
- Apomorphine potentiated haloperidol-induced catalepsy but not molindone-induced catalepsy.
Conclusions:
- The findings challenge simple interpretations based solely on D1 and D2 receptor blockade.
- Catalepsy may involve complex interactions beyond direct D1/D2 antagonism.