Increased S(-)-apomorphine-induced vacuous chewing and attenuated effect of chronic haloperidol treatment in streptozotocin-induced diabetic rat.
The incidence of S(-)-apomorphine-induced vacuous chewing movements (VCMs) as a model for tardive dyskinesia was investigated in streptozotocin (STZ)-induced diabetic rats. A single dose of STZ (65 mg/kg, intravenously) caused a diabetic state (hyperglycemia, 480-490 vs. 116-118 mg/dl in naive rats). S(-)-apomorphine (250 micrograms/kg, subcutaneously)-induced VCMs were significantly intensified in diabetic rats which had received STZ 9 weeks previously. The enhancement of VCMs was also observed in nondiabetic rats which received subsequent treatment with depot haloperidol (4 mg/kg, intramuscularly, once a week, every week for 4 weeks) followed by a 2-week washout period. The ability of haloperidol to enhance VCMs was attenuated in diabetic rats. The implications of these results in relation to altered neurotransmissions in STZ-induced diabetes are discussed.