Hauber W, Andersen R
Biologisches Institut, Abteilung Tierphysiologie, Universität Stuttgart, Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1993 Nov;348(5):486-90. doi: 10.1007/BF00173207.
The effects of the non-NMDA glutamate receptor antagonist GYKI 52466 (2.4 and 4.8 mg/kg, i.p.) on spontaneous locomotor activity and haloperidol-induced catalepsy (0.5 mg/kg, i.p.) were assessed in naive rats and in rats pretreated with the NMDA antagonist dizocilpine (0.08 mg/kg, i.p.). GYKI 52466 given alone did not alter locomotor activity and haloperidol-induced catalepsy, but significantly antagonized the dizocilpine-induced locomotor stimulation and counteracted the anti-cataleptic effects of dizocilpine on haloperidol-induced catalepsy. Thus blockade of non-NMDA glutamate receptors antagonized the behavioural stimulant effects of a NMDA receptor blockade.
在未用药的大鼠以及用NMDA拮抗剂地佐环平(腹腔注射0.08mg/kg)预处理过的大鼠中,评估了非NMDA谷氨酸受体拮抗剂GYKI 52466(腹腔注射2.4和4.8mg/kg)对自发运动活性以及氟哌啶醇诱导的僵住症(腹腔注射0.5mg/kg)的影响。单独给予GYKI 52466不会改变运动活性以及氟哌啶醇诱导的僵住症,但能显著拮抗地佐环平诱导的运动兴奋,并抵消地佐环平对氟哌啶醇诱导僵住症的抗僵住症作用。因此,非NMDA谷氨酸受体的阻断拮抗了NMDA受体阻断的行为兴奋作用。