No abstract

Intraperitoneal injection of ketamine (100 mg/kg body weight) significantly reduces the levels of cholecystokinin (CCK), somatostatin (SRIF), and substance P (SP)-like immunoreactivity in various regions of rat brain. No significant change in thyrotropin releasing hormone (TRH)-like immunoreactivity was observed. Neuropeptide systems may be involved in the neuropharmacologic effects of ketamine.

Intraperitoneal (ip) injection of ketamine increased the concentration of dynorphin in the cortex of rat brain, while decreased it in the septal area. The affinity of ethylketocyclazocine (EKC) receptor binding was decreased in the cortex, but increased in the septal area after pretreating the rats with ketamine. This suggests that the dynorphin neuronal system is stimulated in the cortex and suppressed in the septal area by ketamine. In other 5 brain areas, ketamine had no effect on neither dynorphin concentration nor EKC receptor binding. As dynorphin was reported to produce seizure and spike discharge in the cortex while suppressed the hippocampal EEG of rat brain, it is likely that the dynorphin neuronal system may play at least a part in ketamine induced electrophysiological changes in the brain.