Ketamine blocks the plasticity associated with prefrontal cortex self-stimulation.
Intracranial self-stimulation (ICSS) at sites within the medial prefrontal cortex (MFC) is acquired slowly but can be hastened by prior exposure to a regimen of noncontingent stimulation delivered to the MFC ICSS electrode. The facilitatory effects of noncontingent MFC stimulation on subsequent ICSS acquisition were blocked by pretreatment with ketamine, a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor. These findings provide further support for the view that the NMDA receptor is importantly involved in mechanisms of neural plasticity.
Corbett
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Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
D000818:Animals; D002540:Cerebral Cortex / Q000033:anatomy & histology / Q000502:physiology*; D004567:Electrodes, Implanted; D005625:Frontal Lobe / Q000033:anatomy & histology / Q000502:physiology*; D007649:Ketamine / Q000494:pharmacology*; D007696:Kindling, Neurologic / Q000502:physiology; D008297:Male; D009473:Neuronal Plasticity / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D012653:Self Stimulation / Q000187:drug effects*
D016194:Receptors, N-Methyl-D-Aspartate; D007649:Ketamine