Excitatory responses evoked in prefrontal cortex by mediodorsal thalamic nucleus stimulation: influence of anaesthesia.
The prefrontal cortex and the mediodorsal thalamic nucleus are reciprocally connected through excitatory amino acid pathways. Cortical excitatory responses resulting from activation of either the mediodorsal thalamic nucleus-prefrontal cortex pathway (short latency) or the recurrent collaterals of prefrontal cortex-mediodorsal thalamic nucleus neurons (long latency) can be discriminated mainly by their latency. The present study was undertaken to compare the effects of halothane and ketamine anaesthesia on these cortical excitatory responses and to establish their pharmacological characteristics using microiontophoretic application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D,L-2-amino-5-phosphonovaleric acid (APV), the specific antagonists of D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptors respectively. The number of prefrontal cortex cells which presented short or long latency excitatory responses was smaller in halothane- than in ketamine-anaesthetized rats. Whatever the anaesthetic used, short latency responses were blocked by CNQX and not affected by APV. Long latency responses were mainly blocked by APV and occasionally by CNQX in halothane-anaesthetized rats, while they were only blocked by CNQX in ketamine-anaesthetized animals. Therefore, halothane seems to preferentially reduce evoked responses mediated by AMPA receptors while ketamine completely abolishes evoked responses involving NMDA receptors. Moreover, the present data confirm that excitatory responses resulting from the activation of the mediodorsal thalamic nucleus-prefrontal cortex pathway are mainly mediated by AMPA receptors. In addition, they demonstrate that cortical responses linked to the activation of recurrent collaterals from prefrontal cortex-mediodorsal thalamic nucleus neurons involve both AMPA and NMDA receptors.
Pirot
S
S
INSERM U114, Collège de France, Paris, France.
Glowinski
J
J
Thierry
A M
AM
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000758:Anesthesia; D000777:Anesthetics / Q000494:pharmacology*; D000818:Animals; D006221:Halothane / Q000494:pharmacology*; D007649:Ketamine / Q000494:pharmacology*; D008297:Male; D017397:Prefrontal Cortex / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D013788:Thalamus / Q000187:drug effects* / Q000502:physiology; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology
D000777:Anesthetics; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D007649:Ketamine; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; D006221:Halothane