[P1-3-34] Distinct neural firing changes are observed in unit recording from the rat prefrontal cortex during anesthesia
キーワード：General anesthesia、Extracellular unit recording、Consciousness
The prefrontal cortex (PFC) is thought to be critically involved in the regulation of consciousness. It has been reported that administering a cholinergic agonist in the PFC restores consciousness during continuous sevoflurane anesthesia in rats. Furthermore, the medial PFC is involved in thalamocortical and corticocortical interactions that modulate both induction and recovery from propofol anesthesia. However, it is not known how various anesthetics and sedatives with distinct molecular targets modulate single unit activities in the rat PFC during the transition into unconsciousness and subsequent recovery. In the present study, unit activities were recorded from implanted electrode in the rat PFC under awake, anesthesia, and recovery conditions with various general anesthetics and sedatives (N = 4). All experiments were approved by Institutional Animal Care and Use Committee at Massachusetts General Hospital. IV anesthetics, propofol, dexmedetomidine, ketamine, or fentanyl were administered via the central venous catheter. At least three days of rest were provided between experiments. After all IV anesthetic experiments were completed, additional experiments were performed with volatile anesthetics (2% isoflurane and 3% sevoflurane). Neural activity was continuously recorded during the awake state (before anesthetic administration), anesthetized state, and recovery state. These states were behaviorally defined by loss and recovery of the righting reflex (LORR and RORR, respectively). The neural firing frequencies were compared with the awake state, and if the firing frequency was higher or lower than the mean ±2 standard deviations, the neural firing frequencies were defined as significantly increased or decreased, respectively. All general anesthetics increased and decreased neural firing frequency in subpopulation (around 30%), but isoflurane only decreased their neural firing frequency in 70% of neurons. The percentage of subpopulations were kept even after RORR with fentanyl, but not others. After RORR, the neural firing frequencies were increased more than half neurons in the subpopulation that showed the neural firing changed. Furthermore, some neurons exhibited a brief increase in firing frequency immediately before LORR. The neurons that increased their firing frequency immediately before LORR may be involved in producing paradoxical brain excitation during the transition to unconsciousness with these drugs. On the other hand, the increase of firing frequency in some population after RORR could be reflected an emergence agitation. These results encourage additional experiments to confirm these findings, and additional analysis to characterize the specific neuron types that exhibit these distinct firing patterns.