Nicotinic activity in the interpeduncular nucleus of the midbrain prolongs recovery from halothane anesthesia

The influence of nicotinic transmission in the interpeduncular nucleus of the ventral midbrain on recovery from general anesthesia (3% halothane in oxygen) was assessed in rats. Immediately upon withdrawal of the anesthetic, nicotine (2 microliters, 10(-5) to 10(-1) M) was injected into the interpeduncular nucleus. Larger doses of nicotine (10(-2) and 10(-1) M) significantly (P < 0.05) prolonged the recovery of righting reflexes (to 371 +/- 55 and 362 +/- 67 sec, respectively, mean +/- SE), compared with injection of saline (187 +/- 19 sec). Prior intramuscular administration of the nicotinic antagonist, mecamylamine (2 mg/kg) significantly reduced the effect of 10(-2) M nicotine (to 211 +/- 43 sec). Injection of the nicotinic antagonist, hexamethonium (10(-1) M) led to a low mean recovery time (181 +/- 21 sec), not significantly different from control. Prolongation of recovery by 10(-2) M nicotine was not found to be significant when sites more dorsal to the interpeduncular nucleus were injected. An observed tendency for injection of nicotine to slow the post-anesthesia rate of breathing was not statistically significant and not correlated anatomically with the injection site in the midbrain. Increased release of acetylcholine has been shown previously to occur in the interpeduncular nucleus during anesthesia. The present results suggest that nicotinic activation of the interpeduncular nucleus facilitates or sums with the mechanisms in the brain that produce anesthesia under halothane.