A mechanism study on propofol's action on middle latency auditory evoked potential by neurons in ventral partition of medial geniculate body in rats.

OBJECTIVES To investigate the effect of propofol on the middle latency auditory evoked potentials (MLAEP) by neurons in the ventral partition of medial geniculate body (MGBv) in rats and study their mechanism. MATERIALS AND METHODS Sprague-Dawley (SD) rats were randomly divided into 7 groups (n = 6): group normal saline (NS), group intralipid (I), and groups of different concentrations of propofol (5.6, 16.8, 56, 168, 560 µmol/L) (P1-P5). These animals were anesthetized with ether, tracheostomized, and mechanically ventilated. After anesthesia, rats were paralyzed with vecuronium and fixed. A recording needle electrode with drugs was inserted into MGBv by means of stereotaxis. After injection of 0.2 µl propofol, normal saline or intralipid, correct insertion was verified by MLAEP response to standard sound. MLAEP including amplitudes and latencies of N0, P0, Na, Pa, and Nb waves were recorded. To identify which ion channel could be impacted by propofol, SD rats were divided into Ni2+ plus propofol (A1 group), Cd2+ plus propofol (A2 group), 4-AP plus propofol (A3 grouop), and TTX plus propofol (A4 group). The changes of MLAEP were recorded between injecting 4 ion channel blockers and propofol. Whole-cell patch clamp technique was used to confirm these variations. RESULTS There was no significant changes in all waves of MLAEP in MGBv after drug administration as compared with the baselins before injection in group NS, I, P1, and P2. The latency of Na, Pa, and Nb wave was significantly prolonged and the amplitude of Pa wave was decreased after injection as compared with the baseline in group P3, P4, and P5. The latency of Na, Pa, and Nb waves was significantly longer and the amplitude of Pa wave was significantly lower in group P3, P4, and P5 than in group NS and I. With TTX, amplitudes were decreased in wave Na-Pa. After given propofol, waves were unchanged in Na-Pa and latency was increased in Na, Pa, and Nb. With Cd2+, latency was unchanged in Na, Pa, and Nb as well as amplitudes decreasing in Na-Pa. Nevertheless, after given Ni2+ and 4-AP, every wave of MLAEP had no changes. After injected propofol, amplitudes were decreased in wave Na-Pa and latency was increased in Na, Pa, and Nb. The results of patch clamp showed 56 µmol/L, 168 µmol/L and 560 µmol/L propofol inhibited the persistent sodium currents and high voltaged activated calcium currents in the brain slices of rats. CONCLUSIONS Propofol in 56 µmol/L, 168 µmol/L and 560 µmol/L can inhibit MLAEP in MGBv of rats in a dose-dependent manner and these changes may be caused by blocking the ion channel of persistent sodium currents and high voltaged activated calcium currents.