Sridhar T S, Liberman M C, Brown M C, Sewell W F
Eaton-Peabody Laboratory, Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston 02114-3096, USA.
J Neurosci. 1995 May;15(5 Pt 1):3667-78. doi: 10.1523/JNEUROSCI.15-05-03667.1995.
This report documents slow changes in cochlear responses produced by electrical stimulation of the olivocochlear bundle (OCB), which provides efferent innervation to the hair cells of the cochlea. These slow changes have time constants of 25-50 sec, three orders of magnitude slower than those reported previously. Such "slow effects" are similar to classically described "fast effects" in that (1) they comprise a suppression of the compound action potential (CAP) of the auditory nerve mirrored by an enhancement of the cochlear microphonic potential (CM) generated largely by the outer hair cells; (2) the magnitude of suppression decreases as the intensity of the acoustic stimulus increases; (3) they share the same dependence on OCB stimulation rate; (4) both are extinguished upon cutting the OCB; and (5) both are blocked with similar concentrations of a variety of cholinergic antagonists as well as with strychnine and bicuculline. These observations suggest that both fast and slow effects are mediated by the same receptor and are produced by conductance changes in outer hair cells. Slow effects differ from fast effects in that (1) fast effects are greatest for acoustic stimulus frequencies between 6 and 10 kHz, whereas slow effects peak for frequencies from 12 to 16 kHz, and (2) fast effects persist over long periods of OCB stimulation, whereas slow effects diminish after 60 sec of stimulation. The time course of the slow effects can be described mathematically by assuming that each shock-burst produces, in addition to a fast effect, a small decrease in CAP amplitude that decays exponentially with a time constant that is long relative to the intershock interval. The long time constant of the slow effect compared to the fast effect suggests that it may arise from a distinct intracellular mechanism, possibly mediated by second-messenger systems.
本报告记录了电刺激橄榄耳蜗束(OCB)所产生的耳蜗反应的缓慢变化,OCB为耳蜗的毛细胞提供传出神经支配。这些缓慢变化的时间常数为25 - 50秒,比先前报道的慢三个数量级。这种“慢效应”与经典描述的“快效应”相似之处在于:(1)它们包括听觉神经复合动作电位(CAP)的抑制,同时耳蜗微音器电位(CM)增强,CM主要由外毛细胞产生;(2)抑制幅度随声刺激强度增加而减小;(3)它们对OCB刺激频率具有相同的依赖性;(4)切断OCB后两者均消失;(5)多种胆碱能拮抗剂以及士的宁和荷包牡丹碱在相似浓度下均可阻断两者。这些观察结果表明,快效应和慢效应均由同一受体介导,且是由外毛细胞的电导变化产生的。慢效应与快效应的不同之处在于:(1)快效应在6至10 kHz的声刺激频率时最大,而慢效应在12至16 kHz频率时达到峰值;(2)快效应在长时间OCB刺激下持续存在,而慢效应在刺激60秒后减弱。慢效应的时间进程可以通过数学方式描述为,假设每个冲击脉冲除了产生快效应外,还会使CAP幅度产生一个小的下降,该下降以相对于脉冲间隔较长的时间常数呈指数衰减。与快效应相比,慢效应的长时间常数表明它可能源于一种独特的细胞内机制,可能由第二信使系统介导。