Li L, Parkins C W, Webster D B
Department of Otorhinolaryngology and Biocommunication, Louisiana State University Medical Center, New Orleans 70112-2234, USA.
Hear Res. 1999 Jul;133(1-2):27-39. doi: 10.1016/s0378-5955(99)00043-x.
Thirty-six drug deafened guinea pigs were studied to determine how electrical stimulation of the cochlea affects spiral ganglion cell (SGC) survival. Animals were divided into two groups, extracochlear and intracochlear stimulation, and each group was further divided into four stimulus subgroups: no stimulation (implanted controls), the inferior colliculus electrically evoked potential (ICEEP) threshold-2 dB, ICEEP threshold+2 dB, and ICEEP threshold+6 dB. Stimuli consisted of 200 micros/phase charge balanced biphasic current pulses presented at 100 pulses per second using monopolar stimulation. Animals were stimulated 5 h/day, 5 days per week, for 8 weeks. The animals were then perfused and the cochleae serially sectioned at 4 microm saving every 8th section. We counted the number of intact SGCs, those containing a nucleus with chromatin, in each 20% segment of the cochlea and also measured SGC densities (number of neurons per mm2 of Rosenthal's canal). The number of surviving spiral ganglion neurons was not significantly different (P > 0.05) between the implanted and the unimplanted ears in any of the experimental groups. However, the spiral ganglion neuron densities were significantly elevated in the electrically stimulated ears (P < 0.001) but not in the implanted but not chronically stimulated ears (P > 0.05). We measured the volume of Rosenthal's canal in one subgroup (ICEEP threshold+2 dB) and found a decrease in this volume in the stimulated ear compared to the unstimulated ear (P < 0.01). These findings support the hypothesis that chronic monopolar electrical intracochlear or extracochlear stimulation is not a neurotrophic factor, increasing spiral ganglion neuron survival, but instead causes a narrowing of Rosenthal's canal that accounts for the increased spiral ganglion neuronal densities seen in the stimulated cochleae.
对36只药物致聋的豚鼠进行研究，以确定耳蜗电刺激如何影响螺旋神经节细胞（SGC）的存活。动物被分为两组，即耳蜗外刺激组和耳蜗内刺激组，每组再进一步分为四个刺激亚组：无刺激（植入对照组）、下丘电诱发电位（ICEEP）阈值 - 2 dB、ICEEP阈值 + 2 dB和ICEEP阈值 + 6 dB。刺激由使用单极刺激以每秒100个脉冲呈现的200微秒/相电荷平衡双相电流脉冲组成。动物每天刺激5小时，每周5天，持续8周。然后对动物进行灌注，并将耳蜗以4微米的厚度连续切片，每隔8个切片保存一次。我们计算了耳蜗每20%节段中完整SGC的数量，即那些含有带染色质细胞核的细胞，并测量了SGC密度（每平方毫米罗斯enthal管中的神经元数量）。在任何实验组中，植入耳和未植入耳之间存活的螺旋神经节神经元数量没有显著差异（P > 0.05）。然而，电刺激耳中的螺旋神经节神经元密度显著升高（P < 0.001），而植入但未长期刺激的耳中则没有（P > 0.05）。我们在一个亚组（ICEEP阈值 + 2 dB）中测量了罗斯enthal管的体积，发现与未刺激耳相比，刺激耳中该体积减小（P < 0.01）。这些发现支持了这样一种假设，即慢性单极耳蜗内或耳蜗外电刺激不是一种神经营养因子，不会增加螺旋神经节神经元的存活，而是导致罗斯enthal管变窄，这解释了在受刺激的耳蜗中看到的螺旋神经节神经元密度增加的现象。
