咖啡因和兰尼碱证明了兰尼碱受体在柯蒂氏器中的作用。
Caffeine and ryanodine demonstrate a role for the ryanodine receptor in the organ of Corti.
作者信息
Bobbin Richard P
机构信息
Kresge Hearing Research Laboratories, Department of Otorhinolaryngology and Biocommunication, Louisiana State University Health Sciences Center, 533 Bolivar Street, 5th Floor, New Orleans, LA 70112-2234, USA.
出版信息
Hear Res. 2002 Dec;174(1-2):172-82. doi: 10.1016/s0378-5955(02)00654-8.
The hypothesis that the release of Ca(2+) from ryanodine receptor activated Ca(2+) stores in vivo can affect the function of the cochlea was tested by examining the effects of caffeine (1-10 mM) and ryanodine (1-333 microM), two drugs that release Ca(2+) from these intracellular stores. The drugs were infused into the perilymph compartment of the guinea pig cochlea while sound (10 kHz) evoked cochlear potentials and distortion product otoacoustic emissions (DPOAEs; 2f(1)-f(2)=8 kHz, f(2)=12 kHz) were monitored. Caffeine significantly suppressed the compound action potential of the auditory nerve (CAP) at low intensity (56 dB SPL; 3.3 and 10 mM) and high intensity (92 dB SPL; 10 mM), increased N1 latency at high and low intensity (3 and 10 mM) and suppressed low intensity summating potential (SP; 10 mM) without an effect on high intensity SP. Ryanodine significantly suppressed the CAP at low intensity (100 and 333 microM) and at high intensity (333 microM), increased N1 latency at low intensity (33, 100 and 333 microM) and at high intensity (333 microM) and suppressed low intensity SP (100 and 333 microM) and increased high intensity SP (333 microM). The cochlear microphonic (CM) evoked by 10 kHz tone bursts was not affected by caffeine at high or low intensity, and ryanodine had no effect on it at low intensity but decreased it at high intensity (10, 33, 100 and 333 microM). In contrast, caffeine (10 mM) and ryanodine (33 and 100 microM) significantly increased CM evoked by l kHz tone bursts and recorded from the round window. Caffeine (10 mM) and ryanodine (100 microM) reversibly suppressed the cubic DPOAEs evoked by low intensity primaries. Overall, low intensity evoked responses were more sensitive and were suppressed to a greater extent by both drugs. This is consistent with the hypothesis that release of Ca(2+) from ryanodine receptor Ca(2+) stores, possibly in outer hair cells and supporting cells, affects the function of the cochlear amplifier.
通过研究咖啡因（1 - 10 mM）和兰尼碱（1 - 333 microM）这两种能从这些细胞内储存库释放Ca(2+)的药物的作用，来检验体内从兰尼碱受体激活的Ca(2+)储存库释放Ca(2+)会影响耳蜗功能这一假设。将药物注入豚鼠耳蜗的外淋巴腔，同时监测声音（10 kHz）诱发的耳蜗电位和畸变产物耳声发射（DPOAE；2f(1)-f(2)=8 kHz，f(2)=12 kHz）。咖啡因在低强度（56 dB SPL；3.3和10 mM）和高强度（92 dB SPL；10 mM）时显著抑制听神经复合动作电位（CAP），在高、低强度（3和10 mM）时增加N1潜伏期，在低强度时抑制总和电位（SP；10 mM），而对高强度SP无影响。兰尼碱在低强度（100和333 microM）和高强度（333 microM）时显著抑制CAP，在低强度（33、100和333 microM）和高强度（333 microM）时增加N1潜伏期，在低强度时抑制SP（100和333 microM），在高强度时增加SP（333 microM）。10 kHz短音诱发的耳蜗微音电位（CM）在高、低强度时均不受咖啡因影响，兰尼碱在低强度时对其无影响，但在高强度时（10、33、100和333 microM）使其降低。相反，咖啡因（10 mM）和兰尼碱（33和100 microM）显著增加1 kHz短音诱发并从圆窗记录的CM。咖啡因（10 mM）和兰尼碱（100 microM）可逆地抑制低强度初级刺激诱发的三次DPOAE。总体而言，低强度诱发反应更敏感，且两种药物对其抑制程度更大。这与以下假设一致，即从兰尼碱受体Ca(2+)储存库释放Ca(2+)，可能在外毛细胞和支持细胞中，会影响耳蜗放大器的功能。
Zotero 插件