GLUTAMATERGIC INHIBITION OF VOLTAGE-OPERATED CALCIUM CHANNELS IN THE AVIAN COCHLEAR NUCLEUS
GLUTAMATERGIC INHIBITION OF VOLTAGE-OPERATED CALCIUM CHANNELS IN THE AVIAN COCHLEAR NUCLEUS
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DOI：
10.1523/jneurosci.15-03-01724.1995
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发表时间：
1995-03-01
影响因子：
5.3
通讯作者：
RUBEL, EW
中科院分区：
文献类型：
--
作者：
LACHICA, EA;RUBSAMEN, R;RUBEL, EW
听觉神经是鸟类耳蜗核（nucleus magnocellularis，NM）中神经元的唯一兴奋性输入。未成熟动物的NM神经元依赖于听觉神经信号;当剥夺它们时，许多NM神经元死亡，其余萎缩。听觉神经末梢释放谷氨酸，其可以通过激活代谢型谷氨酸受体（mGluR）来刺激第二信使系统。因此，它是可能的mGluR刺激的信号转导系统的效应需要NM神经元的生存。这项研究表明，NM神经元中的mGluR激活减弱了[Ca 2 +]（i）的电压依赖性变化。电压依赖性Ca 2+内流也减弱增加cAMP与毛喉素，VIP，或8-溴-cAMP，表明mGluR激活可能会刺激腺苷酸环化酶。主要结果可归纳如下。NM神经元具有高电压激活的Ca 2+通道，其由使君子酸、谷氨酸和（+/-）trans-ACPD按效力顺序调制。谷氨酸能抑制Ca ~（2+）内流不被L-AP_3或L-AP_4阻断，它们拮抗mGluRs在其他神经系统中的作用;它被丝氨酸-O-磷酸盐阻断。最后，电压依赖性Ca ~（2+）内流的衰减被cAMP抑制剂复制。由于NM神经元具有较高的自发活动率和较高的驱动活动率，这种mGluR的表达证明是非常有价值的：没有它，[Ca 2 +]（i）可以达到致死浓度。这些结果提供了一个重要的线索，身份的细胞内信号，可能发挥重要作用，NM神经元的生存。
The auditory nerve serves as the only excitatory input to neurons in the avian cochlear nucleus, nucleus magnocellularis (NM). NM neurons in immature animals are dependent upon auditory nerve signals; when deprived of them, many NM neurons die, and the rest atrophy. Auditory nerve terminals release glutamate, which can stimulate second messenger systems by activating a metabotropic glutamate receptor (mGluR). Therefore, it is possible that the effecters of mGluR-stimulated signal transduction systems are needed for NM neuronal survival. This study shows that mGluR activation in NM neurons attenuates voltage-dependent changes in [Ca2+](i). Voltage-dependent Ca2+ influx was also attenuated by increasing cAMP with forskolin, VIP, or 8-bromo-cAMP, indicating that mGluR activation may stimulate adenylate cyclase. The main results may be summarized as follows. NM neurons possess high voltage-activated Ca2+ channels that were modulated by quisqualate, glutamate, and (+/-)trans-ACPD, in that order of potency. Glutamatergic inhibition of Ca2+ influx was not blocked by L-AP3 or L-AP4, which antagonize the actions of mGluRs in other neural systems; it was blocked by serine-O-phosphate. Finally, the attenuation of voltage-dependent Ca2+ influx was duplicated by cAMP accumulators. Since NM neurons have high rates of spontaneous activity and higher rates of driven activity, the expression of this mGluR turns out to be very valuable: without it, [Ca2+](i) could reach lethal concentrations. These results provide an important clue as to the identity of an intracellular signal that may play an important role in NM neuronal survival.