Maturation of calcium-dependent GABA, glycine, and glutamate release in the glycinergic MNTB-LSO pathway.
Maturation of calcium-dependent GABA, glycine, and glutamate release in the glycinergic MNTB-LSO pathway.
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DOI：
10.1371/journal.pone.0075688
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Gillespie DC
中科院分区：
文献类型：
--
作者：
Alamilla J;Gillespie DC
斜方体内侧核（MNTB）是听觉脑干中高保真时间处理的关键核团，是声音定位的基础。虽然甘氨酸能主细胞的MNTB项目的所有初级核的上级橄榄，在发展过程中的投影从MNTB到外侧上级橄榄（LSO）是感兴趣的，因为这种不成熟的抑制性投影是已知的，在出生后早期进行tonotopic细化，因为在此期间，个别MNTB终端在LSO短暂释放甘氨酸GABA和谷氨酸。据了解，钙依赖性释放的发育变化是允许各种听觉核团跟随高频活动所需的;然而，人们对MNTB-LSO通路中钙依赖性释放的成熟知之甚少，人们推测该通路对高保真度的要求不太严格时间跟随。在急性脑干切片的大鼠出生后第1天至15天，我们记录了全细胞反应LSO主要神经元电刺激的MNTB，以测量对外部钙的敏感性，不同的电压门控钙通道亚型的贡献囊泡释放，和成熟的GABA/甘氨酸和谷氨酸传输这些措施。我们的研究结果表明，在MNTB-LSO突触谷氨酸的释放是钙依赖性的。虽然没有显着的发展变化是明显的谷氨酸释放，GABA/甘氨酸释放经历了实质性的变化，在出生后的前两周：出生后不久L型，N型和P/Q型电压门控钙通道（VGCC）一起介导的释放，但在听力发作P/Q型VGCC占主导地位。P/Q型VGCC的阻断降低了P5-8时GABA/gly和谷氨酸传递的估计量子数和P12-15时诱发的微型甘氨酸能事件的频率，对神经递质的自发释放没有明显影响，支持了一个模型，其中成熟的同步突触传递需要P/Q型VGCC，但自发囊泡释放不需要。
The medial nucleus of the trapezoid body (MNTB) is a key nucleus in high-fidelity temporal processing that underlies sound localization in the auditory brainstem. While the glycinergic principal cells of the MNTB project to all primary nuclei of the superior olive, during development the projection from MNTB to the lateral superior olive (LSO) is of interest because this immature inhibitory projection is known to undergo tonotopic refinement during an early postnatal period, and because during this period individual MNTB terminals in the LSO transiently release glycine GABA and glutamate. Developmental changes in calcium-dependent release are understood to be required to allow various auditory nuclei to follow high frequency activity; however, little is known about maturation of calcium-dependent release in the MNTB-LSO pathway, which has been presumed to have less stringent requirements for high-fidelity temporal following. In acute brainstem slices of rats age postnatal day 1 to 15 we recorded whole-cell responses in LSO principal neurons to electrical stimulation in the MNTB in order to measure sensitivity to external calcium, the contribution of different voltage-gated calcium channel subtypes to vesicular release, and the maturation of these measures for both GABA/glycine and glutamate transmission. Our results establish that release of glutamate at MNTB-LSO synapses is calcium-dependent. Whereas no significant developmental changes were evident for glutamate release, GABA/glycine release underwent substantial changes over the first two postnatal weeks: soon after birth L-type, N-type, and P/Q-type voltage-gated calcium channels (VGCCs) together mediated release, but after hearing onset P/Q-type VGCCs predominated. Blockade of P/Q-type VGCCs reduced the estimated quantal number for GABA/gly and glutamate transmission at P5–8 and the frequency of evoked miniature glycinergic events at P12–15, without apparent effects on spontaneous release of neurotransmitter, supporting a model in which P/Q-type VGCCs are required for mature synchronous synaptic transmission, but not for spontaneous vesicle release.
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