In vivo optical recordings of synaptic transmission and intracellular Ca2+ and Cl– in the superior colliculus of fetal rats
In vivo optical recordings of synaptic transmission and intracellular Ca2+ and Cl– in the superior colliculus of fetal rats
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DOI：
10.1111/j.1460-9568.2006.04683.x
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发表时间：
2006-03
影响因子：
3.4
通讯作者：
Y. Sakata;T. Fujioka;H. Endoh;Shoji Nakamura
中科院分区：
文献类型：
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作者：
Y. Sakata;T. Fujioka;H. Endoh;Shoji Nakamura
尽管N-甲基-d-天冬氨酸(NMDA)受体在胎儿上丘(SC)突触连接的活性依赖性重塑中起重要作用，但其对胎儿SC神经元电活动的作用尚未确定。此外，γ-氨基丁酸(GABA)介导的抑制是在产前就发生，还是只在睁开眼睛后发生，一直存在争议。因此，我们使用电压敏感、钙离子和氯离子敏感的荧光染料进行光学记录，以分析胎鼠SC中突触传递和细胞内钙离子和氯离子的变化，这些细胞内的钙离子和氯离子仍通过脐带连接。刺激局部SC可引起兴奋性和抑制性反应。兴奋性突触反应由早成分和晚成分组成。早期成分主要由非NMDA受体和NMDA受体介导，晚期成分主要由NMDA受体介导。高电流的序列脉冲刺激需要诱导这种抑制，荷包牡丹碱可拮抗这种抑制，并通过荷包牡丹碱暴露掩蔽的兴奋性突触反应阻断GABA介导的抑制。局灶性SC刺激可引起[Cl-]i和[Ca2+]i的升高，分别由GABA-A受体和NMDA受体介导。GABA拮抗剂能增强SC诱导的[Ca~(2+)]i升高。这些结果表明，在胎儿SC中，兴奋性和抑制性突触传递发生在出生前，NMDA受体是兴奋性突触传递的主要贡献者，并使[Ca~(2+)]i升高，GABA-A受体已经起到抑制兴奋性神经传递的作用。
Although the N‐methyl‐d‐aspartate (NMDA) receptor is known to play a crucial role in activity‐dependent remodeling of synaptic connections in the fetal superior colliculus (SC), its contribution to the electrical activity of fetal SC neurons has not been determined. Furthermore, whether γ‐aminobutyric acid (GABA)‐mediated inhibition occurs either as early as prenatal periods or only after eye opening has been controversial. We therefore performed optical recordings using voltage‐, Ca2+‐ and Cl–‐sensitive fluorescent dyes to analyse synaptic transmission and changes in intracellular Ca2+ and Cl– in the SC of fetal rats that were still connected with the dams by the umbilical cord. Excitatory and inhibitory responses were evoked by focal SC stimulation. The excitatory synaptic responses are composed of early and late components. The early component was mediated by both non‐NMDA and NMDA receptors, whereas the late component occurred mainly via NMDA receptors. Train pulse stimulation at higher currents was required for induction of the inhibition, which was antagonized by bicuculline, and blocking of the GABA‐mediated inhibition by bicuculline uncovered masked excitatory synaptic responses. Focal SC stimulation induced increases in [Cl–]i and [Ca2+]i that were mediated by GABA‐A receptors and mainly by NMDA receptors, respectively. GABA antagonists augmented SC‐induced increases in [Ca2+]i. These results indicate that, in the fetal SC, excitatory and inhibitory synaptic transmissions occur before birth, that the NMDA receptor is a major contributor to excitatory synaptic transmission and increased [Ca2+]i, and that the GABA‐A receptor is already functioning to inhibit excitatory neurotransmission.