Regulation of burst activity through presynaptic and postsynaptic GABAB receptors in mouse superior colliculus
Regulation of burst activity through presynaptic and postsynaptic GABAB receptors in mouse superior colliculus
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DOI：
10.1523/jneurosci.4666-07.2008
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发表时间：
2008-01-23
影响因子：
5.3
通讯作者：
Isa, Tadashi
中科院分区：
文献类型：
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作者：
Kaneda, Katsuyuki;Phongphanphanee, Penphimon;Isa, Tadashi
在切片制备中，当GABA（A）受体（GABA（A）R）介导的抑制减少时，电刺激上级丘（SC）的浅灰质层（SGS）诱导中间灰质层（SGI）神经元的EPSC爆发。该制剂已被用作模型系统，以研究涉及对视觉刺激（如扫视眼球运动）的短潜伏期定向反应的执行的信号处理。在本研究中，我们研究的作用，GABA（B）受体（GABA（B）Rs）在上述途径中的调制信号传递的全细胞膜片钳记录从GAD 67-GFP基因敲入小鼠获得的SC切片。用GABA（B）R拮抗剂CGP 52432（CGP）灌注脑片可显著延长EPSC爆发的持续时间。局部应用CGP的SGS，但不SGI产生类似的效果。由于当GABA（A）受体被阻断时，SGS刺激引起SGS中GABA能神经元的爆发，这些结果表明爆发后释放的GABA激活SGS中的GABA（B）受体，导致爆发持续时间缩短。我们发现突触后和突触前的行动GABA（B）Rs的SGS;激活突触后GABABR诱导外向电流在窄场垂直细胞，而它引起分流抑制在远端树突在宽场垂直细胞。另一方面，突触前GABABR的激活抑制了SGS中非GABA能神经元的兴奋性突触传递。这些结果表明，突触释放的GABA可以激活SGS中的突触前和突触后GABA（B）受体，并限制SC局部回路中爆发反应的持续时间。
In slice preparations, electrical stimulation of the superficial gray layer (SGS) of the superior colliculus (SC) induces EPSC bursts in neurons in the intermediate gray layer (SGI) when GABA(A) receptor (GABA(A)R)-mediated inhibition is reduced. This preparation has been used as a model system to study signal processing involved in execution of short-latency orienting responses to visual stimuli such as saccadic eye movements. In the present study, we investigated the role of GABA(B) receptors(GABA(B)Rs) in modulating signal transmission in the above pathway with whole-cell patch-clamp recordings in SC slices obtained from GAD67-GFP knock-in mice. Perfusion of the slice with the GABA(B)R antagonist CGP52432 (CGP) greatly prolonged the duration of the EPSC bursts. Local application of CGP to the SGS but not to the SGI produced similar effects. Because SGS stimulation elicited bursts in GABAergic neurons in the SGS when GABA(A)Rs were blocked, these results suggest that GABA released after bursts activates GABA(B)Rs in the SGS, leading to reduced burst duration. We found both postsynaptic and presynaptic actions of GABA(B)Rs in the SGS; activation of postsynaptic GABABRs induced outward currents in narrow-field vertical cells, whereas it caused shunting inhibition in distal dendrites in wide-field vertical cells. On the other hand, activation of presynaptic GABABRs suppressed excitatory synaptic transmissions to non-GABAergic neurons in the SGS. These results indicate that synaptically released GABA can activate both presynaptic and postsynaptic GABA(B)Rs in the SGS and limit the duration of burst responses in the SC local circuit.