Synaptic pharmacology in the turtle accessory optic system.
Synaptic pharmacology in the turtle accessory optic system.
复制标题
乌龟辅助光学系统中的突触药理学。
DOI：
10.1007/s00221-002-1231-5
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发表时间：
2002
影响因子：
2
通讯作者：
Ariel,Michael
中科院分区：
文献类型：
--
作者：
Kogo,Naoki;Fan,TianXing;Ariel,Michael
海龟的辅助视系统（基底视核，BON）接受兴奋性和抑制性输入，这些输入是方向敏感的。当背侧中脑被消融时，仅保留从视网膜到BON的单突触方向敏感输入。为了更好地了解由辅助视系统执行的中央视觉处理，本研究确定了介导BON细胞突触兴奋和抑制的神经递质及其受体。我们使用简化的体外龟脑干制备，其中双眼和大脑被分离。当药物被施加到大脑时，在BON神经元上进行贴片记录，眼睛浸泡在控制介质中，并暴露于视觉模式运动或受到电刺激。将谷氨酸受体亚型AMPA（α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid，α-氨基-3-羟基-5-甲基-4-异恶唑丙酸）的拮抗剂应用于脑室内阻断视觉反应。在响应于电刺激的兴奋性和抑制性突触事件被阻止在BON细胞，大概是通过阻止直接兴奋的视网膜神经节细胞轴突在BON和间接兴奋的抑制性中间神经元在脑干的其他地方。即使在无镁培养基中去极化的BON细胞中测量反应，NMDA受体拮抗剂也无效。BON细胞上的GABAA受体介导对视网膜刺激的抑制反应。对侧眼注射利多卡因引起自发抑制性突触后电位（IPSP）增加，表明存在一种紧张性视网膜输出，可减少脑干对BON细胞的抑制。此外，可能存在从脑干内到BON神经元的兴奋性路径的紧张性抑制，因为荷包牡丹碱增加了在没有视网膜输入的BON细胞中观察到的自发兴奋性突触后电位（EPSP）。这些结果表明，BON是一个复杂的视觉处理的竞争视觉信号的网站，并提供洞察如何在辅助光学系统的兴奋和抑制的相互作用创建一个视网膜滑动信号。
The accessory optic system of the turtle (the basal optic nucleus, BON) receives both excitatory and inhibitory inputs that are direction-sensitive. When the dorsal midbrain is ablated, only the monosynaptic direction-sensitive input from the retina to the BON remains. To better understand the central visual processing performed by the accessory optic system, this study identifies the neurotransmitters and their receptors that mediate the synaptic excitation and inhibition of BON cells. We used a reduced in vitro turtle brainstem preparation in which the two eyes and brain were isolated pharmacologically. Patch recordings were made on BON neurons while drugs were applied to the brain, with the eyes bathed in control media and either exposed to visual pattern motion or subjected to electrical stimulation. An antagonist of the AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) subtype of glutamate receptor applied within the brain chamber blocked the visual responses. In response to electrical stimulation both excitatory and inhibitory synaptic events were blocked in BON cells, presumably by blocking direct excitation by retinal ganglion cell axons in the BON and indirect excitation of inhibitory interneurons elsewhere in the brainstem. An NMDA receptor antagonist was ineffective, even when the response was measured in a BON cell depolarized in Mg2+-free media. A GABAAreceptor on the BON cell mediates the inhibitory responses to retinal stimulation. Injection of lidocaine into the contralateral eye caused an increase in spontaneous inhibitory post-synaptic potentials (IPSPs), suggesting that a tonic retinal output exists that reduces brainstem inhibition of BON cells. Also, there may be tonic inhibition of an excitatory path to BON neurons from within the brainstem, because bicuculline increased spontaneous excitatory post-synaptic potentials (EPSPs) observed in a BON cell without retinal input. These results indicate that the BON is a site of complex visual processing of competing visual signals and provide insight into how an interaction of excitation and inhibition creates a retinal slip signal in the accessory optic system.