EXCITATORY AND DIFFERENTIAL DISINHIBITORY ACTIONS OF ACETYLCHOLINE IN THE LATERAL GENICULATE-NUCLEUS OF THE CAT
EXCITATORY AND DIFFERENTIAL DISINHIBITORY ACTIONS OF ACETYLCHOLINE IN THE LATERAL GENICULATE-NUCLEUS OF THE CAT
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DOI：
10.1113/jphysiol.1986.sp015932
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发表时间：
1986-01-01
影响因子：
5.5
通讯作者：
VANSCHAYCK, R
中科院分区：
文献类型：
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作者：
EYSEL, UT;PAPE, HC;VANSCHAYCK, R
在外侧膝状体背侧核（d.l.g.n.）用氟烷、一氧化二氮和氧气的混合物麻醉的成年猫。多筒玻璃微电极填充有乙酸钠、L-谷氨酸、乙酰胆碱（ACh）、γ-谷氨酰胺、γ-谷氨酰胺和γ-谷氨酰胺。氨基丁酸（GABA）和荷包牡丹碱。在正常神经支配的，自发活动的d.l.g.n.细胞，乙酰胆碱和L-谷氨酸引起的放电率增加。在通过视网膜光凝消除来自视网膜的兴奋性输入后，ACh和L-谷氨酸的作用相似。这证明两种药物对d.l.g.n.都有直接的兴奋作用。细胞和解除抑制是不是最突出的影响ACh在d.l.g.n.乙酰胆碱对背根神经节中继细胞的兴奋作用。受到巴比妥类药物的强烈影响。亚麻醉水平的戊巴比妥钠完全取消了乙酰胆碱的兴奋，而L-谷氨酸的反应保持不变。激发，中心-周围的拮抗作用和周边的影响引起的光点和大场相位反转光栅与和没有中央保留的感受野面积。双眼抑制引起的相位反转光栅呈现给非优势眼。在视网膜感受野区域的局部破坏后，在急性去传入的d.l.g.n.中观察到retinogeniculate兴奋停止和孤立的侧抑制。细胞这种抑制的时间过程和强度被披露，提高了背景放电与microionophoretically应用L-谷氨酸。随着视网膜病变大小的增加，孤立性侧抑制的强度呈指数下降。从d.l.g.n.中去传入神经的横向范围的计算中得出大于1000 μ m的最大膝状体内范围。这种抑制作用超越了d.l.g.n.的经典环绕抑制。细胞，因此被命名为长距离侧抑制。微电泳应用GABA在d.l.g.n.被荷包牡丹碱拮抗的细胞。中心-环绕拮抗、双眼抑制和长程抑制被荷包牡丹碱阻断，因此被证明是GABA能的。每一类抑制的差异影响microionophoretically应用乙酰胆碱。长距离抑制被解除，中心-周围拮抗作用增强，双眼抑制无显著变化。与ACh兴奋相反，戊巴比妥不能抑制ACh的去抑制作用。有人建议，远程抑制介导的经常性途径，通过周围的膝状体神经元，而更具体的类型的抑制（中心环绕和双眼）可能会出现从膝状体内interneurones。胆碱能系统似乎是一种选择性机制，调节全局抑制，使特定类型不受影响。
Single neurones were recorded in the dorsal lateral geniculate nucleus (d.l.g.n.) of adult cats anaesthetized with a mixture of halothane, nitrous oxide and oxygen. The multibarrel-glass micro-electrodes were filled with sodium acetate, L-glutamate, acetylcholine (ACh), .gamma.-aminobutyric acid (GABA) and bicuculline. In normally innervated, spontaneously active d.l.g.n. cells, ACh and L-glutamate elicited increased firing rates. After elimination of the excitatory input from the retina by retinal photocoagulation, the effects of ACh and L-glutamate were similar. This proves that both drugs have direct excitatory effects on d.l.g.n. cells and that disinhibition is not the most prominent influence of ACh in the d.l.g.n. The excitatory action of ACh on relay cells in the d.l.g.n. was strongly influenced by barbiturates. Sub-narcotic levels of sodium pentobarbitone completely abolished the excitation by ACh while the response to L-glutamate remained unchanged. Excitation, centre-surround antagonism and periphery effects were elicited by spots of light and by large field phase-reversing gratings with and without central sparing of the receptive field area. Binocular inhibition was elicited with the phase-reversing grating presented to the non-dominant eye. After localized destruction of the retinal receptive field area, retinogeniculate excitation ceased and an isolated lateral inhibition was observed in the acutely deafferented d.l.g.n. cells. The time course and strength of this inhibition was disclosed by raising the background discharge with microiontophoretically applied L-glutamate. With increasing size of retinal lesions the strength of isolated lateral inhibition decreased exponentially. A maximal intrageniculate range of more than 1000 .mu.m was derived from computations of the lateral extent of deafferentiation in the d.l.g.n. The inhibition acted beyond the classic surround inhibition of d.l.g.n. cells and thus was named long-range lateral inhibition. Microiontophoretically applied GABA elicits a strong inhibitory effect at the d.l.g.n. cells which is antagonized by bicuculline. Centre-surround antagonism, binocular inhibition and long-range inhibition were blocked by bicuculline and thus proven to be GABAergic. Each class of inhibition was differentially influenced by microiontophoretically applied ACh. Long-range inhibition was disinhibited, centre-surround antagonism was enhanced, and binocular inhibition was not significantly changed. In contrast to ACh excitation, the disinhibitory action of ACh was not suppressed by pentobarbitone. It is suggested that long-range inhibition is mediated by the recurrent pathway via perigeniculate neurones while the more specific types of inhibition (centre surround and binocular) might arise from intrageniculate interneurones. The cholinergic system seems to serve as a selective mechanism to modulate global inhibition and leave the specific types unaffected.