Kita H, Yamada H, Tanifuji M, Murase K
University of Tennessee, College of Medicine, Department of Anatomy and Neurobiology, Memphis 38163, USA.
Exp Brain Res. 1995;106(2):187-95. doi: 10.1007/BF00241114.
Effects of GABA and glutamate antagonists as well as dopamine agonists and antagonists on the optical responses of neostriatal (Str) slices to local electrical stimulation were examined using a voltage-sensitive dye and a high-speed image sensor. A single local stimulation applied to the Str slices evoked optical responses lasting for 40-80 ms and propagating in every direction up to about 1.5 mm. Bath application of bicuculline methiodide increased the intensity and duration of optical responses, while their spatial response patterns were unchanged. Bath application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) greatly reduced the late part of responses occurring about 4 ms after stimulation, but the early part of responses was unaffected by CNQX. The early part of the response was eliminated by application of tetrodotoxin. Bath application of N-methyl-D-aspartate antagonists, 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid and 2-amino-5-phosphonovaleric acid resulted in only small changes in the optical responses. Bath application of D1 agonist 6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5,-tetrahydro-1H-3-benz aze pine hydrobromide consistently increased the intensity but decreased the speed of propagation and duration of the optical response. Bath application of D2 agonist quinpirole had no effect on the optical response. D1 antagonist SCH 23390 and D2 antagonist sulpiride also failed to change optical responses. These results indicate that the early part of the response is due to direct activation of the neuronal elements by electrical stimulation, while the late part of the response is due mainly to glutamatergic ex-citatory postsynaptic potentials (EPSPs) mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptors. This study also suggests that dopamine may modulate AMPA/kainate responses through D1 receptors.
使用电压敏感染料和高速图像传感器,研究了γ-氨基丁酸(GABA)和谷氨酸拮抗剂以及多巴胺激动剂和拮抗剂对新纹状体(Str)切片对局部电刺激的光学反应的影响。对Str切片施加单次局部刺激可诱发持续40 - 80毫秒并向各个方向传播至约1.5毫米的光学反应。浴槽中加入甲磺酸荷包牡丹碱可增加光学反应的强度和持续时间,但其空间反应模式不变。浴槽中加入6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX)可大大减少刺激后约4毫秒出现的反应后期部分,但反应早期部分不受CNQX影响。应用河豚毒素可消除反应的早期部分。浴槽中加入N-甲基-D-天冬氨酸拮抗剂3-(2-羧基哌嗪-4-基)-丙基-1-膦酸和2-氨基-5-膦酰基戊酸,光学反应仅有微小变化。浴槽中加入D1激动剂6-氯-7,8-二羟基-3-烯丙基-1-苯基-2,3,4,5-四氢-1H-3-苯并氮杂卓氢溴酸盐可持续增加光学反应的强度,但降低其传播速度和持续时间。浴槽中加入D2激动剂喹吡罗对光学反应无影响。D1拮抗剂SCH 23390和D2拮抗剂舒必利也未能改变光学反应。这些结果表明,反应的早期部分是由于电刺激直接激活神经元成分所致,而反应的后期部分主要是由于由α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)/海人藻酸受体介导的谷氨酸能兴奋性突触后电位(EPSP)。本研究还表明,多巴胺可能通过D1受体调节AMPA/海人藻酸反应。