GABAergic modulation of D-1 dopamine receptor-mediated 3H-acetylcholine release from rabbit retina.
GABAergic modulation of D-1 dopamine receptor-mediated 3H-acetylcholine release from rabbit retina.
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GABA 能调节 D-1 多巴胺受体介导的兔视网膜 3H-乙酰胆碱释放。
DOI：
10.1007/bf00175793
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Dubocovich,ML
中科院分区：
文献类型：
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作者：
Hensler,JG;Dubocovich,ML
多巴胺通过激活D-1多巴胺受体，诱导3h -乙酰胆碱从体外3h -胆碱标记的过量兔视网膜中钙依赖性释放。本研究探讨了内源性多巴胺对该受体的激活作用，以及gaba能激动剂和拮抗剂对3h -乙酰胆碱从3h -胆碱标记的兔视网膜自发释放和多巴胺诱导释放的调节作用。内源性多巴胺通过间接胺酪胺或d -安非他明从多巴胺能无突神经元释放，引起兔视网膜3h -乙酰胆碱的钙依赖性释放。选择性D-1拮抗剂SCH 23390 （0.1 μM）和多巴胺摄取抑制剂nomifenine （3 μM）可减弱酪胺（10 μM）和d -安非他明（10 μM）诱导的3h -乙酰胆碱释放。GABA和muscimol分别在1 mM和1 μM浓度下抑制3h -胆碱体外标记兔视网膜氚的自发释放。Picrotoxin和bicuculline （10 μM）增加了氚的自发释放。GABA和GABA激动剂muscimol （0.01 ~ 100 μM）对100 μM多巴胺诱导的3h -乙酰胆碱释放呈浓度依赖性，ic50值分别为4.5 μM和0.02 μM。GABA （10 μM）和muscimol （0.1 μM）对多巴胺诱导的3h -乙酰胆碱释放的抑制作用被GABA拮抗剂双核碱和微毒素拮抗。乳杆菌毒素和双核碱（10 μM）增加了氚的自发释放，并增强了100 μM多巴胺引起的3h -乙酰胆碱的释放，这与对兔视网膜胆碱能神经元的强直、抑制性gaba能输入一致。多巴胺在兔视网膜中引起的乙酰胆碱释放可能具有重要的生理意义，因为内源性多巴胺可以诱导D-1多巴胺受体介导的3h -乙酰胆碱释放增加。此外，GABA受体位点的激活调节了自发和多巴胺诱发的兔视网膜乙酰胆碱释放。
Dopamine evokes calcium-dependent release of3H-acetylcholine from superfused rabbit retina labeled in vitro with3H-choline, through activation of a D-1 dopamine receptor. This study investigates the activation of this receptor by endogenous dopamine and the modulation of the spontaneous and dopamine-evoked release of3H-acetylcholine from rabbit retina labeled with3H-choline by GABAergic agonists and antagonists. Endogenous dopamine, released from dopaminergic amacrine neurons by the indirect amines tyramine or D-amphetamine evoked the calcium-dependent release of3H-acetylcholine from rabbit retina. The release of3H-acetylcholine elicited by tyramine (10 μM) or D-amphetamine (10 μM) was attenuated by the selective D-1 antagonist SCH 23390 (0.1 μM) and by the dopamine uptake inhibitor nomifensine (3 μM). At concentrations of 1 mM and 1 μM respectively, GABA and muscimol inhibited the spontaneous release of tritium from rabbit retina labeled in vitro with3H-choline. Picrotoxin and bicuculline (10 μM) increased the spontaneous release of tritium. GABA and the GABA agonist muscimol (0.01–100 μM) inhibited in a concentration-dependent manner the release of3H-acetylcholine elicited by 100 μM dopamine with IC50values of 4.5 μM and 0.02 μM respectively. The inhibition of dopamine-evoked3H-acetylcholine release by GABA (10 μM) and muscimol (0.1 μM) was antagonized by the GABA antagonists bicuculline and picrotoxin. Picrotoxin and bicuculline (10 μM) increased the spontaneous release of tritium, and potentiated the release of3H-acetylcholine evoked by 100 μM dopamine consistant with a tonic, inhibitory GABAergic input to the cholinergic amacrine neurons in rabbit retina. Dopamine-evoked acetylcholine release in rabbit retina may be of physiological importance as D-1 dopamine receptor-mediated increases in3H-acetylcholine release from rabbit retina can be elicited by endogenous dopamine. In addition, activation of GABA receptor sites modulates the spontaneous and dopamine-evoked acetylcholine release from rabbit retina.