CAJ | 학술논문

小脑间位核（interpositusnucleus，IN）主要接受1一氨基丁酸（GABA）能纤维支配，同时接受组胺能纤维的调节．本研究在小脑脑片上研究了GABA和组胺对单个IN神经元电活动的共同作用．持续灌流组胺或同时施加组胺和GABA，81．2％（69／85）神经元，GABA及其激动剂的效应都被组胺削弱（持续灌流n=33；同时施加n=36）．这种削弱效应能够被纽胺H，受体阻断剂ranitidine（n=10）和PK。抑制剂H一89阻断（n=8），fors—kolin模拟组胺的效应（n=9）．结果表明组胺和GABA对IN神经元的电活动具有交互调节作用：通过激活H：受体偶联的G—protein—AC—PK。信号通路，磷酸化GABAB和GABA^受体，降低受体功能．推测受体间的对话的工作模式，可能是整个大脑神经元活动的某些药理作用和生理活动调节的基础；如果对话紊乱，可能导致大脑功能障碍．
소뇌간위핵（interpositusnucleus，IN）주요접수1일안기정산（GABA）능섬유지배，동시접수조알능섬유적조절．본연구재소뇌뇌편상연구료GABA화조알대단개IN신경원전활동적공동작용．지속관류조알혹동시시가조알화GABA，81．2％（69／85）신경원，GABA급기격동제적효응도피조알삭약（지속관류n=33；동시시가n=36）．저충삭약효응능구피뉴알H，수체조단제ranitidine（n=10）화PK。억제제H일89조단（n=8），fors—kolin모의조알적효응（n=9）．결과표명조알화GABA대IN신경원적전활동구유교호조절작용：통과격활H：수체우련적G—protein—AC—PK。신호통로，린산화GABAB화GABA^수체，강저수체공능．추측수체간적대화적공작모식，가능시정개대뇌신경원활동적모사약리작용화생리활동조절적기출；여과대화문란，가능도치대뇌공능장애．
Previous studies suggested that the activity of neurons in the cerebellar interpositus nucleus （ IN）, is major under the influence of GABAergic fibers afferent, and also regulation of histaminergic fibers afferent. In this study, the brain slice preparation of adult rats was used to examine the combined effect of y-aminobutyric acid （GABA） and histamine on the spontaneous unitary discharge of IN neurons and the underlying mecha- nism. When the effect of GABA was tested during sequential application of histamine or co-application of GABA and histamine, the magnitude of GABA-induced response was modified in 81.2% （69/85） of the cells （n = 33, 36）. Histamine-induced diminishment of GABA response was abolished by the H2 receptor antagonist ranit- idine （n = 10）, and also prevented by PKA inhibitor H-89 （n = 8）. And histamine-induced diminishment of GABA response was mimicked by the adenylyl cyclase activator （AC） forskolin （n = 9）. Our results indicated that a reciprocal modulation between the effects of GABA and histamine on neuronal firing activity via Hi recep- tors and H2 receptors linked intracellular G-protein-AC-PKA signaling pathway, and result in an activation of in- tracellular phosphmylation of GABAR and GABAA receptors, ultimately, a depression of GABA receptor func- tion, suggesting that the disruption of the working model of receptors cross-talk may be responsible for some ofthe pharmacological action and physiological regulation of neuronal activity through the brain.