Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.
Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.
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DOI：
10.1113/jphysiol.1992.sp019078
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发表时间：
1992-04
期刊：
影响因子：
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通讯作者：
M. Washburn;H. C. Moises
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文献类型：
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作者：
M. Washburn;H. C. Moises
1.从大鼠腹侧前脑切片中基底外侧杏仁核（BLA）中的锥体型神经元获得细胞内记录，并用于比较外源性拟胆碱药的作用与电刺激基底前脑杏仁核胆碱能传入产生的作用。2.卡巴胆碱的浴应用使锥体细胞去极化，伴随输入电阻（Ri）的相关增加，减少了一系列电流诱发动作电位后的缓慢后超极化（AHP），并阻断了棘波频率调节。所有这些作用都被毒蕈碱拮抗剂阿托品逆转，但不能被烟碱拮抗剂六甲双铵逆转。3.电刺激外囊内的杏仁核传入引起一系列突触电位，包括非胆碱能快速兴奋性突触后电位（EPSP），随后是早期和晚期抑制性突触后电位（IPSP）。卡巴胆碱以阿托品敏感的方式降低了这些突触电位中的每一个。4.对锥体细胞局部应用卡巴胆碱产生短潜伏期超极化，随后是延长的去极化。氨甲酰胆碱引起的超极化和去极化可被阿托品阻断，但不被六甲双铵阻断。5.卡巴胆碱诱导的超极化与Ri降低相关，并且具有与早期IPSP几乎相同的逆转电位。灌注含有河豚毒素（TTX），荷包牡丹碱或印防己毒素的培养基阻断抑制反应，而随后的去极化不受影响。根据这些数据，可以得出结论，毒蕈碱超极化介导的突触前GABA能中间神经元在切片中的快速兴奋。6.卡巴胆碱诱导的去极化与Ri增加相关，通常具有低于-80 mV的逆转电位，对细胞外钾浓度的变化敏感，并被钾通道阻滞剂铯的细胞内离子电泳阻断，这一发现表明它是由一种或多种钾电导的毒蕈碱阻滞引起的。7.重复刺激含有胆碱能传入的切片内的站点诱发了一系列快速EPSP，然后是IPSP。这些非胆碱能电位之后是持续10 s-4 min的慢EPSP。慢EPSP被艾司氯胺酮增强，并被阿托品阻断。它也被TTX或镉阻断，表明它依赖于尖峰传播和乙酰胆碱（ACh）的钙依赖性释放。8.刺激胆碱能传入的切片模仿卡巴胆碱产生的其他影响，包括封锁的慢AHP和住宿的动作电位放电，这些行动被加强的埃斯帕酮和阿托品阻断。（400字处截断摘要）
1. Intracellular recordings were obtained from pyramidal‐type neurons in the basolateral amygdaloid nucleus (BLA) in slices of rat ventral forebrain and used to compare the actions of exogenously applied cholinomimetics to the effects produced by electrical stimulation of amygdalopetal cholinergic afferents from basal forebrain. 2. Bath application of carbachol depolarized pyramidal cells with an associated increase in input resistance (Ri), reduced the slow after‐hyperpolarization (AHP) that followed a series of current‐evoked action potentials and blocked spike frequency accommodation. All of these effects were reversed by the muscarinic antagonist atropine but not by the nicotinic antagonist hexamethonium. 3. Electrical stimulation of amygdaloid afferents within the external capsule evoked a series of synaptic potentials consisting of a non‐cholinergic fast excitatory postsynaptic potential (EPSP), followed by early and late inhibitory postsynaptic potentials (IPSPs). Each of these synaptic potentials was reduced by carbachol in an atropine‐sensitive manner. 4. Local application of carbachol to pyramidal cells produced a short‐latency hyperpolarization followed by a prolonged depolarization. The hyperpolarization and depolarization to carbachol were blocked by atropine but not hexamethonium. 5. The carbachol‐induced hyperpolarization was associated with a decrease in Ri and had a reversal potential nearly identical to that of the early IPSP. The inhibitory response was blocked by perfusion of medium containing tetrodotoxin (TTX), bicuculline or picrotoxin, while the subsequent depolarization was unaffected. On the basis of these data, it is concluded that the muscarinic hyperpolarization is mediated through the rapid excitation of presynaptic GABAergic interneurons in the slice. 6. The findings that the carbachol‐induced depolarization was associated with an increase in Ri, often had a reversal potential below ‐80 mV, was sensitive to changes in extracellular potassium concentration and was blocked by intracellular ionophoresis of the potassium channel blocker caesium suggest that it resulted from a muscarinic blockade of one or more potassium conductances. 7. Repetitive stimulation of sites within the slice containing cholinergic afferents evoked a series of fast EPSPs followed by IPSPs. These non‐cholinergic potentials were followed by a slow EPSP that lasted from 10 s‐4 min. The slow EPSP was enhanced by eserine and blocked by atropine. It was also blocked by TTX or cadmium, indicating that it was dependent on spike propagation and calcium‐dependent release of acetylcholine (ACh). 8. Stimulation of cholinergic afferents in the slice mimicked other effects produced by carbachol including blockade of the slow AHP and accommodation of action potential discharge and these actions were potentiated by eserine and blocked by atropine.(ABSTRACT TRUNCATED AT 400 WORDS)