Serotonergic modulation of neurotransmission in the rat basolateral amygdala
Serotonergic modulation of neurotransmission in the rat basolateral amygdala
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DOI：
10.1152/jn.1999.82.1.69
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发表时间：
1999-07-01
影响因子：
2.5
通讯作者：
Rainnie, DG
中科院分区：
文献类型：
--
作者：
Rainnie, DG
大鼠基底外侧杏仁核神经传递的血清素调节。[j] .中国生物医学工程。69 - 85年,1999年。对大鼠基底外侧杏仁核（BLA）的投射神经元和中间神经元进行全细胞膜片钳记录，以了解形态学鉴定神经元的局部网络相互作用及其受血清素的调节。根据其固有的膜特性和突触特性，对投射神经元和中间神经元进行了形态学和电生理表征。投射神经元的突触突触活性主要由多相自发性抑制性突触后电流（IPSCs）控制，其振幅可达181 +/- 38 pA，持续时间为296 +/- 27 mS，并被GABA(A)受体拮抗剂双丘碱（30 μ M）阻断。在中间神经元中，自发突触活动的特征是爆发放电模式（200 +/- 40 Hz），与6-氰基-7-硝基喹啉-2,3-二酮敏感的高振幅（260 +/- 42 pA），长时间（139 +/- 19 mS）内向兴奋性突触后电流（EPSCs）的发生相关。复合抑制突触后电位（IPSP）的事件间隔为831 +/- 344 mS， EPSC爆发的事件间隔为916 +/- 270 mS，表明投射神经元自发性IPSP/Cs是由中间神经元的动作电位爆发驱动的。因此，BLA中间神经元可能调节投射神经元的兴奋性，从而决定BLA神经元群内的同步程度。在中间神经元5-羟色胺草酸（5-HT）诱发直接，剂量依赖性。45 +/- 6.9 pA向内电流介导膜去极化，反向电位为-90 mV。5-HT的作用可被5-HT2受体激动剂α -甲基-5-羟色胺（α -甲基-5-HT）模拟，但不能被5-HT1A受体激动剂（+/-）8-羟二丙胺四溴化氢（8-QH-DPAT）或5-HT1B激动剂CGS 12066A模拟。在投射神经元中，5-HT诱发了间接膜超极化（类似于2 mV），并伴有75 +/- 42 pA的向外电流和-70 mV的逆转电位。反应不受5-HT浓度的影响，呈阻滞状态；由TTX还原，α -甲基-5- ht模拟，8-OH-DPAT模拟。在中间神经元中，5-HT降低了EPSC的振幅，在TTX （0.6 μ M）存在下，减少了微型EPSC的频率，但没有减少其量子含量。在投射神经元中，5-HT也引起EPSCs和IPSCs刺激幅度的剂量依赖性降低。这些结果表明，急性血清素释放会通过激活5-HT2受体直接激活BLA的gaba能中间神经元，并增加投射神经元中抑制性突触事件的频率。慢性5 -羟色胺释放，或高水平的5 -羟色胺，将减少兴奋驱动到中间神经元，并可能作为一种反馈机制，以防止过度抑制在核。
Serotonergic modulation of neurotransmission in the rat basolateral amygdala. J. Neurophysiol. 82. 69-85, 1999. Whole cell patch-clamp recordings were obtained from projection neurons and interneurons of the rat basolateral amygdala (BLA) to understand local network interactions in morphologically identified neurons and their modulation by serotonin. Projection neurons and interneurons were characterized morphologically and electrophysiologically according to their intrinsic membrane properties and synaptic characteristics. Syn aptic activity in projection neurons was dominated by spontaneous inhibitory postsynaptic currents (IPSCs) that were multiphasic, reached 181 +/- 38 pA in amplitude, lasted 296 +/- 27 mS, and were blocked by the GABA(A) receptor antagonist, bicuculline methiodide (30 mu M). In interneurons, spontaneous synaptic activity was characterized by a burst-firing discharge patterns (200 +/- 40 Hz) that correlated with the occurrence of 6-cyano-7-nitroquinoxaline-2,3-dione-sensitive high-amplitude (260 +/- 42 pA), long-duration (139 +/- 19 mS) inward excitatory postsynaptic currents (EPSCs). The interevent interval of 831 +/- 344 mS for compound inhibitory postsynaptic potentials (IPSPs), and 916 +/- 270 mS for EPSC bursts, suggested that spontaneous IPSP/Cs in projection neurons are driven by burst of action potentials in interneurons. Hence, BLA interneurons may regulate the excitability of projection neurons and thus determine the degree of synchrony within ensembles of BLA neurons. In interneurons 5-hydroxytryptamine oxalate (5-HT) evoked a direct, dose-dependent. membrane depolarization mediated by a 45 +/- 6.9 pA inward current, which had a reversal potential of -90 mV. The effect of 5-HT was mimicked by the 5-HT2 receptor agonist, alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT), but not by the 5-HT1A receptor agonist, (+/-) 8-hydroxydipropylaminotetralin hydrobromide (8-QH-DPAT), or the 5-HT1B agonist, CGS 12066A. In projection neurons, 5-HT evoked an indirect membrane hyperpolarization (similar to 2 mV) that was associated with a 75 +/- 42 pA outward current and had a reversal potential of -70 mV. The response was independent of 5-HT concentration, blocked;ed by TTX, mimicked by alpha-methyl-5-HT but nut by 8-OH-DPAT. In interneurons, 5-HT reduced the amplitude of the evoked EPSC and in the presence of TTX (0.6 mu M) reduced the frequency of miniature EPSCs but not their quantal content. In projection neurons, 5-HT also caused a dose-dependent reduction in the amplitude of stimulus evoked EPSCs and IPSCs. These results suggest that acute serotonin release would directly activate GABAergic interneurons of the BLA, via an activation of 5-HT2 receptors, and increase the frequency of inhibitory synaptic events in projection neurons. Chronic serotonin release, or high levels of serotonin, would reduce the excitatory drive onto interneurons and may act as a feedback mechanism to prevent excess inhibition within the nucleus.