Muscarinic receptor activation induces depolarizing plateau potentials in bursting neurons of the rat subiculum
Muscarinic receptor activation induces depolarizing plateau potentials in bursting neurons of the rat subiculum
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DOI：
10.1152/jn.1999.82.5.2590
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发表时间：
1999-11-01
影响因子：
2.5
通讯作者：
Avoli, M
中科院分区：
文献类型：
--
作者：
Kawasaki, H;Palmieri, C;Avoli, M
毒蕈碱受体激活诱导大鼠下托爆发神经元的去极化平台电位。神经生理学杂志。82：2590-2601，1999.乙酰胆碱在哺乳动物脑中作为一种神经调质，通过与特定受体结合，从而引起神经元兴奋性的深刻变化。毒蕈碱受体的激活通常导致皮质细胞的兴奋性增加。然而，这种作用是否存在于下托中尚不清楚，下托是一种可能参与认知过程以及癫痫发作传播的边缘结构。大多数大鼠下托神经元被赋予内在的膜特性，使他们的火灾动作电位爆发。使用细胞内记录这些爆裂细胞在切片制备，我们在这里报告的应用胆碱能激动剂卡巴胆碱，（CCh，30-100 μ M）的培养基中含有离子型兴奋性氨基酸受体拮抗剂减少爆发后超极化（猝发-AHP），并公开了比触发电流脉冲持续时间长140-2的去极化平台电位，这些平台电位出现在CCh浓度>50 μ M时，并且依赖于静息膜电位和触发脉冲的强度/持续时间;在应用河豚毒素期间记录（1 μ M，n = 5个神经元），但明显减少，取代82%的细胞外Na+与等摩尔胆碱（n = 6）。通过施加Co 2+（2 mM; n = 5）或Cd 2+（1 mM; n = 2）以及通过用含有Ca 2+螯合剂双（2-氨基苯氧基）乙烷-N，N，N '，N'-四乙酸（0.2 M; n = 6）的电极记录，平台电位也被消除。毒蕈碱拮抗剂阿托品（0.5 μ M，n = 7）可逆转CCh诱导的爆发-AHP降低和平台电位。总之，我们的研究结果表明，一个强大的毒蕈碱调制的内在兴奋性的下托爆裂细胞，主要是由平台电位的外观。这些兴奋性的变化可能有助于生理过程，如学习或记忆，并在癫痫样去极化的产生中发挥作用。我们建议，在其他边缘结构，毒蕈碱平台电位下托主要是由于钙依赖性的非选择性阳离子电导。
Muscarinic receptor activation induces depolarizing plateau potentials in bursting neurons of the rat subiculum. J. Neurophysiol. 82: 2590-2601, 1999. Acetylcholine functions as a neuromodulator in the mammalian brain by binding to specific receptors and thus bringing about profound changes in neuronal excitability. Activation of muscarinic receptors often results in an increased excitability of cortical cells. It is, however, unknown whether such an action is present in the subiculum, a limbic structure that may be involved in cognitive processes as well as in seizure propagation. Most rat subicular neurons are endowed of intrinsic membrane properties that make them fire action potential bursts. Using intracellular recordings from these bursting cells in a slice preparation, we report here that application of the cholinergic agonist carbachol (CCh, 30-100 mu M) to medium containing ionotropic excitatory amino acid receptor antagonists reduces burst-afterhyperpolarizations (burst-AHPs) and discloses depolarizing plateau potentials that outlast the triggering current pulses by 140-2,800 ms. These plateau potentials appear with CCh concentrations >50 mu M and are dependent on the resting membrane potential and on the intensity/duration of the triggering pulse; are recorded during application of tetrodotoxin (1 mu M, n = 5 neurons); but are markedly reduced by replacing 82% of extracellular Na+ with equimolar choline (n = 6). Plateau potentials also are abolished by Co2+ (2 mM; n = 5) or Cd2+ (1 mM; n = 2) application and by recording with electrodes containing the Ca2+ chelator bis(2-aminophenoxy)ethane-N, N,N',N'-tetraacetic acid (0.2 M; n = 6). CCh-induced burst-AHP reduction and plateau potentials are reversed by the muscarinic antagonist atropine (0.5 mu M, n = 7). In conclusion, our findings demonstrate a powerful muscarinic modulation of the intrinsic excitability of subicular bursting cells that is predominated by the appearance of plateau potentials. These changes in excitability may contribute to physiological processes such as learning or memory and play a role in the generation of epileptiform depolarizations. We propose that, as in other limbic structures, muscarinic plateau potentials in the subiculum are mainly due to a Ca2+-dependent nonselective cationic conductance.