γ-氨基丁酸B型受体激活可抑制大鼠黑质网状部神经元的刺激诱发爆发式放电。
Gamma-aminobutyric acid(B) receptor activation suppresses stimulus-evoked burst firing in rat substantia nigra reticulata neurons.
作者信息
Shen Ke-Zhong, Johnson Steven W
机构信息
Department of Neurology, Oregon Health and Science University, Portland, Oregon 97239, USA.
出版信息
Neuroreport. 2012 Jan 4;23(1):40-4. doi: 10.1097/WNR.0b013e32834e4899.
Previous whole-cell patch-pipette studies showed that focal electrical stimulation of the subthalamic nucleus (STN) evokes a long-lasting complex excitatory postsynaptic currents (EPSC) and synaptically evoked bursts of action potentials in substantia nigra pars reticulata (SNR) neurons. Although synaptically evoked bursting may play a role in normal physiology, excessive burst firing correlates with symptoms of Parkinson's disease. We used patch-pipette recordings in rat brain slices to study the effects of baclofen on complex EPSCs and STN-induced burst firing in SNR neurons. Baclofen (1 µM) caused a reversible, 73% reduction in complex EPSCs, and this effect was blocked by the γ-aminobutyric acid(B) antagonist CGP35348 (100 µM). Using the loose-patch method to record extracellular potentials, a lower concentration of baclofen (100 nM) inhibited STN-evoked bursts, while leaving spontaneous firing of action potentials less affected. We suggest that strategies that selectively inhibit burst firing in the SNR might have therapeutic potential in the treatment of Parkinson's disease.
以往的全细胞膜片钳研究表明，对丘脑底核（STN）进行局部电刺激可在黑质网状部（SNR）神经元中诱发持久的复合兴奋性突触后电流（EPSC）以及突触诱发的动作电位爆发。虽然突触诱发的爆发可能在正常生理过程中发挥作用，但过度的爆发式放电与帕金森病的症状相关。我们在大鼠脑片中使用膜片钳记录来研究巴氯芬对SNR神经元中复合EPSC和STN诱发的爆发式放电的影响。巴氯芬（1 μM）使复合EPSC可逆性降低了73%，且这种效应被γ-氨基丁酸B（GABAB）拮抗剂CGP35348（100 μM）阻断。使用松散膜片法记录细胞外电位，较低浓度的巴氯芬（100 nM）可抑制STN诱发的爆发式放电，而对动作电位的自发放电影响较小。我们认为，选择性抑制SNR中爆发式放电的策略可能在帕金森病的治疗中具有治疗潜力。
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