Center for Translational Neuroscience, Dept. of Neurobiology and Developmental Sciences, Univ. of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
J Neurophysiol. 2012 Feb;107(3):772-84. doi: 10.1152/jn.00677.2011. Epub 2011 Nov 16.
The parafascicular nucleus (Pf) receives cholinergic input from the pedunculopontine nucleus, part of the reticular activating system involved in waking and rapid eye movement (REM) sleep, and sends projections to the cortex. We tested the hypothesis that Pf neurons fire maximally at gamma band frequency (30-90 Hz), that this mechanism involves high-threshold voltage-dependent P/Q- and N-type calcium channels, and that this activity is enhanced by the cholinergic agonist carbachol (CAR). Patch-clamped 9- to 25-day-old rat Pf neurons (n = 299) manifested a firing frequency plateau at gamma band when maximally activated (31.5 ± 1.5 Hz) and showed gamma oscillations when voltage-clamped at holding potentials above -20 mV, and the frequency of the oscillations increased significantly with age (24.6 ± 3.8 vs. 51.6 ± 4.4 Hz, P < 0.001) but plateaued at gamma frequencies. Cells exposed to CAR showed significantly higher frequencies early in development compared with those without CAR (24.6 ± 3.8 vs. 41.7 ± 4.3 Hz, P < 0.001) but plateaued with age. The P/Q-type calcium channel blocker ω-agatoxin-IVA (ω-Aga) blocked gamma oscillations, whereas the N-type blocker ω-conotoxin-GVIA (ω-CgTx) only partially decreased the power spectrum amplitude of gamma oscillations. The blocking effect of ω-Aga on P/Q-type currents and ω-CgTx on N-type currents was consistent over age. We conclude that P/Q- and N-type calcium channels appear to mediate Pf gamma oscillations during development. We hypothesize that the cholinergic input to the Pf could activate these cells to oscillate at gamma frequency, and perhaps relay these rhythms to cortical areas, thus providing a stable high-frequency state for "nonspecific" thalamocortical processing.
束旁核（Pf）接收来自脑桥被盖脚核（pedunculopontine nucleus）的胆碱能输入，脑桥被盖脚核是参与觉醒和快速眼动（REM）睡眠的网状激活系统的一部分，并向皮层发送投射。我们检验了这样一个假说，即 Pf 神经元以伽马频段（30-90Hz）的最大频率放电，该机制涉及高阈值电压依赖性 P/Q 和 N 型钙通道，而这种活动可被胆碱能激动剂 carbachol（CAR）增强。我们对 9 至 25 天龄的大鼠 Pf 神经元（n=299）进行了膜片钳记录，结果显示当最大激活时（31.5±1.5Hz）神经元以伽马频段表现出放电频率平台，当在高于-20mV 的钳制电位下进行电压钳制时表现出伽马振荡，并且振荡频率随年龄显著增加（24.6±3.8 与 51.6±4.4Hz，P<0.001），但在伽马频段达到平台。与无 CAR 组相比，早期接触 CAR 的细胞表现出明显更高的频率（24.6±3.8 与 41.7±4.3Hz，P<0.001），但随年龄增长达到平台。P/Q 型钙通道阻断剂 ω-agatoxin-IVA（ω-Aga）阻断了伽马振荡，而 N 型钙通道阻断剂 ω-conotoxin-GVIA（ω-CgTx）仅部分降低了伽马振荡的功率谱幅度。ω-Aga 对 P/Q 型电流和 ω-CgTx 对 N 型电流的阻断作用在整个年龄范围内都是一致的。我们得出结论，P/Q 和 N 型钙通道似乎在发育过程中介导 Pf 伽马振荡。我们假设 Pf 中的胆碱能输入可以激活这些细胞以伽马频率振荡，并可能将这些节律传递到皮层区域，从而为“非特异性”丘脑皮质处理提供稳定的高频状态。
