Rose H J, Metherate R
Department of Neurobiology and Behavior, University of California, 2205 Biological Sciences II, Irvine, CA 92697-4550, USA.
Neuroscience. 2001;106(2):331-40. doi: 10.1016/s0306-4522(01)00282-2.
Stimulation of the medial geniculate body in an auditory thalamocortical slice elicits a short-latency current sink in the middle cortical layers, as would be expected following activation of thalamocortical relay neurons. However, corticothalamic neurons can have axon collaterals that project to the middle layers, thus, a middle-layer current sink could also result from antidromic activation of corticothalamic neurons and their axon collaterals. The likelihood of thalamic stimulation activating corticothalamic neurons would be reduced substantially if the corticothalamic pathway was not well preserved in the slice, and/or if the threshold for antidromic activation was significantly higher than for orthodromic activation. To determine the prevalence and threshold of antidromic activation, we recorded intracellularly from day 14-17 mouse brain slices containing infragranular cortical neurons while stimulating the medial geniculate or thalamocortical pathway. Antidromic spikes were confirmed by spike collision and characterized according to spike latency "jitter" and the ability to follow a high-frequency (100 Hz) stimulus train. The ability to follow a 100-Hz tetanus was a reliable indicator of antidromic activation, but both antidromic and orthodromic spikes could have low jitter. Thalamic stimulation produced antidromic activation in two of 69 infragranular cortical neurons (<3%), indicating the presence of antidromic activity, but implying a limited corticothalamic connection in the slice. Antidromic spikes in 13 additional neurons were obtained by stimulating axons in the thalamocortical pathway. The antidromic threshold averaged 214+/-40.6 microA (range 6-475 microA), over seven times the orthodromic threshold for medial geniculate-evoked responses in layer IV extracellular (28+/-5.4 microA) or intracellular (27+/-5.6 microA) recordings. We conclude that medial geniculate stimulation activates relatively few corticothalamic neurons. Conversely, low-intensity thalamic stimulation strongly activates thalamocortical neurons. Thus, at low-stimulus intensities, the auditory thalamocortical slice can be used to probe mechanisms of thalamocortical function with limited antidromic activation of corticothalamic neurons.
在听觉丘脑皮质切片中刺激内侧膝状体，会在皮质中间层引发一个短潜伏期的电流汇集，这正如丘脑皮质中继神经元激活后所预期的那样。然而，皮质丘脑神经元可能有轴突侧支投射到中间层，因此，中间层的电流汇集也可能是皮质丘脑神经元及其轴突侧支的逆向激活所致。如果皮质丘脑通路在切片中保存不佳，和/或如果逆向激活的阈值显著高于顺向激活的阈值，那么丘脑刺激激活皮质丘脑神经元的可能性将大幅降低。为了确定逆向激活的发生率和阈值，我们在含有颗粒下层皮质神经元的第14 - 17天小鼠脑切片中进行细胞内记录，同时刺激内侧膝状体或丘脑皮质通路。通过锋电位碰撞确认逆向锋电位，并根据锋电位潜伏期“抖动”以及跟随高频（100Hz）刺激序列的能力对其进行特征描述。跟随100Hz强直刺激的能力是逆向激活的可靠指标，但逆向和顺向锋电位都可能具有低抖动。丘脑刺激在69个颗粒下层皮质神经元中的2个（<3%）产生了逆向激活，表明存在逆向活动，但意味着切片中皮质丘脑连接有限。通过刺激丘脑皮质通路中的轴突，在另外13个神经元中获得了逆向锋电位。逆向阈值平均为214±40.6微安（范围为6 - 475微安），是在细胞外（28±5.4微安）或细胞内（27±5.6微安）记录中内侧膝状体诱发反应顺向阈值的七倍多。我们得出结论，内侧膝状体刺激激活的皮质丘脑神经元相对较少。相反，低强度丘脑刺激强烈激活丘脑皮质神经元。因此，在低刺激强度下，听觉丘脑皮质切片可用于探究丘脑皮质功能机制，同时对皮质丘脑神经元的逆向激活有限。
