Schwarz D W, Tennigkeit F, Adam T, Finlayson P, Puil E
J Otolaryngol. 1998 Dec;27(6):311-7.
We investigated if auditory neurons have an intrinsic ability to radically transform auditory signals.
We surveyed membrane properties that control coding by neurons, identified with intracellular staining or infrared-DIC videomicroscopy, in three stations of the auditory pathway. We used intracellular and patch-clamp techniques in slices, to study the voltage responses to current pulse injections and distinguished voltage-gated conductances with selective blockers.
First order spherical bushy cells in the anteroventral cochlear nucleus responded at a short, stable latency with single spikes, due to a perithreshold interaction of Na+ and Ca2+ conductances. Two K+ conductances suppressed firing after this onset-spike. Second-order principal neurons of the lateral superior olive use unspecified mechanisms to secure stable onset latencies but maintained a very regular tonic firing, resulting in a chopper pattern. Other intrinsic properties induced a marked accommodation in spike rate. When depolarized as during alert states, neurons in the medial geniculate body (MGB) of the thalamus fired with variable latencies in a tonic mode. At negative resting potentials characteristic of sleep states, they responded at the onset of a depolarization and the offset of a hyperpolarization with phasic bursts due to a transient low threshold Ca2+ current. In the phasic, but not tonic mode, MGB neurons produced high-threshold Ca2+ spikes that may couple signal transmission to the neuron's metabolism. The three neuron types exhibit analogue computing abilities that transform the same input into entirely different output patterns. Isoflurane anaesthesia induces a current shunt in MGB neurons, radically changing the properties and preventing normal responses. Thus, thalamocortical auditory codes are compromised under anaesthesia.
At all investigated stations of the auditory pathway, input signals are transformed by activation of voltage-controlled conductances and other intrinsic membrane properties.
我们研究了听觉神经元是否具有从根本上转换听觉信号的内在能力。
我们在听觉通路的三个部位,对通过细胞内染色或红外微分干涉相差显微镜鉴定的、控制神经元编码的膜特性进行了研究。我们在脑片中使用细胞内和膜片钳技术,研究对电流脉冲注入的电压反应,并用选择性阻滞剂区分电压门控电导。
前腹侧耳蜗核中的一级球形毛细胞由于Na⁺和Ca²⁺电导的阈下相互作用,以短而稳定的潜伏期对单个尖峰做出反应。在此起始尖峰之后,两种K⁺电导抑制放电。外侧上橄榄核的二级主神经元利用未明确的机制来确保稳定的起始潜伏期,但维持非常规则的紧张性放电,从而形成一种斩波模式。其他内在特性导致尖峰频率明显适应。当在警觉状态下 depolarized 时,丘脑内侧膝状体(MGB)中的神经元以紧张性模式以可变潜伏期放电。在睡眠状态特有的负静息电位下,它们在去极化开始和超极化结束时由于短暂的低阈值Ca²⁺电流而以相位爆发做出反应。在相位模式而非紧张性模式下,MGB神经元产生高阈值Ca²⁺尖峰,这可能将信号传递与神经元的代谢耦合起来。这三种神经元类型表现出模拟计算能力,可将相同的输入转换为完全不同的输出模式。异氟烷麻醉在MGB神经元中诱导电流分流,从根本上改变其特性并阻止正常反应。因此,麻醉状态下丘脑皮质听觉编码受到损害。
在听觉通路的所有研究部位,输入信号通过电压控制电导和其他内在膜特性的激活而被转换。