L-type calcium channel-mediated plateau potentials in barrelette cells during structural plasticity
L-type calcium channel-mediated plateau potentials in barrelette cells during structural plasticity
复制标题
DOI：
10.1152/jn.2002.88.2.794
复制
发表时间：
2002-08-01
影响因子：
2.5
通讯作者：
Erzurumlu, RS
中科院分区：
文献类型：
--
作者：
Lo, FS;Erzurumlu, RS
啮齿动物三叉神经通路上胡须特异性模式的发育和维持取决于发育敏感/关键时期完整的感觉外围。脑干三叉神经核的桶状细胞是第一组形成胡须特异性模式的神经元。主感觉核（PrV）中的那些将这些模式传递给腹基底丘脑，从而传递给体感皮层。因此，PrV 桶状细胞是第一组容易受到外周损伤影响的中枢神经元。之前我们表明，桶状细胞的膜特性早在出生后第 1 天（PND 1）就不同，并且在新生大鼠幼崽的外周去神经后保持不变（Lo 和 Erzurumlu 2001）。在本研究中，我们研究了突触传递的变化。在正常 PND 1 大鼠的桶状细胞中，三叉神经束 (TrV) 的弱刺激（TrV）是诱导 Na+ 尖峰的阈值以下，会引发兴奋性突触后电位 - 抑制性突触后电位 (EPSP-IPSP) 序列，这与老年大鼠中观察到的反应相似 (Lo et al. 1999)。出生时眶下神经横断不会改变桶状细胞的兴奋性和抑制性突触连接。这些观察结果表明，PrV 中的局部神经元回路在出生时就已建立，并在传入神经阻滞后保持完整。 TrV 的强烈刺激会在去神经支配的神经元中诱导持续的去极化（平台电位），但在正常的桶状神经元中不会。平台电位与 EPSP-IPSP 序列的不同之处在于 1) 持续 (>80 ms) 去极化高于 -40 mV； 2) 到超极化膜水平的缓慢下降斜率 (1 mV/ms)。平台电位由 L 型 Ca2+ 通道介导，并由 N-甲基-D-天冬氨酸 (NMDA) 受体介导的 EPSP 触发。 γ-氨基丁酸-A (GABA(A)) 受体介导的 IPSP 动态调节平台电位的潜伏期和持续时间。这些结果表明，新生儿外周损伤后，中枢三叉神经输入会通过桶状神经元中的 L 型 Ca2+ 通道引起大量且持久的 Ca2+ 流入。 Ca2+ 进入的增加可能在损伤诱导的结构重塑和/或突触细胞死亡中发挥关键作用。
Development and maintenance of whisker-specific patterns along the rodent trigeminal pathway depends on an intact sensory periphery during the sensitive/critical period in development. Barrelette cells of the brain stem trigeminal nuclei are the first set of neurons to develop whisker-specific patterns. Those in the principal sensory nucleus (PrV) relay these patterns to the ventrobasal thalamus, and consequently, to the somatosensory cortex. Thus PrV barrelette cells are among the first group of central neurons susceptible to the effects of peripheral damage. Previously we showed that membrane properties of barrelette cells are distinct as early as postnatal day 1 (PND 1) and remain unchanged following peripheral denervation in newborn rat pups (Lo and Erzurumlu 2001). In the present study, we investigated the changes in synaptic transmission. In barrelette cells of normal PND 1 rats, weak stimulation of the trigeminal tract (TrV) that was subthreshold for inducing Na+ spikes evoked an excitatory postsynaptic potential-inhibitory postsynaptic potential (EPSP-IPSP) sequence that was similar to the responses seen in older rats (Lo et al. 1999). Infraorbital nerve transection at birth did not alter excitatory and inhibitory synaptic connections of the barrelette cells. These observations suggested that local neuronal circuits are already established in PrV at birth and remain intact after deafferentation. Strong stimulation of the TrV induced a sustained depolarization (plateau potential) in denervated but not in normal barrelette neurons. The plateau potential was distinct from the EPSP-IPSP sequence by 1) a sustained (>80 ms) depolarization above -40 mV; 2) a slow decline slope (1 mV/ms) to a hyperpolarizing membrane level. The plateau potential was mediated by L-type Ca2+ channels and triggered by a N-methyl-D-aspartate (NMDA) receptor-mediated EPSP. gamma-aminobutyric acid-A (GABA(A)) receptor-mediated IPSP dynamically regulated the latency and duration of the plateau potential. These results indicate that after neonatal peripheral damage, central trigeminal inputs cause a large and long-lasting Ca2+ influx through L-type Ca2+ channels in barrelette neurons. Increased Ca2+ entry may play a key role in injury-induced structural remodeling, and/or transsynaptic cell death.