Gulledge Allan T, Stuart Greg J
Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT 0200, Australia.
J Neurosci. 2003 Dec 10;23(36):11363-72. doi: 10.1523/JNEUROSCI.23-36-11363.2003.
Somatic and dendritic whole-cell recording was used to examine action potential (AP) initiation and propagation in layer 5 pyramidal neurons of the rat prelimbic prefrontal cortex. APs generated by somatic current injection, or via antidromic stimulation, were reliably recorded at apical dendritic locations as far as 480 microm from the soma. Although the backpropagation of single APs into the apical dendrite was robust, frequency-dependent attenuation was observed during AP trains delivered at 10-100 Hz. APs were usually initiated close to the soma (presumably in the axon); however, strong depolarizing input to the apical dendrite could generate dendritic spikes that preceded somatic APs. AP backpropagation was dependent solely on activation of dendritic voltage-gated sodium channels and did not require activation of dendritic calcium channels. Despite not playing a role in AP backpropagation, calcium-imaging experiments demonstrated that dendritic calcium channels are activated by backpropagating APs, leading to transient increases in intracellular calcium. In addition, calcium imaging revealed that AP backpropagation into the distal apical tuft was frequency dependent. Finally, we tested whether dopamine, a prominent neuromodulator associated with prefrontal activity, could alter AP initiation or backpropagation. Bath-applied dopamine (10 or 100 microm) did not effect AP backpropagation, frequency-dependent depression, local dendritic spike initiation, or AP-induced calcium signaling. These data indicate that AP backpropagation in prefrontal layer 5 pyramidal neurons is robust but frequency dependent in the distal tuft, requires dendritic sodium rather than calcium channel activation, and, unlike other aspects of neuronal excitability, insensitive to modulation by dopamine.
采用体细胞和树突全细胞记录法，研究大鼠前边缘前额叶皮层第5层锥体神经元动作电位（AP）的起始和传播。通过体细胞电流注入或逆向刺激产生的动作电位，在距离胞体最远达480微米的顶端树突位置能够可靠记录。尽管单个动作电位向顶端树突的逆向传播很强劲，但在10 - 100赫兹发放动作电位串期间，观察到了频率依赖性衰减。动作电位通常在靠近胞体处起始（推测在轴突）；然而，对顶端树突的强去极化输入可产生先于体细胞动作电位的树突棘波。动作电位的逆向传播仅依赖于树突电压门控钠通道的激活，不需要树突钙通道的激活。尽管钙成像实验表明树突钙通道在动作电位逆向传播中不起作用，但动作电位逆向传播可激活树突钙通道，导致细胞内钙短暂增加。此外，钙成像显示动作电位向远端顶端树突的逆向传播具有频率依赖性。最后，我们测试了多巴胺（一种与前额叶活动相关的重要神经调质）是否能改变动作电位的起始或逆向传播。浴加多巴胺（10或100微摩尔）对动作电位逆向传播、频率依赖性抑制、局部树突棘波起始或动作电位诱导的钙信号均无影响。这些数据表明，前额叶第5层锥体神经元的动作电位逆向传播很强劲，但在远端树突具有频率依赖性，需要树突钠通道而非钙通道的激活，并且与神经元兴奋性的其他方面不同，对多巴胺调节不敏感。
