| Short-term activation of synaptic transmission by acute KCl application significantly reduces somatic A-type K+ current. |
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Jung-Yop Song, Hye-Ji Kim, Sung-Cherl Jung, Moon-Seok Kang |
Correspondence:
Moon-Seok Kang, Email: wanzon@botamedi.com
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| Abstract |
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A-type K+ (IA) channels are transiently activated in the suprathreshold membrane potential and then rapidly inactivated. These channels play roles to control the neuronal excitability in pyramidal neurons in hippocampi. We here electrophysiologically tested if regulatory functions of IA channels might be targeted by acute activation of glutamatergic synaptic transmission in cultured hippocampal neurons (DIV 6~8). The application of high KCl in recording solutions (10 mM, 2 min) to increase presynaptic glutamate release, significantly reduced the peak of somatic IA without changes of gating kinetics. This indicates that neuronal excitation induced by the enhancement of synaptic transmission may process with distinctive signaling cascades to affect voltage-dependent ion channels in hippocampal neurons. Therefore, it is possible that short-lasting enhancement of synaptic transmission is functionally restricted in local synapses without effects on intracellular signaling cascades affecting a whole neuron, efficiently and rapidly enhancing synaptic functions in hippocampal network. |
| Key Words:
A-type, K+, channel, glutamate, transient |
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