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Molecular mechanisms regulating action potential generation in neocortical fast-spiking interneurons
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Molecular mechanisms regulating action potential generation in neocortical fast-spiking interneurons
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Dissertation
Molecular mechanisms regulating action potential generation in neocortical fast-spiking interneurons
2011
Overview
Ion channels are critical regulators of neuronal excitability in the central nervous system and mutations in these proteins produce human disease such as epilepsy and ataxia. Potassium channels are by far the most diverse group of ion channels and influence many aspects of neuronal communication from subthreshold synaptic integration to action potential generation and neurotransmitter release. In this thesis, I investigate the functional roles of Kv1 potassium channels in a specialized subtype of neocortical GABAergic interneuron known as the fast-spiking (FS) cell. Fast and reliable operation of these neurons is thought to be essential for normal cortical function. Using immunohistochemical methods, we show that Kv1.1 protein subunits are highly enriched at the axon initial segment of FS cells--the site of action potential generation. By recording FS cell activity in response to naturalistic fluctuating inputs combined with Kv1 specific pharmacology and recordings in Kv1.1 null mice, we show that Kv1 channels with specific biophysical properties are important determinants of input selectivity and precise spike generation in FS cells. These studies may have implications for the mechanisms regulating FS cell action potential generation in vivo and for the cellular basis of seizures in animal models of epilepsy.
