Abstract

Although multiple ionic conductances underlie nerve action potentials, K⁺ conductances play a key role in regulating neuronal excitability. The K⁺ channels make up the largest and most diverse family of ion channels, showing varying sensitivities to voltage and to intracellular second messengers, and present distinct patterns of expression in different cells and species. The goal of this dissertation was to investigate regulation of Ca²⁺-dependent K⁺ currents underlying the afterhyperpolarization (AHP) using perforated-patch and whole-cell recording techniques. Although learning-related increases in postsynaptic neuronal excitability resulting from reductions in the post-burst AHP in CA1 pyramidal neurons have been substantiated, the precise mechanisms mediating these learning-related changes are still unclear. Although small conductance (SK) K⁺ channels, voltage-gated Ca²+ channels, and metabotropic (second messenger-mediated) receptors have been shown to regulate late components of the AHP, and thus influence neuronal excitability, no single set of studies have assessed all these mechanisms in the same population of neurons. This study has systematically done so in young rat CA1 pyramidal neurons.