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Abstract
Small-conductance Ca²⁺-activated potassium (SK) channels regulate neuronal excitability by coupling intracellular Ca²⁺ signals to membrane hyperpolarization. This thesis examines the role of SK2 isoforms in hippocampal synaptic plasticity and identifies distinct Ca²⁺ sources activating SK and Kv4.2 channels. We show that SK2-L directs synaptic localization of SK channels and is essential for normal long-term potentiation (LTP), while SK2-S alone cannot support synaptic SK function. Additionally, Ca²⁺ influx through NMDA receptors activates SK channels, whereas R-type Ca²⁺ channels engage Kv4.2 channels via KChIP-dependent mechanisms, revealing two separate Ca²⁺ signaling pathways within dendritic spines.