SK Channels Modulate the Excitability and Firing Precision of Projection Neurons in the Robust Nucleus of the Arcopallium (RA) in Adult Male Zebra Finches

Small-conductance Ca2+-activated K+ channels (SK channels) are insensitive to the change of membrane potential and widely expressed throughout the nervous system in mammals [1-4]. There are three subtypes (SK1, SK2 and SK3) of SK channels and all of them have been found to express in the mammalian brain [1]. These channels are activated by rises in intracellular calcium concentration and can be specifically blocked by the bee toxin apamin. SK channels contribute to the after hyperpolarization (AHP) following action potential [5]. In central nervous system, SK channels are important in controlling firing frequency of neurons, regulating dendritic excitability, synaptic transmission and synaptic plasticity [6-9]. In rat globus pallidus neurons, blockade of SK channels by apamin reduces the amplitude of AHP and increases the firing rate. Apamin also varies spike threshold and disrupts the precision of firing. These changes make it difficult for neurons to encode accurate information through spike time and firing rate [10]. 10-fold overexpression of SK2 subunits causes an approximately 4-fold increase in the apamin-sensitive current in CA1 neurons of transgenic mice, compared with wild-type littermates. EPSPs synaptically evoked from SK2 overexpressed CA1 neurons are increased in amplitude after SK channel blockade by 2-fold over that in wild-type CA1 neurons. In addition, SK2 overexpression decreases long-term potentiation (LTP) and weakens hippocampusand amygdala-dependent learning, as compared to wild-type littermates [11]. Therefore, SK channels play a critical role in regulating synaptic transmission, synaptic plasticity and learning and memory.