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Small conductance calcium-activated potassium (SK) channels are present at glutamatergic synapses where they limit synaptic transmission and plasticity. Here, we show that \u03b2 adrenoceptor activation regulates synaptic SK channels in lateral amygdala pyramidal neurons, through activation of protein kinase A. We show that SK channels are constitutively recycled from the postsynaptic membrane and that activation of \u03b2 adrenoceptors removes SK channels from excitatory synapses. This results in enhanced synaptic transmission and plasticity. Our findings demonstrate a novel mechanism by which \u03b2 adrenoceptors control synaptic transmission and plasticity, through regulation of SK channel trafficking, and suggest that modulation of synaptic SK channels may contribute to \u03b2 adrenoceptor-mediated potentiation of emotional memories.<\/jats:p>","DOI":"10.1523\/jneurosci.1796-08.2008","type":"journal-article","created":{"date-parts":[[2008,10,22]],"date-time":"2008-10-22T17:39:55Z","timestamp":1224697195000},"page":"10803-10813","source":"Crossref","is-referenced-by-count":105,"title":["Modulation of SK Channel Trafficking by Beta Adrenoceptors Enhances Excitatory Synaptic Transmission and Plasticity in the Amygdala"],"prefix":"10.1523","volume":"28","author":[{"given":"E. S. 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