Your browser version may not work well with NCBI's Web applications. More information here...
1: Nat Neurosci. 2005 May;8(5):635-41. Epub 2005 Apr 24.
Related Articles, Links
Click here to read Click here to read
Comment in:
SK channels regulate excitatory synaptic transmission and plasticity in the lateral amygdala.

Faber ES, Delaney AJ, Sah P.

The Queensland Brain Institute, University of Queensland, Brisbane, Queensland 4072, Australia.

At glutamatergic synapses, calcium influx through NMDA receptors (NMDARs) is required for long-term potentiation (LTP); this is a proposed cellular mechanism underlying memory and learning. Here we show that in lateral amygdala pyramidal neurons, SK channels are also activated by calcium influx through synaptically activated NMDARs, resulting in depression of the synaptic potential. Thus, blockade of SK channels by apamin potentiates fast glutamatergic synaptic potentials. This potentiation is blocked by the NMDAR antagonist AP5 (D(-)-2-amino-5-phosphono-valeric acid) or by buffering cytosolic calcium with BAPTA. Blockade of SK channels greatly enhances LTP of cortical inputs to lateral amygdala pyramidal neurons. These results show that NMDARs and SK channels are colocalized at glutamatergic synapses in the lateral amygdala. Calcium influx through NMDARs activates SK channels and shunts the resultant excitatory postsynaptic potential. These results demonstrate a new role for SK channels as postsynaptic regulators of synaptic efficacy.

Publication Types:
PMID: 15852010 [PubMed - indexed for MEDLINE]