SK channels regulate excitatory synaptic transmission and plasticity in the lateral amygdala.

Abstract:

: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.

journal_name

Nat Neurosci

journal_title

Nature neuroscience

authors

Faber ES,Delaney AJ,Sah P

doi

10.1038/nn1450

subject

Has Abstract

pub_date

2005-05-01 00:00:00

pages

635-41

issue

5

eissn

1097-6256

issn

1546-1726

pii

nn1450

journal_volume

8

pub_type

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