Format

Send to

Choose Destination
See comment in PubMed Commons below
PLoS One. 2011;6(9):e24915. doi: 10.1371/journal.pone.0024915. Epub 2011 Sep 26.

The A-current modulates learning via NMDA receptors containing the NR2B subunit.

Author information

1
División de Neurociencias, Universidad Pablo de Olavide de Sevilla, Sevilla, Spain. angela.fontan@cabimer.es

Abstract

Synaptic plasticity involves short- and long-term events, although the molecular mechanisms that underlie these processes are not fully understood. The transient A-type K(+) current (I(A)) controls the excitability of the dendrites from CA1 pyramidal neurons by regulating the back-propagation of action potentials and shaping synaptic input. Here, we have studied how decreases in I(A) affect cognitive processes and synaptic plasticity. Using wild-type mice treated with 4-AP, an I(A) inhibitor, and mice lacking the DREAM protein, a transcriptional repressor and modulator of the I(A), we demonstrate that impairment of I(A) decreases the stimulation threshold for learning and the induction of early-LTP. Hippocampal electrical recordings in both models revealed alterations in basal electrical oscillatory properties toward low-theta frequencies. In addition, we demonstrated that the facilitated learning induced by decreased I(A) requires the activation of NMDA receptors containing the NR2B subunit. Together, these findings point to a balance between the I(A) and the activity of NR2B-containing NMDA receptors in the regulation of learning.

PMID:
21966384
PMCID:
PMC3180285
DOI:
10.1371/journal.pone.0024915
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Support Center