07.01.2013 Views

[Abstract Title]. - Society for Neuroscience

[Abstract Title]. - Society for Neuroscience

[Abstract Title]. - Society for Neuroscience

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

Rats were randomly assigned to one of 3 groups: trained, pseudoconditioned (pseudo), and naïve.<br />

The trained group received 30 paired tone CS and corneal airpuff US separated by a 250ms trace<br />

interval. Pseudo rats were given 30 CS and 30 US in an unpaired manner. Both groups had 5<br />

training sessions (2sessions/day). Hippocampal slices were cut in ice-cold aCSF 1 d after the last<br />

training session using a vibratome. The CA1/S was isolated from the hippocampal slice, and<br />

SK2, hippocalcin and CaV1.2 L-type Ca 2+ channel protein levels were determined by western<br />

blotting. Here we report an increase in SK2 and hippocalcin, but a decrease in CaV1.2 levels in<br />

CA1/S region from rats that learned as compared to naïve and pseudo rats. These data strongly<br />

suggest that the reduction in the amount of CaV1.2 is one source of the learning-related AHP<br />

reduction observed in CA1 neurons after trace EBC. Although hippocalcin is proposed to be a<br />

mediator of the slow AHP current, it does not contribute to the learning-related AHP reduction.<br />

Rather, the increase in hippocalcin levels suggests that a compensatory mechanism may occur<br />

after learning in response to a decreased cytosolic Ca 2+ level. The enhanced SK2 levels suggest<br />

that a homeostatic regulation may occur after learning. The increased SK2 level in the spines<br />

would filter out extraneous synaptic noise by establishing a higher threshold <strong>for</strong> the postsynaptic<br />

response to occur, but a strong signal that passes the SK2 filter would be readily passed on to the<br />

next element in the neural circuit because of the significantly reduced somatic slow AHP.<br />

Our present findings of molecular changes that occur with trace EBC directly link the reductions<br />

in CaV1.2 to the learning-related AHP reduction in CA1 neurons.<br />

Disclosures: M.M. Oh, None; D.P. Srivastava, None; B.M. McKay, None; K. Schoedel,<br />

None; P. Penzes, None; J.F. Disterhoft, None.<br />

Poster<br />

240. Intrinsic Membrane Properties: Modulation of Neuronal Firing Properties by Inputs<br />

and Activity<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 240.16/E38<br />

Topic: B.10.c. Activity-dependent plasticity of intrinsic membrane properties<br />

Support: NIH RR-015497<br />

NIH NS-35180<br />

NIH MH-067564<br />

NIH MH-074866

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!