[Abstract Title]. - Society for Neuroscience

gated HVA calcium current in our dynamic clamp circuit. As previously established, we found
that in the presence of the SK channel blocker apamin (100nM), DCN neurons exhibited high
frequency bursting behavior brought on by elimination of the sAHP. When simulated synaptic
conductance patterns were applied before and after the addition of apamin, we found that
synaptic responses remained precisely locked to specific input events in both conditions.
However, responses to small depolarizing synaptic events were reduced after apamin application,
whereas responses to larger depolarizing events were increased. In addition, the responses to
larger depolarizing event consisted of short high frequency bursts rather than a single spike. The
application of artificial SK conductance could restore the regular spontaneous firing pattern as
well as a synaptic response function closely resembling that seen before apamin application. The
short bursts to large synaptic events seen during apamin application were also restored to single
spike responses. These data suggest that the SK currents play a role in defining the sensitivity
and gain function of synaptic responses in DCN neurons. Modulation of the SK channels or the
calcium dynamics triggering SK activation could thus allow for tuning of DCN responsiveness to
synaptic input.
Disclosures: S.S. Feng , None; T. Sangrey, None; D. Jaeger, None.
Poster
237. Synaptic Integration II
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 237.17/D42
Topic: B.07.c. Synaptic integration
Support: NSERC
FRSQ
Title: Impact of altered chloride extrusion capacity on cell excitability
Authors: N. DOYON 1 , H. KROGER 2 , S. A. PRESCOTT 3 , *Y. DE KONINCK 4 ;
1 Cell. Neurobio., 2 Laval Univ., Quebec, QC, Canada; 3 Neurobio., Univ. of Pittsburgh,
Pittsburgh, PA; 4 Cell. Neurobiol, Laval Univ. / CRULRG, Quebec, Canada
Abstract: Hyperpolarizing inhibition mediated by GABAA receptors is highly dependent on Cl
homeostasis since its efficacy depends on the neuron‟s ability to maintain a strong
transmembrane Cl gradient. A decrease in Cl extrusion capacity (e.g., resulting from diminished
KCC2 activity or expression) can cause a change in the Cl gradient with consequences on the
excitability of the cell (Prescott et al., Mol. Pain, 2007). In addition, a collapse in Cl gradient can