An increased N-methyl-D-aspartate receptor conductance is associated with intrinsic bursting behavior
© Martell et al; licensee BioMed Central Ltd. 2007
Published: 6 July 2007
Seizure activity is often accompanied by an increase in the number of intrinsically bursting neurons . The N-methyl-D-aspartate (NMDA) receptor, a channel known to be involved in many seizure models, represents one mechanism by which intrinsic bursting may arise, since 30–50% of these channels are bound at ambient concentrations of glutamate. In adult rat, intrinsic bursting has been induced in pyramidal neurons of the prefrontal cortex (PFC) through a combination of NMDA and dopamine type 1 (D1) receptor agonist . Here we used the in vitro mouse neocortex and a computational model to further investigate the basis for bursting in the context of epileptiform activity.
The NMDA receptor is associated with production of intrinsic bursting behavior in mouse cortical pyramidal neurons, and, together with a calcium-activated K conductance, is sufficient to cause spontaneous bursting in a computational model of pyramidal neuron. These and previous results indicate that the NMDA receptor has the potential to drive the bursting behavior that characterizes seizures.
This work was supported in part by the Falk Foundation and the Linn family.
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