GABA-A Receptor-Induced Changes in Firing Pattern Mediated by Ionotropic Receptors in Mitral Cells of the Main Olfactory Bulb


Meeting Abstract

P3.183  Monday, Jan. 6 15:30  GABA-A Receptor-Induced Changes in Firing Pattern Mediated by Ionotropic Receptors in Mitral Cells of the Main Olfactory Bulb WANG, Z.-J.; HEINBOCKEL, T.*; Howard University, Washington, DC; Howard University, Washington, DC theinbockel@howard.edu

In the main olfactory bulb, we observed that one type of output neuron, the mitral cell (MC), exhibits two modes of integrative behavior: long-lasting depolarizations with a burst of action potentials and regular firing of action potentials. We hypothesize that these integrative behaviors distinguish two physiologically distinct mitral cell populations. We used whole-cell patch-clamp recording in mouse brain slices and tested if blockade of GABA-A receptors modified the firing pattern of MCs. In MCs with spontaneous regular firing, the GABA-A receptor antagonist gabazine evoked burst firing in ~57% of these cells. In MCs with spontaneous bursting, gabazine greatly enhanced the strength of bursting. Gabazine-evoked burst firing was reversed by blocking ionotropic glutamate receptors with CNQX and APV, indicating that the transformation of firing pattern was mediated by ionotropic glutamate receptors. In voltage-clamp recording, the burst firing of MCs was expressed as a rhythmic long-lasting depolarizing current (LLC). Both spontaneous LLCs and gabazine-evoked LLCs were blocked by CNQX plus D-AP5, indicating that they share the same mechanism of LLC initiation. This suggests that inhibition of GABA-A receptors was involved in the transformation of firing pattern via activation of ionotropic glutamate receptors. Our results suggest the existence of two MC subtypes: one subtype might be involved in dendrodendritic transmission between MCs in a single glomerulus, and, therefore, exhibits bursting or can be transformed from regular to burst firing. Another MC subtype generates regular firing, possibly due to the lack of dendrodendritic interactions. Support: Whitehall Foundation, U.S.-PHS grants GM08016, MD007597.

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