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Publication : GABAergic inhibition at dendrodendritic synapses tunes gamma oscillations in the olfactory bulb.

First Author  Lagier S Year  2007
Journal  Proc Natl Acad Sci U S A Volume  104
Issue  17 Pages  7259-64
PubMed ID  17428916 Mgi Jnum  J:120906
Mgi Id  MGI:3708228 Doi  10.1073/pnas.0701846104
Citation  Lagier S, et al. (2007) GABAergic inhibition at dendrodendritic synapses tunes {gamma} oscillations in the olfactory bulb. Proc Natl Acad Sci U S A 104(17):7259-64
abstractText  In the olfactory bulb (OB), odorants induce oscillations in the gamma range (20-80 Hz) that play an important role in the processing of sensory information. Synaptic transmission between dendrites is a major contributor to this processing. Glutamate released from mitral cell dendrites excites the dendrites of granule cells, which in turn mediate GABAergic inhibition back onto mitral cells. Although this reciprocal synapse is thought to be a key element supporting oscillatory activity, the mechanisms by which dendrodendritic inhibition induces and maintains gamma oscillations remain unknown. Here, we assessed the role of the dendrodendritic inhibition, using mice lacking the GABA(A) receptor alpha1-subunit, which is specifically expressed in mitral cells but not in granule cells. The spontaneous inhibitory postsynaptic current frequency in these mutants was low and was consistent with the reduction of GABA(A) receptor clusters detected by immunohistochemistry. The remaining GABA(A) receptors in mitral cells contained the alpha3-subunit and supported slower decaying currents of unchanged amplitude. Overall, inhibitory-mediated interactions between mitral cells were smaller and slower in mutant than in WT mice, although the strength of sensory afferent inputs remained unchanged. Consequently, both experimental and theoretical approaches revealed slower gamma oscillations in the OB network of mutant mice. We conclude, therefore, that fast oscillations in the OB circuit are strongly constrained by the precise location, subunit composition and kinetics of GABA(A) receptors expressed in mitral cells.
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