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1 Anatomy and Neurobiology, University of Tennessee, Memphis, Tennessee, USA
2 Anatomy and Neurobiology, University of Tennessee, Memphis, Tennessee, USA; Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
* To whom correspondence should be addressed. E-mail: mennis{at}utmem.edu.
The group I metabotropic glutamate receptor (mGluR) subtype, mGluR1, is highly expressed on the apical dendrites of olfactory bulb mitral cells, and thus may be activated by glutamate released from olfactory nerve (ON) terminals. Previous studies have shown that mGluR1 agonists directly excite mitral cells. In the present study, we investigated the involvement of mGluR1 in ON-evoked responses in mitral cells in rat olfactory bulb slices using patch-clamp electrophysiology. In voltage clamp recordings, the average EPSC evoked by single ON shocks or brief trains of ON stimulation (6 pulses at 50 Hz) in normal physiological conditions were not significantly affected by the non-selective mGluR antagonist LY341495 (50 - 100 µM) or the mGluR1 specific antagonist LY367385 (100 µM); ON-evoked responses were attenuated, however, in a subset (36%) of cells. In the presence of blockers of ionotropic glutamate and GABA receptors, application of the glutamate uptake inhibitors THA (300 µM) and TBOA (100 µM) revealed large amplitude, long duration responses to ON stimulation, while responses elicited by antidromic activation of mitral/tufted cells were unaffected. The magnitude of the ON-evoked responses elicited in the presence of THA-TBOA were dependent on stimulation intensity and frequency, and were maximal during high frequency (50 Hz) bursts of ON spikes, which occur during odor stimulation. ON-evoked responses elicited in the presence of THA-TBOA were significantly reduced or completely blocked by LY341495 or LY367385 (100 µM). These results demonstrate that glutamate transporters tightly regulate access of synaptically-evoked glutamate from ON terminals to postsynaptic mGluR1s on mitral cell apical dendrites. Taken together with other findings, the present results suggest that mGluR1s may not play a major role in phasic responses to ON input, but instead may play an important role in shaping slow oscillatory activity in mitral cells and/or activity-dependent regulation of plasticity at ON-mitral cell synapses.
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