7e Colloque de la Société des neurosciences

May 18-20, 2005, Lille (France)

For lectures and symposia, time indicates the beginning of the session.
For posters, authors are expected to be present at the time indicated.

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First author: Argence, Meritxell (poster)

Poster C-6 - 18/05/05, 14:00 - Lille Métropole I
Session C - Molecular and Cellular Neurobiology I
Ref.: 7e Colloque de la Société des neurosciences, Lille 2005, C.6.

Author(s) Argence M. , Saez I. , Sassu R. , Vassias I. , Vidal P. P. & De Waele C.
Addresse(s) LNRS, Paris, France.
Title Modulation of inhibitory synaptic transmission in the inferior colliculus of unilateral cochleectomized rats.
Text In this study, we investigated whether inhibitory synaptic transmission mediated through glycinergic receptor (GLYR) and GAD, the synthetizing enzyme of GABA, was modulated in the inferior colliculus (CIC) following unilateral cochleectomy. In situ hybridization and immunohistofluorescence experiments were performed in shamed and lesioned rats at various times following the lesion: 1 to 150 days. Our data showed that unilaterally cochleectomy induced a strong Gly alpha 1 (50%) and moderate GAD (25%) mRNA decreases in the contralateral CIC. It began at day post-lesion 3, peaked on day 8, and remained unchanged until day post-lesion 150. This mRNA decrease was associated with a decrease of GLY alpha 1 and GAD immunofluorescent signal intensity. A bilateral simultaneous or sequential cochlectomy induced a bilateral diminution of GAD mRNA but no difference could be detected for Gly alpha 1 between the CIC of lesioned and controls rats at any times following the lesion. Finally, no modulation could be detected for any of the other probes used recognizing either GLYR beta subunit, gephyrin, GluR2, R3 subunits of AMPA receptors, NR1 and NR2A transcripts of NMDA receptors and the calcium dependent potassium channels (SK1-3). Thus, unilateral cochlear removal specifically decreased and for a long period of time the alpha 1 subunit of GLYR and GAD in the deafferented CIC. We hypothesized that these neurochemical changes could be at the origin of the tinnitus frequently encountered in patients who suffered from a sudden hearing loss.