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Publication : Null mutations in EphB receptors decrease sharpness of frequency tuning in primary auditory cortex.

First Author  Intskirveli I Year  2011
Journal  PLoS One Volume  6
Issue  10 Pages  e26192
PubMed ID  22022561 Mgi Jnum  J:179580
Mgi Id  MGI:5302728 Doi  10.1371/journal.pone.0026192
Citation  Intskirveli I, et al. (2011) Null mutations in EphB receptors decrease sharpness of frequency tuning in primary auditory cortex. PLoS One 6(10):e26192
abstractText  Primary auditory cortex (A1) exhibits a tonotopic representation of characteristic frequency (CF). The receptive field properties of A1 neurons emerge from a combination of thalamic inputs and intracortical connections. However, the mechanisms that guide growth of these inputs during development and shape receptive field properties remain largely unknown. We previously showed that Eph family proteins help establish tonotopy in the auditory brainstem. Moreover, other studies have shown that these proteins shape topography in visual and somatosensory cortices. Here, we examined the contribution of Eph proteins to cortical organization of CF, response thresholds and sharpness of frequency tuning. We examined mice with null mutations in EphB2 and EphB3, as these mice show significant changes in auditory brainstem connectivity. We mapped A1 using local field potential recordings in adult EphB2(-/-);EphB3(-/-) and EphB3(-/-) mice, and in a central A1 location inserted a 16-channel probe to measure tone-evoked current-source density (CSD) profiles. Based on the shortest-latency current sink in the middle layers, which reflects putative thalamocortical input, we determined frequency receptive fields and sharpness of tuning (Q(20)) for each recording site. While both mutant mouse lines demonstrated increasing CF values from posterior to anterior A1 similar to wild type mice, we found that the double mutant mice had significantly lower Q(20) values than either EphB3(-/-) mice or wild type mice, indicating broader tuning. In addition, we found that the double mutants had significantly higher CF thresholds and longer onset latency at threshold than mice with wild type EphB2. These results demonstrate that EphB receptors influence auditory cortical responses, and suggest that EphB signaling has multiple functions in auditory system development.
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