AI Article Synopsis
- The study examined how glutamate co-transmission at synapses between the medial nucleus of the trapezoid body (MNTB) and lateral superior olive (LSO) is affected by cochlear damage in developing rats treated with kanamycin.
- Rats treated with kanamycin showed cochlear hair cell damage and increased glutamatergic activity in postsynaptic currents, indicating a disruption in normal auditory processing.
- The findings suggest that glutamate co-transmission relies on functional cochlear structures, with enhanced activity observed in damaged conditions, indicating a potential compensatory mechanism.
Article Abstract
Cochlear dependency of glutamate co-transmission at the medial nucleus of the trapezoid body (MNTB)--the lateral superior olive (LSO) synapses was investigated using developing rats treated with high dose kanamycin. Rats were treated with kanamycin from postnatal day (P) 3 to P8. A scanning electron microscopic study on P9 demonstrated partial cochlear hair cell damage. A whole cell voltage clamp experiment demonstrated the increased glutamatergic portion of postsynaptic currents (PSCs) elicited by MNTB stimulation in P9-P11 kanamycin-treated rats. The enhanced VGLUT3 immunoreactivities (IRs) in kanamycin-treated rats and asymmetric VGLUT3 IRs in the LSO of unilaterally cochlear ablated rats supported the electrophysiologic data. Taken together, it is concluded that glutamate co-transmission is cochlear-dependent and enhanced glutamate co-transmission in kanamycin-treated rats is induced by partial cochlear damage.
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| http://dx.doi.org/10.1016/j.bbrc.2010.12.129 | DOI Listing |
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