Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1931122 | Biochemical and Biophysical Research Communications | 2011 | 6 Pages |
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.
Research highlights► Glutamate co-transmission is enhanced in kanamycin-treated rats. ► VGLUT3 expression is increased in kanamycin-treated rats. ► GlyR expression is decreased in kanamycin-treated rats. ► GlyR, VGLUT3 expression patterns are asymmetric in unilaterally cochlear ablated rat.