| First Author | Schraven SP | Year | 2012 |
| Journal | J Assoc Res Otolaryngol | Volume | 13 |
| Issue | 3 | Pages | 323-33 |
| PubMed ID | 22350511 | Mgi Jnum | J:324095 |
| Mgi Id | MGI:6870574 | Doi | 10.1007/s10162-011-0311-2 |
| Citation | Schraven SP, et al. (2012) Altered phenotype of the vestibular organ in GLAST-1 null mice. J Assoc Res Otolaryngol 13(3):323-33 |
| abstractText | Various studies point to a crucial role of the high-affinity sodium-coupled glutamate aspartate transporter GLAST-1 for modulation of excitatory transmission as shown in the retina and the CNS. While 2-4-month-old GLAST-1 null mice did not show any functional vestibular abnormality, we observed profound circling behavior in older (7 months) animals lacking GLAST-1. An unchanged total number of otoferlin-positive vestibular hair cells (VHCs), similar ribbon numbers in VHCs, and an unchanged VGLUT3 expression in type II VHCs were detected in GLAST-1 null compared to wild-type mice. A partial loss of supporting cells and an apparent decline of a voltage-gated channel potassium subunit (KCNQ4) was observed in postsynaptic calyceal afferents contacting type I VHCs, together with a reduction of neurofilament- (NF200-) and vesicular glutamate transporter 1- (VGLUT1-) positive calyces in GLAST-1 null mice. Taken together, GLAST-1 deletion appeared to preferentially affect the maintenance of a normal postsynaptic/neuronal phenotype, evident only with increasing age. |
