Axonal sprouting in the dorsal cochlear nucleus affects gapprepulse inhibition following noise exposure.
Int J Mol Med
; 44(4): 1473-1483, 2019 Oct.
Article
em En
| MEDLINE
| ID: mdl-31432095
ABSTRACT
One of the primary theories of the pathogenesis of tinnitus involves maladaptive auditorysomatosensory plasticity in the dorsal cochlear nucleus (DCN), which is assumed to be due to axonal sprouting. Although a disrupted balance between auditory and somatosensory inputs may occur following hearing damage and may induce tinnitus, examination of this phenomenon employed a model of hearing damage that does not account for the causal relationship between these changes and tinnitus. The present study aimed to investigate changes in auditorysomatosensory innervation and the role that axonal sprouting serves in this process by comparing results between animals with and without tinnitus. Rats were exposed to a noiseinducing temporary threshold shift and were subsequently divided into tinnitus and nontinnitus groups based on the results of gap prepulse inhibition of the acoustic startle reflex. DCNs were collected from rats divided into three subgroups according to the number of weeks (1, 2 or 3) following noise exposure, and the protein levels of vesicular glutamate transporter 1 (VGLUT1), which is associated with auditory input to the DCN, and VGLUT2, which is in turn primarily associated with somatosensory inputs, were assessed. In addition, factors related to axonal sprouting, including growthassociated protein 43 (GAP43), postsynaptic density protein 95, synaptophysin, αthalassemia/mental retardation syndrome Xlinked homolog (ATRX), growth differentiation factor 10 (GDF10), and leucinerich repeat and immunoglobulin domaincontaining 1, were measured by western blot analyses. Compared to the nontinnitus group, the tinnitus group exhibited a significant decrease in VGLUT1 at 1 week and a significant increase in VGLUT2 at 3 weeks postexposure. In addition, rats in the tinnitus group exhibited significant increases in GAP43 and GDF10 protein expression levels in their DCN at 3 weeks following noise exposure. Results from the present study provided further evidence that changes in the neural input distribution to the DCN may cause tinnitus and that axonal sprouting underlies these alterations.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Estimulação Acústica
/
Núcleo Coclear
/
Inibição Pré-Pulso
/
Crescimento Neuronal
/
Ruído
Tipo de estudo:
Diagnostic_studies
/
Etiology_studies
/
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article