Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation.

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation. Abstract Text:

Leqin Yan,Sanoj K Suneja,Steven J Potashner,

Glycinergic synaptic inhibition is part of acoustic information processing in brain stem auditory pathways and contributes to the regulation of neuronal excitation. We found previously that unilateral cochlear ablation (UCA) in young adult guinea pigs decreased [3H]strychnine binding activity in several brain stem auditory nuclei. This study determined if the UCA-induced deficit could be regulated by protein kinase C (PKC), protein kinase A (PKA) or Ca2+/calmodulin-dependent protein kinase II (CaMKII). The specific binding of [3H]strychnine was measured in slices of the dorsal (DCN), posteroventral (PVCN) and anteroventral (AVCN) cochlear nucleus (CN), the lateral (LSO) and medial (MSO) superior olive, and the inferior colliculus (IC) 145 days after UCA. Tissues from age-matched unlesioned animals served as controls. UCA induced deficits in specific binding in the AVCN, PVCN, and LSO on the ablated side and in the MSO bilaterally. These deficits were reversed by 3 microM phorbol 1,2-dibutyrate, a PKC activator, or 0.2 mM dibutyryl-cAMP, a PKA activator. However, 50 nM Ro31-8220, a PKC inhibitor, and 2 microM H-89, a PKA inhibitor, had no effect in unlesioned controls and after UCA. In contrast, 4 microM KN-93, a CaMKII inhibitor, relieved or reversed the UCA-induced binding deficits and elevated binding in the IC. These findings suggest that a UCA-induced down-regulation of glycine receptor synthesis may have occurred via reduced phosphorylation of proteins that control receptor synthesis; this effect was reversed by diminishing CaMKII activity or increasing PKC and PKA activity.

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation. Publishing Authors By Initials

L Yan,SK Suneja,SJ Potashner,

For similar tritium research abstracts see: tritium research

PUBMED ID PMID:

MEDLINE DATE:

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Brain research

VOLUME: 1135

Page Numbers: 102-6

Journal Abbreviation: Brain Res.

ISSN: 0006-8993

DAY: 2

MONTH: 01

YEAR: 2007

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 45503

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation. Keywords Mesh Terms:

KEYWORDS: Tritium

MESH TERMS: metabolism

Chemical & Substance for Abstract: Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation. Information

Substance Name: Protein Kinases

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation.

AFFILIATION: Department of Neuroscience, University of Connecticut Health Center, Farmington, CT 06030-3401, USA.

Country: Netherlands

AGENCY: United States NIDCD

GRANT: R01-DC00199

ACRONYM: DC

MEDLINETA: Brain Res

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation Related Publications

• Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation.