Using microdissection and quantitative microassay, choline acetyltransferase (ChAT) activity was mapped in the cochlear nucleus (CN) and in the source nuclei of the olivocochlear bundle, the lateral superior olive and ventral nucleus of the trapezoid body. In control rats, gradients of ChAT activity
Effects of cochlear ablation on muscarinic acetylcholine receptor binding in the rat cochlear nucleus
β Scribed by Yong-Ming Jin; Donald A. Godfrey
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 332 KB
- Volume
- 83
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
β¦ Synopsis
Cholinergic synapses in the cochlear nucleus (CN) have been reported to modulate spontaneous activity via muscarinic acetylcholine receptors. In this study, muscarinic receptor binding was measured as specific binding of 1-[N-methyl-(3)H]scopolamine in CN regions of control rats and 7 days, 1 month, and 2 months after unilateral cochlear ablation. In control rats, the strongest binding was found in granular regions, followed in order by fusiform soma, molecular, and deep layers of the dorsal cochlear nucleus (DCN), with much lower binding in the anteroventral CN (AVCN) and posteroventral CN (PVCN). After unilateral cochlear ablation, binding in the AVCN, PVCN, and their associated granular regions on the lesion side became progressively greater than on the control side through 2 months after lesion. A significant asymmetry, with binding higher on the lesion side, was also found in the DCN fusiform soma layer at 7 days, and there and in the DCN deep layer at 1 and 2 months after lesion. There was also evidence of increased binding on the control side in most CN regions. By contrast, binding in the ipsilateral facial nucleus decreased, compared with the control side, by 7 days after the lesion and showed some recovery toward symmetry by 2 months after lesion, and there was no evidence for contralateral changes. These muscarinic receptor binding changes reflect receptor plasticity after loss of auditory nerve innervation. Such plasticity may underlie some of the central auditory functional changes that occur following peripheral lesions, such as tinnitus and hyperacusis.
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