AMPA receptor binding in adult guinea pig brain stem auditory nuclei afterunilateral cochlear ablation

This study determined if an asymmetric hearing loss, due to unilateral coch lear ablation, could induce the regulation of intracellular AMPA receptors in brain stem auditory nuclei. In young adult guinea pigs, the high-affinit y specific binding of [H-3]AMPA was measured in the cochlear nucleus (CN), the superior olivary complex (SOC), and the auditory midbrain at 2-147 post lesion days. After correction for tissue shrinkage, changes in specific bin ding relative to that in age-matched unlesioned controls were interpreted a s altered numbers and/or activity of intracellular AMPA receptors. In the C N, transient elevations and/or deficits in binding were evident in most reg ions, which usually recovered by 147 days. However, persistently deficient binding was evident ipsilaterally in the anterior part of the anteroventral CN (AVCNa). In the SOC, transient elevations in binding were evident at 2 days in the medial limb of the lateral superior olive (LSOmed) and the medi al superior olive. Between 7 and 147 days, most SOC nuclei exhibited transi ent, temporally synchronized postlesion deficits in binding. However, late in the survival period, deficits persisted ipsilaterally in the LSOmed and the lateral (LSOIat) limb of the lateral superior olive. In the midbrain, t ransient elevations and/or deficits in binding were evident in the dorsal n ucleus of the lateral lemniscus as well as in the central and dorsal nucleu s of the inferior colliculus. A persistent deficit was evident in the inter mediate nucleus of the lateral lemniscus. The findings implied that auditor y neurons contain regulatory mechanisms that control the numbers and/or act ivity of intracellular AMPA receptors. Regulation was induced by cochlear n erve destruction and probably by changes in the excitation of glutamatergic neurons. Many of the regulatory changes were transient, except in the ipsi lateral AVCNa and LSO, where postlesion downregulations were persistent. Th e downregulation in the ipsilateral AVCNa was probably induced directly by the loss of cochlear nerve endings. However, other regulatory changes may h ave been induced by signals carried on pathways emerging from the ipsilater al CN and on centrifugal auditory pathways. (C) 2000 Academic Press.