| Literature DB >> 2918077 |
R L Saint Marie1, E M Ostapoff, D K Morest, R J Wenthold.
Abstract
Neurons in the lateral superior olive are optimally excited by stimulation of the ipsilateral ear, as are those in the inferior colliculus by stimulation of the contralateral ear. This reversal of ear dominance may result, in part, from distinct crossed excitatory and uncrossed inhibitory pathways ascending from the lateral superior olive. To explore this possibility, immunoreactivity for two putative inhibitory neurotransmitters, glycine and GABA, was examined in projection neurons that retrogradely transported horseradish peroxidase from the cat inferior colliculus. The results suggest that the projection from the lateral superior olive can be segregated, immunocytochemically, into three components: 1) a crossed, glycine-negative (-) projection; 2) an uncrossed, glycine-positive (+) projection; and 3) an uncrossed, glycine(-) projection. Additional evidence suggests that the terminal fields of the two uncrossed projections may distribute differently within the inferior colliculus. Glycine(+) or glycine(-) projection neurons, crossed or uncrossed, do not differ in the size, shape, or location of their somata. However, most glycine(-) neurons are heavily encrusted with glycine(+) endings; glycine(+) neurons have 40-60% fewer of these endings. Glycine(-) neurons located in the lateral limb have fewer glycine (+) perisomatic endings than those in the medial limb. Few projection neurons are GABA(+), and GABA(+) perisomatic endings are rare in the lateral superior olive. Thus, there is a heavy uncrossed projection from the cat lateral superior olive to the inferior colliculus that may be glycinergic and inhibitory. Furthermore, there is a bilateral projection that is not glycinergic or GABAergic, which may be excitatory. The potential contribution of these pathways to contralateral ear dominance in the inferior colliculus is discussed.Entities:
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Year: 1989 PMID: 2918077 DOI: 10.1002/cne.902790305
Source DB: PubMed Journal: J Comp Neurol ISSN: 0021-9967 Impact factor: 3.215