Expression of GABA sub(B) receptor in the avian auditory brainstem: Ontogeny, afferent deprivation, and ultrastructure

• Published in: Journal of comparative neurology (1911) Vol. 489; no. 1; pp. 11 - 22
• Main Authors: Burger, RMichael, Pfeiffer, Joshua D, Westrum, Lesnick E, Bernard, Amy, Rubel, Edwin W
• Format: Journal Article
• Language: English
• Published: 01-01-2005
• ISSN: 0021-9967; 1096-9861
• DOI: 10.1002/cne.20607

Nucleus magnocellularis (NM), nucleus angularis (NA), and nucleus laminaris (NL), second- and third-order auditory neurons in the avian brainstem, receive GABAergic input primarily from the superior olivary nucleus (SON). Previous studies have demonstrated that both GABA sub(A) and GABA sub(B) receptors (GABA sub(B)Rs) influence physiological properties of NM neurons. We characterized the distribution of GABA sub(B)R expression in these nuclei during development and after deafferentation of the excitatory auditory nerve (nVIII) inputs. We used a polyclonal antibody raised against rat GABA sub(B)Rs in the auditory brainstem during developmental periods that are thought to precede and include synaptogenesis of GABAergic inputs. As early as embryonic day (E)14, dense labeling is observed in NA, NM, NL, and SON. At earlier ages immunoreactivity is present in somas as diffuse staining with few puncta. By E21, when the structure and function of the auditory nuclei are known to be mature, GABA sub(B) immunoreactivity is characterized by dense punctate labeling in NM, NL, and a subset of NA neurons, but label is sparse in the SON. Removal of the cochlea and nVIII neurons in posthatch chicks resulted in only a small decrease in immunoreactivity after survival times of 14 or 28 days, suggesting that a major proportion of GABA sub(B)Rs may be expressed postsynaptically or on GABAergic terminals. We confirmed this interpretation with immunogold TEM, where expression at postsynaptic membrane sites is clearly observed. The characterization of GABA sub(B)R distribution enriches our understanding of the full complement of inhibitory influences on central auditory processing in this well-studied neuronal circuit. J. Comp. Neurol. 489:11-22, 2005.