Maintenance of pharmacologically-immature glutamate receptors by aberrant synapses in the chick cochlear nucleus.

Surgical destruction of the otocyst in chick embryos prevents formation of the *** ear, abolishes normal cochlear input to the cochlear nucleus (nucleus magnocellularis, NM) and results in axons from the contralateral NM forming (in addition to their normal bilateral endings in nucleus laminaris, NL) a novel and functional aberrant projection to the deafferented NM. We studied the pharmacology of synaptic transmission at aberrant synapses in an in vitro preparation of the brainstem in chick embryos and hatchlings. Transmission at the aberrant synapses (as with cochlear nerve synapses in NM and NM synapses in NL) is blocked by the quinoxalinedione antagonists CNQX and NBQX, confirming the presence of excitatory amino acid receptors of the non-NMDA subtype. At cochlear nerve synapses in NM, the antagonist potency of NBQX normally decreases rapidly after embryonic day (E)18 (IC50 = 0.69 +/- 0.06 microM, mean +/- S.E.M.), reaching an asymptotic value by E21 (IC50 = 2.7 +/- 0.4 microM) that is maintained at least through posthatching day (P)14 (IC50 = 3.6 +/- 0.3 microM). In the case of the aberrant endings, the potency of NBQX remained (from E21 [IC50 = 0.6 +/- 0.1 microM] through at least P14[IC50 = 0.5 +/- 0.1 microM]) at levels that are statistically indistinguishable from the E18 value for normal cochlear nerve synapses.(ABSTRACT TRUNCATED AT 250 WORDS)