Formula omitted] receptors may mediate ipsilateral excitation at lateral superior olivary synapses

Abstract

Principal cells of the lateral superior olivary nucleus (LSO) are thought to receive a direct excitatory input from spherical bushy cells located in the ipsilateral ventral cochlear nucleus (VCN) and an indirect input from the contralateral VCN globular bushy cells via a secure synapse in the medial nucleus of the trapezoid body (MNTB). MNTB bushy cells project to the somata and proximal dendrites of LSO principal cells. LSO neurons display phasic ‘chopper’ temporal response patterns to ipsilateral tone-burst stimuli at characteristic frequency (CF), while binaural stimuli suppress this ipsilaterally evoked activity. This suppression is sensitive to interaural differences in intensity, phase and time, suggesting a role for these neurons in the localization of sound in space. In the present study, the nature of the neurotransmitter mediating fast ipsilateral excitation of LSO neurons was examined using iontophoretic application of excitant amino acid (EAA) agonists and antagonists. N- methyl- d-aspartate (NMDA) and quisqualate (QUIS) were used as agonists, while the selective NMDA receptor antagonists d. l-2-amino-5-phosphonovaleric acid (APV), and the non-selective receptor EAA antagonist cis-2,3-piperidine-dicarboxylic acid (PDA) were used to study ipsilaterally evoked neuronal responses. In 3 additional experiments the selective non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) replaced PDA. Ipsilateral, tone-evoked and spontaneous activities were generally enhanced by EAA agonists while partial blockade of tone-evoked, ipsilateral excitation was observed with EAA antagonists. Both PDA and DNQX more effectively blocked ipsilateral tone-evoked excitations and spontaneous activity than did the NMDA-receptor antagopnist, APV, QUIS application enhanced both spontaneous and tone-evoked responses to a greater extent than did NMDA application. These findings indicate that EAA receptors are present on LSO principal cells and suggest that if an EAA mediates fast ipsilateral excitatory responses in LSO it is unlikely to utilize slow NMDA receptors but is acting through non-NMDA receptors of the QUIS or kainate receptors types.