title: Glycinergic "inhibition" mediates selective excitatory responses to combinations of sounds.
abstract: In the mustached bat's inferior colliculus (IC), combination-sensitive neurons display time-sensitive facilitatory interactions between inputs tuned to distinct spectral elements in sonar or social vocalizations. Here we compare roles of ionotropic receptors to glutamate (iGluRs), glycine (GlyRs), and GABA (GABA(A)Rs) in facilitatory combination-sensitive interactions. Facilitatory responses to 36 single IC neurons were recorded before, during, and after local application of antagonists to these receptors. The NMDA receptor antagonist CPP [(+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid], alone (n = 14) or combined with AMPA receptor antagonist NBQX (n = 22), significantly reduced or eliminated responses to best frequency (BF) sounds across a broad range of sound levels, but did not eliminate combination-sensitive facilitation. In a subset of neurons, GABA(A)R blockers bicuculline or gabazine were applied in addition to iGluR blockers. GABA(A)R blockers did not "uncover" residual iGluR-mediated excitation, and only rarely eliminated facilitation. In nearly all neurons for which the GlyR antagonist strychnine was applied in addition to iGluR blockade (22 of 23 neurons, with or without GABA(A)R blockade), facilitatory interactions were eliminated. Thus, neither glutamate nor GABA neurotransmission are required for facilitatory combination-sensitive interactions in IC. Instead, facilitation may depend entirely on glycinergic inputs that are presumed to be inhibitory. We propose that glycinergic inputs tuned to two distinct spectral elements in vocal signals each activate postinhibitory rebound excitation. When rebound excitations from two spectral elements coincide, the neuron discharges. Excitation from glutamatergic inputs, tuned to the BF of the neuron, is superimposed onto this facilitatory interaction, presumably mediating responses to a broader range of acoustic signals.
authors.affiliation: Department of Neurobiology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272, USA.
authors.forename: Jason Tait
authors.initials: JT
authors.lastname: Sanchez
authors.forename: Donald
authors.initials: D
authors.lastname: Gans
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Wenstrup
mesh_terms: D000161:Acoustic Stimulation / Q000379:methods; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001306:Auditory Pathways / Q000502:physiology*; D002685:Chiroptera / Q000502:physiology; D004307:Dose-Response Relationship, Radiation; D004347:Drug Interactions; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018682:GABA Agents / Q000494:pharmacology; D005998:Glycine / Q000502:physiology*; D018684:Glycine Agents / Q000494:pharmacology; D007245:Inferior Colliculi / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D007478:Iontophoresis / Q000379:methods; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D010879:Piperazines / Q000494:pharmacology; D018079:Receptors, GABA / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology; D013016:Sound
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018682:GABA Agents; D018684:Glycine Agents; D010879:Piperazines; D018079:Receptors, GABA; D016194:Receptors, N-Methyl-D-Aspartate; C050592:3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid; D005998:Glycine