title: Glycinergic inhibition creates a form of auditory spectral integration in nuclei of the lateral lemniscus.
abstract: For analyses of complex sounds, many neurons integrate information across different spectral elements via suppressive effects that are distant from the neurons' excitatory tuning. In the mustached bat, suppression evoked by sounds within the first sonar harmonic (23-30 kHz) or in the subsonar band (<23 kHz) alters responsiveness to the higher best frequencies of many neurons. This study examined features and mechanisms associated with low-frequency (LF) suppression among neurons of the lateral lemniscal nuclei (NLL). We obtained extracellular recordings from neurons in the intermediate and ventral nuclei of the lateral lemniscus, observing different forms of LF suppression related to the two above-cited frequency bands. To understand the mechanisms underlying this suppression in NLL neurons, we examined the roles of glycinergic and GABAergic input through local microiontophoretic application of strychnine, an antagonist to glycine receptors (GlyRs), or bicuculline, an antagonist to gamma-aminobutyric acid type A receptors (GABA(A)Rs). With blockade of GABA(A)Rs, neurons showed an increase in firing rate to best frequency (BF) and/or LF tones but retained LF suppression of BF sounds. For neurons that displayed LF suppression tuned to 23-30 kHz, the suppression was eliminated or nearly eliminated by GlyR blockade. In contrast, GABA(A)R blockade did not eliminate nor had any consistent effect on suppression tuned to these frequencies. We conclude that LF suppression tuned in the 23- to 30-kHz range results from neuronal inhibition within the NLL via glycinergic inputs. For neurons displaying suppression tuned <23 kHz, neither GlyR nor GABAR blockade altered LF suppression. We conclude that such suppression originates at a lower auditory level, perhaps a result of cochlear mechanisms. These findings demonstrate that neuronal interactions within NLL create a particular form of LF suppression that contributes to the analysis of complex acoustic signals.
authors.affiliation: Department of Anatomy and Neurobiology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272, USA.
authors.forename: Diana Coomes
authors.initials: DC
authors.lastname: Peterson
authors.forename: Kiran
authors.initials: K
authors.lastname: Nataraj
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Wenstrup
mesh_terms: D000161:Acoustic Stimulation; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001307:Auditory Perception / Q000187:drug effects / Q000502:physiology*; D001640:Bicuculline / Q000494:pharmacology; D001933:Brain Stem / Q000187:drug effects / Q000502:physiology*; D002685:Chiroptera; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D005998:Glycine / Q000502:physiology*; D018684:Glycine Agents / Q000494:pharmacology; D008839:Microelectrodes; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011963:Receptors, GABA-A / Q000378:metabolism; D018009:Receptors, Glycine / Q000037:antagonists & inhibitors / Q000378:metabolism; D013331:Strychnine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D018684:Glycine Agents; D011963:Receptors, GABA-A; D018009:Receptors, Glycine; D005680:gamma-Aminobutyric Acid; D013331:Strychnine; D005998:Glycine; D001640:Bicuculline