title: Lateral olivocochlear (LOC) neurons of the mouse LSO receive excitatory and inhibitory synaptic inputs with slower kinetics than LSO principal neurons.
abstract: We examined membrane properties and synaptic responses of neurons in the mouse lateral superior olivary nucleus (LSO). Two clear populations were identified consistent with: principal neurons which are involved in detecting interaural intensity differences (IIDs) and efferent neurons of the lateral olivocochlear (LOC) system which project to the cochlea. Principal neurons fired a short latency action potential (AP) often followed by an AP train during maintained depolarization. They possessed sustained outward K(+) currents, with little or no transient K(+) current (I(A)) and a prominent hyperpolarization-activated non-specific cation conductance, I(H). On depolarization, LOC neurons exhibited a characteristic delay to the first AP. These neurons possessed a prominent transient outward current I(A), but had no I(H). Both LOC and principal neurons received glutamatergic and glycinergic synaptic inputs. LOC synaptic responses decayed more slowly than those of principal neurons; the mean decay time constant of AMPA receptor-mediated EPSCs was around 1 ms in principal neurons and 4 ms in LOC neurons. Decay time constants for glycinergic IPSCs were around 5 ms in principal neurons and 10 ms in LOC neurons. We conclude that principal cells receive fast synaptic responses appropriate for integration of IID inputs, while the LOC cells possess excitatory and inhibitory receptors with much slower kinetics.
authors.affiliation: Department of Cell Physiology & Pharmacology, University of Leicester, Leicester, UK.
authors.forename: Jessica C
authors.initials: JC
authors.lastname: Sterenborg
authors.forename: Nadia
authors.initials: N
authors.lastname: Pilati
authors.forename: Craig J
authors.initials: CJ
authors.lastname: Sheridan
authors.forename: Osvaldo D
authors.initials: OD
authors.lastname: Uchitel
authors.forename: Ian D
authors.initials: ID
authors.lastname: Forsythe
authors.forename: Margaret
authors.initials: M
authors.lastname: Barnes-Davies
mesh_terms: D000818:Animals; D001306:Auditory Pathways / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D003056:Cochlear Nerve / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D054815:Cyclic Nucleotide-Gated Cation Channels / Q000378:metabolism; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D018698:Glutamic Acid / Q000378:metabolism; D005998:Glycine / Q000378:metabolism; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D066298:In Vitro Techniques; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects; D007700:Kinetics; D051379:Mice; D008808:Mice, Inbred CBA; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009476:Neurons, Efferent / Q000502:physiology; D018377:Neurotransmitter Agents / Q000494:pharmacology; D009847:Olivary Nucleus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D011930:Reaction Time
chemical_list: D054815:Cyclic Nucleotide-Gated Cation Channels; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D018377:Neurotransmitter Agents; D015221:Potassium Channels; D018698:Glutamic Acid; D011188:Potassium; D005998:Glycine