Membrane properties that shape the auditory code in three nuclei of the central nervous system.
OBJECTIVE
We investigated if auditory neurons have an intrinsic ability to radically transform auditory signals.


METHODS
We surveyed membrane properties that control coding by neurons, identified with intracellular staining or infrared-DIC videomicroscopy, in three stations of the auditory pathway. We used intracellular and patch-clamp techniques in slices, to study the voltage responses to current pulse injections and distinguished voltage-gated conductances with selective blockers.


RESULTS
First order spherical bushy cells in the anteroventral cochlear nucleus responded at a short, stable latency with single spikes, due to a perithreshold interaction of Na+ and Ca2+ conductances. Two K+ conductances suppressed firing after this onset-spike. Second-order principal neurons of the lateral superior olive use unspecified mechanisms to secure stable onset latencies but maintained a very regular tonic firing, resulting in a chopper pattern. Other intrinsic properties induced a marked accommodation in spike rate. When depolarized as during alert states, neurons in the medial geniculate body (MGB) of the thalamus fired with variable latencies in a tonic mode. At negative resting potentials characteristic of sleep states, they responded at the onset of a depolarization and the offset of a hyperpolarization with phasic bursts due to a transient low threshold Ca2+ current. In the phasic, but not tonic mode, MGB neurons produced high-threshold Ca2+ spikes that may couple signal transmission to the neuron's metabolism. The three neuron types exhibit analogue computing abilities that transform the same input into entirely different output patterns. Isoflurane anaesthesia induces a current shunt in MGB neurons, radically changing the properties and preventing normal responses. Thus, thalamocortical auditory codes are compromised under anaesthesia.


CONCLUSIONS
At all investigated stations of the auditory pathway, input signals are transformed by activation of voltage-controlled conductances and other intrinsic membrane properties.
Schwarz
D W
DW
Tennigkeit
F
F
Adam
T
T
Finlayson
P
P
Puil
E
E
D018685:Anesthetics, Inhalation / Q000494:pharmacology; D000818:Animals; D001306:Auditory Pathways / Q000502:physiology*; D015220:Calcium Channels / Q000502:physiology; D020013:Calcium Signaling / Q000502:physiology; D017626:Cochlear Nucleus / Q000502:physiology*; D004396:Coloring Agents; D005071:Evoked Potentials / Q000502:physiology; D005829:Geniculate Bodies / Q000187:drug effects / Q000502:physiology*; D005849:Gerbillinae; D015640:Ion Channel Gating / Q000502:physiology; D007530:Isoflurane / Q000494:pharmacology; D008526:Medulla Oblongata / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D018715:Microscopy, Video; D009431:Neural Conduction / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000502:physiology; D051381:Rats; D011930:Reaction Time; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D012890:Sleep / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology
D018685:Anesthetics, Inhalation; D015220:Calcium Channels; D004396:Coloring Agents; D015221:Potassium Channels; D015222:Sodium Channels; D007530:Isoflurane