Context-dependent synaptic action of glycinergic and GABAergic inputs in the dorsal cochlear nucleus.
Cartwheel cells are prominent interneurons in the dorsal cochlear nucleus (DCN) that bear considerable homology to cerebellar Purkinje cells. They contact other cartwheel cells as well as fusiform cells, the principal cells of the DCN. In fusiform cells, the inhibition from cartwheel cells interacts with excitation mediated by granule cells and auditory nerve fibers, and shapes the output of the DCN in its ascent to the inferior colliculi. With intracellular recordings from anatomically identified cells in slices, synaptic inputs to fusiform and cartwheel cells were analyzed pharmacologically. Shocks to the auditory nerve and granule cell domains evoked glutamatergic, glycinergic, and GABA(A)ergic postsynaptic potentials (PSPs) in both cartwheel and fusiform cells. The temporal patterns of spontaneous and evoked glycinergic PSPs in fusiform and cartwheel cells were similar and mirrored the pattern of firing of cartwheel cells, probably reflecting the anatomical connections between these cell types and supporting the conclusion that cartwheel cells are glycinergic. In fusiform cells, glycinergic and GABA(A)ergic IPSPs evoked with shocks reversed at -68 mV on average. In marked contrast, glycinergic and GABA(A)ergic PSPs in cartwheel cells, as well as responses to exogenous application of 50-100 mM glycine or 100 microns muscimol, were depolarizing. Reversal potentials of PSPs and responses to glycine and muscimol were similar and averaged -52 mV. Glycinergic and GABA(A)ergic PSPs could elicit firing from cartwheel cells at their resting potentials, but could also reduce rapid firing during strong depolarizations. Thus, the action of glycinergic and GABA(A)ergic inputs on cartwheel cells depends on the electrophysiological context in which they occur.
Golding
N L
NL
Department of Neurophysiology, University of Wisconsin, Madison 53706, USA.
Oertel
D
D
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D017626:Cochlear Nucleus / Q000166:cytology / Q000502:physiology*; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000502:physiology; D005998:Glycine / Q000494:pharmacology / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D051379:Mice; D008808:Mice, Inbred CBA; D009118:Muscimol / Q000494:pharmacology; D009433:Neural Inhibition / Q000502:physiology; D009474:Neurons / Q000502:physiology; D011810:Quinoxalines / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D011810:Quinoxalines; D009118:Muscimol; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; C056723:FG 9041; D015763:2-Amino-5-phosphonovalerate; D005998:Glycine