Inhibitory synaptic transmission differs in mouse type A and B medial vestibular nucleus neurons in vitro.
Fast inhibitory synaptic transmission in the medial vestibular nucleus (MVN) is mediated by GABA(A) receptors (GABA(A)Rs) and glycine receptors (GlyRs). To assess their relative contribution to inhibition in the MVN, we recorded miniature inhibitory postsynaptic currents (mIPSCs) in physiologically characterized type A and type B MVN neurons. Transverse brain stem slices were prepared from mice (3-8 wk old), and whole cell patch-clamp recordings were obtained from visualized MVN neurons (CsCl internal; Vm = -70 mV; 23 degrees C). In 81 MVN neurons, 69% received exclusively GABA(A)ergic inputs, 6% exclusively glycinergic inputs, and 25% received both types of mIPSCs. The mean amplitude of GABA(A)R-mediated mIPSCs was smaller than those mediated by GlyRs (22.6 +/- 1.8 vs. 35.3 +/- 5.3 pA). The rise time and decay time constants of GABA(A)R- versus GlyR-mediated mIPSCs were slower (1.3 +/- 0.1 vs. 0.9 +/- 0.1 ms and 10.5 +/- 0.3 vs. 4.7 +/- 0.3 ms, respectively). Comparison of type A (n = 20) and type B (n = 32) neurons showed that type A neurons received almost exclusively GABA(A)ergic inhibitory inputs, whereas type B neurons received GABA(A)ergic inputs, glycinergic inputs, or both. Intracellular labeling in a subset of MVN neurons showed that morphology was not related to a MVN neuron's inhibitory profile (n = 15), or whether it was classified as type A or B (n = 29). Together, these findings indicate that both GABA and glycine contribute to inhibitory synaptic processing in MVN neurons, although GABA dominates and there is a difference in the distribution of GABA(A) and Gly receptors between type A and type B MVN neurons.
Camp
Aaron J
AJ
School of Biomedical Sciences and Hunter Medical Research Institute, Faculty of Health, The University of Newcastle, Callaghan, Australia.
Callister
Robert J
RJ
Brichta
Alan M
AM
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D001710:Biotin / Q000031:analogs & derivatives / Q000493:pharmacokinetics; D002586:Cesium / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D004347:Drug Interactions; D017097:Electric Impedance; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D018756:GABA Antagonists / Q000494:pharmacology; D005998:Glycine / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000502:physiology / Q000528:radiation effects; D008698:Mesylates / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000145:classification* / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques / Q000379:methods; D026941:Sodium Channel Blockers / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D014726:Vestibular Nuclei / Q000166:cytology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D002712:Chlorides; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D008698:Mesylates; D026941:Sodium Channel Blockers; C070614:neurobiotin; C045880:methanesulfonic acid; D002586:Cesium; D013779:Tetrodotoxin; D005680:gamma-Aminobutyric Acid; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D001710:Biotin; C028019:cesium chloride; D005998:Glycine; D001640:Bicuculline