The nonuniform distribution of the GABA(A) receptor alpha 1 subunit influences inhibitory synaptic transmission to motoneurons within a motor nucleus.
Using immunohistochemistry we studied the distribution of GABA(A) and glycine receptor alpha1 subunits in the rat hypoglossal nucleus during postnatal development. In the neonate [postnatal day (P) 1-3] and adult nucleus (P28-30), GABA(A) receptor alpha1 subunit labeling was relatively modest. However, in the juvenile nucleus (P9-13), labeling was strong in the ventrolateral region and moderate in the dorsal region. Glycine receptor alpha1 subunit labeling was strong and uniform in the juvenile and adult nucleus and absent in the neonate nucleus. GABA and glycine neurotransmitter labeling was uniform throughout the neonatal and juvenile nucleus. To study the functional consequences of this regional differential GABA(A) receptor alpha1 subunit distribution, we voltage clamped juvenile hypoglossal motoneurons (HMs) from the ventrolateral and dorsal regions and recorded spontaneous miniature IPSCs (mIPSCs). Pure GABAergic events had slower decay times than glycinergic events. Although pure GABAergic and glycinergic decay times did not differ depending on HM location, the decays of mixed mIPSCs from ventrolateral HMs, recorded without GABA(A) and glycine receptor antagonists, had significantly slower decays than mIPSCs from dorsal HMs. Focally applied GABA and glycine onto outside-out patches revealed that the GABAergic to glycinergic peak current amplitude ratio was larger for patches from ventrolateral HMs compared with dorsal HMs. Dual component mIPSCs, presumably caused by co-release of GABA and glycine, were recorded more frequently in the ventrolateral nucleus. These data suggest that the number of synapses using GABA(A) receptor-mediated transmission is greater on ventrolateral HMs than dorsal HMs, demonstrating a nonuniformity of synaptic function within a defined motor nucleus.
O'Brien
J A
JA
Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195-7290, USA.
Berger
A J
AJ
D000375:Aging / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D018756:GABA Antagonists / Q000494:pharmacology; D018757:GABA Modulators / Q000494:pharmacology; D005998:Glycine / Q000378:metabolism / Q000494:pharmacology; D018684:Glycine Agents / Q000494:pharmacology; D007002:Hypoglossal Nerve / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008526:Medulla Oblongata / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009046:Motor Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D021122:Protein Subunits; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000378:metabolism*; D018009:Receptors, Glycine / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism / Q000494:pharmacology
D018756:GABA Antagonists; D018757:GABA Modulators; D018684:Glycine Agents; D021122:Protein Subunits; D011963:Receptors, GABA-A; D018009:Receptors, Glycine; D005680:gamma-Aminobutyric Acid; D005998:Glycine