Effects of GABAergic agonists and antagonists on oscillatory signal propagation in the guinea-pig accessory olfactory bulb slice revealed by optical recording.
To investigate the action of GABAergic agents on oscillatory signal propagation induced by electrical stimulation of the vomeronasal nerve layer, optical and electrophysiological recordings were carried out in slice preparations of the guinea-pig accessory olfactory bulb. In response to electrical stimuli, characteristic optical signals appeared in each layer: in the vomeronasal nerve layer, a transient presynaptic response; in the glomerular layer, pre- and postsynaptic responses; in the external plexiform, mitral cell and granule cell layers, a damped oscillatory response. Application of the GABAergic agonists, that is, GABA, muscimol (a GABAA receptor agonist) and baclofen (a GABAB receptor agonist), suggested that the GABAB action existed mainly in the glomeruli, whereas the GABAA action was present in both the glomeruli and the external plexiform layer. Bicuculline (a GABAA receptor antagonist) produced long-lasting but nonoscillating excitation in the external plexiform and mitral cell layers, indicating that the GABAA action contributes to the formation of oscillatory responses. When double-pulse stimulation was applied to the vomeronasal nerve layer, the test responses in the glomerular layer and external plexiform and mitral cell layers were depressed, but those in the vomeronasal nerve layer were not. Application of 2-hydroxysaclofen (a GABAB receptor antagonist) mostly blocked paired-pulse depression occurring in the glomerular layer and restored the reduced transmission to mitral cells, but had only a small effect on the depressed oscillatory response in the external plexiform and mitral cell layers. These observations suggest that GABAB action in the glomerular layer might, at least, regulate information flow from vomeronasal afferents to apical dendrites of mitral cells, like a gate inhibition. However, actions other than GABAB could also be involved in the depression of the oscillation in the external plexiform and mitral cell layers.
Sugai
T
T
Department of Physiology, Kanazawa Medical University, Uchinada, Ishikawa, Japan. tokio@kanazawa-med.ac.jp
Sugitani
M
M
Onoda
N
N
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D004558:Electric Stimulation; D004594:Electrophysiology; D004597:Electroshock; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018755:GABA Agonists / Q000494:pharmacology*; D018756:GABA Antagonists / Q000494:pharmacology*; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D006168:Guinea Pigs; D066298:In Vitro Techniques; D009296:Nasal Cavity / Q000294:innervation; D009300:Nasal Septum / Q000294:innervation; D009424:Nervous System Physiological Phenomena; D009830:Olfactory Bulb / Q000502:physiology*; D055095:Optics and Photonics; D009991:Oscillometry; D013779:Tetrodotoxin / Q000494:pharmacology
D018691:Excitatory Amino Acid Antagonists; D018755:GABA Agonists; D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D013779:Tetrodotoxin; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione