Inhibitory synaptic inputs to the respiratory rhythm generator in the medulla isolated from newborn rats.
Involvement of chloride-dependent, gamma-aminobutyric acid-(GABA-) like synaptic inhibition in the generation of respiratory rhythm was studied in brainstem-spinal cord preparations isolated from newborn rats. Primary respiratory rhythm is presumably generated within the rostral ventrolateral medulla, the site of Pre-I neurones, the firing of which precedes inspiration. Therefore, we examined the responses of Pre-I and inspiratory neurones to GABA antagonists (picrotoxin and bicuculline), a glycine antagonist (strychnine) and reduced chloride concentration in the perfusate. These antagonists (2-20 microM) and reduction of chloride concentration reversibly blocked the transient inhibition of Pre-I activity that occurred during the inspiratory phase. The rhythmic Pre-I and inspiratory neurone activity remained. Changes in the firing properties of Pre-I and inspiratory neurones in 10 microM bicuculline, 10 microM picrotoxin, 5 microM strychnine or reduction of chloride concentration to 40% of normal were analysed statistically. Burst rate of Pre-I neurones tended to increase during these treatments. Delay time from initiation of Pre-I firing to the peak of C4 motorneurone inspiratory activity tended to decrease except during reduced chloride concentration. Changes in mean intraburst firing frequency of Pre-I neurones were not consistent; increase (32%), no change (38%) or decrease (30%). Burst duration of inspiratory neurones decreased. Intraburst firing frequency of inspiratory neurones tended to increase except in 5 microM strychnine. GABA (0.1 mM) or glycine (0.2 mM) reduced the intraburst firing frequency and burst rate of Pre-I neurones, but did not affect the intraburst firing frequency of inspiratory neurones. The burst duration of inspiratory neurones increased during GABA and glycine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Onimaru
H
H
Department of Physiology, Showa University School of Medicine, Tokyo, Japan.
Arata
A
A
Homma
I
I
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001640:Bicuculline / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D018756:GABA Antagonists; D005998:Glycine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D008526:Medulla Oblongata / Q000502:physiology* / Q000648:ultrastructure; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D010852:Picrotoxin / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism; D012119:Respiration / Q000502:physiology*; D013331:Strychnine / Q000494:pharmacology; D013569:Synapses / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism / Q000494:pharmacology
D001640:Bicuculline; D002712:Chlorides; D018756:GABA Antagonists; D005998:Glycine; D010852:Picrotoxin; D011963:Receptors, GABA-A; D013331:Strychnine; D005680:gamma-Aminobutyric Acid