Medullary lateral tegmental field neurons influence the timing and pattern of phrenic nerve activity in cats.
In an effort to characterize the role of the medullary lateral tegmental field (LTF) in regulating respiration, we tested the effects of selective blockade of excitatory (EAA) and inhibitory amino acid (IAA) receptors in this region on phrenic nerve activity (PNA) of vagus-intact and vagotomized cats anesthetized with dial-urethane. We found distinct patterns of changes in central respiratory rate, duration of inspiratory and expiratory phases of PNA (Ti and Te, respectively), and I-burst amplitude after selective blockade of EAA and IAA receptors in the LTF. First, blockade of N-methyl-D-aspartate (NMDA) receptors significantly (P < 0.05) decreased central respiratory rate primarily by increasing Ti but did not alter I-burst amplitude. Second, blockade of non-NMDA receptors significantly reduced I-burst amplitude without affecting central respiratory rate. Third, blockade of GABAA receptors significantly decreased central respiratory rate by increasing Te and significantly reduced I-burst amplitude. Fourth, blockade of glycine receptors significantly decreased central respiratory rate by causing proportional increases in Ti and Te and significantly reduced I-burst amplitude. These changes in PNA were markedly different from those produced by blockade of EAA or IAA receptors in the pre-Bötzinger complex. We propose that a proper balance of excitatory and inhibitory inputs to several functionally distinct pools of LTF neurons is essential for maintaining the normal pattern of PNA in anesthetized cats.
Orer
Hakan S
HS
Dept. of Pharmacology and Toxicology, Michigan State Univ., East Lansing, MI 48824, USA.
Gebber
Gerard L
GL
Barman
Susan M
SM
D000818:Animals; D002415:Cats / Q000502:physiology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D045853:Exhalation / Q000502:physiology; D018756:GABA Antagonists / Q000494:pharmacology; D018684:Glycine Agents / Q000494:pharmacology; D001239:Inhalation / Q000502:physiology; D008526:Medulla Oblongata / Q000502:physiology*; D009046:Motor Neurons / Q000502:physiology*; D009588:Nitrogen Mustard Compounds / Q000494:pharmacology; D010791:Phrenic Nerve / Q000502:physiology*; D011724:Pyridazines / Q000494:pharmacology; D011810:Quinoxalines / Q000494:pharmacology; D017459:Receptors, Amino Acid / Q000037:antagonists & inhibitors / Q000502:physiology; D011963:Receptors, GABA-A / Q000502:physiology; D017470:Receptors, Glutamate / Q000502:physiology; D018009:Receptors, Glycine / Q000037:antagonists & inhibitors / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology; D012125:Respiratory Center / Q000502:physiology*; D015656:Respiratory Mechanics / Q000502:physiology; D013331:Strychnine / Q000494:pharmacology; D013997:Time Factors
D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D018684:Glycine Agents; D009588:Nitrogen Mustard Compounds; D011724:Pyridazines; D011810:Quinoxalines; D017459:Receptors, Amino Acid; D011963:Receptors, GABA-A; D017470:Receptors, Glutamate; D018009:Receptors, Glycine; D016194:Receptors, N-Methyl-D-Aspartate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; C100119:imidazole mustard; C049853:gabazine; D013331:Strychnine