NDLI: Spinal NMDA receptor activation is necessary for de novo, but not the maintenance of, A2a receptor-mediated phrenic motor facilitation.

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Spinal NMDA receptor activation is necessary for de novo, but not the maintenance of, A2a receptor-mediated phrenic motor facilitation.

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Spinal NMDA receptor activation is necessary for de novo, but not the maintenance of, A2a receptor-mediated phrenic motor facilitation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Golder, F. J.
Description	Country affiliation: United States Author Affiliation: Golder FJ ( Dept. of Clinical Studies-Philadelphia, School of Veterinary Medicine, Univ. of Pennsylvania, 3900 Delancey St., Philadelphia, PA 19104, USA. golderf@vet.upenn.edu)
Abstract	Adenosine 2a (A2a) receptor agonists elicit persistent increases in phrenic nerve activity by transactivating the neurotrophin receptor, TrkB, near phrenic motoneurons. Our working model proposes that A2a receptor-mediated TrkB receptor activation strengthens glutamatergic synapses onto phrenic motoneurons. Activation of glutamate N-methyl d-aspartate (NMDA) receptors has been implicated in other models of phrenic motor plasticity. Thus we hypothesized that NMDA receptor activation also would contribute to A2a receptor-mediated phrenic motor facilitation. Adult male Sprague-Dawley rats were anesthetized with urethane, mechanically ventilated, neuromuscularly paralyzed, and bilaterally vagotomized. The A2a receptor agonist CGS-21680 and the NMDA receptor-channel blocker MK-801 were administered intrathecally over the C4 spinal segment. Phrenic nerve activity was recorded before, during, and after drug administration. MK-801 (concentration range 0.1, 1.0, 10.0, and 100 microM) was administered 30 min before CGS-21680 (50 microM). MK-801 dose-dependently blocked A2a receptor-mediated phrenic motor facilitation. When administered at 60 min post-CGS-21680, MK-801 prevented further increases in phrenic nerve activity compared with the CGS-21680 alone (CGS-21680 alone at 120 min: 114 +/- 19%; CGS-21680 and MK-801 at 60 min post-CGS-21680: 61 +/- 11%, above baseline, P < 0.05) but did not return phrenic motor output to baseline values. Our data suggest that NMDA receptor activation is necessary for de novo A2a receptor-mediated phrenic motor facilitation and that the maintenance of preexisting phrenic motor facilitation does not involve NMDA receptor-dependent mechanisms.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
Journal	Journal of Applied Physiology
Issue Number	1
Volume Number	107
Language	English
Publisher	American Physiological Society
Publisher Date	2009-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Motor Neurons Physiology Phrenic Nerve Receptor, Adenosine A2a Metabolism Receptors, N-methyl-d-aspartate Spinal Cord Injuries Spinal Cord Adenosine Analogs & Derivatives Pharmacology Adenosine A2 Receptor Antagonists Animals Antihypertensive Agents Disease Models, Animal Dizocilpine Maleate Drug Interactions Drug Effects Neuroprotective Agents Phenethylamines Rats, Sprague-dawley Receptor, Trkb Antagonists & Inhibitors Drug Therapy Etiology Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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