Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-11-6
pubmed:abstractText
N-methyl-D-aspartate (NMDA) receptor-mediated synaptic transmission is implicated in activity-dependent developmental reorganization in mammalian brain, including sensory systems and spinal motoneuron circuits. During normal development, synaptic interactions important in activity-dependent modification of neuronal circuits may be driven spontaneously (Shatz 1990b). The respiratory system exhibits substantial spontaneous activity in utero; this activity may be critical in assuring essential and appropriate breathing movements from birth. We tested the hypothesis that NMDA receptors are necessary for prenatal development of central neural circuits underlying respiratory rhythm generation by comparing the responsiveness of control mice and mutant mice lacking the NMDA receptor R1 subunit (NMDAR1) gene to glutamate receptor agonists and antagonists and comparing endogenous respiratory-related oscillations generated in vitro by brain stem-spinal cord and medullary slice preparations from control and mutant mice. In control mice, local application of NMDA and the non-NMDA receptor agonist, (R,S)-alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid hydrobromide (AMPA), over the pre-Bötzinger Complex, the C4 cervical motor neuron pool, and the hypoglossal motor nucleus produced profound increases in inspiratory frequency, tonic discharge on C4 ventral nerve roots, and inward currents in inspiratory hypoglossal motoneurons, respectively. Responses of mutant mice to AMPA were similar. However, mutant mice were completely unresponsive to NMDA applications. Preparations from mutant mice generated a respiratory rhythm virtually identical to control. Results demonstrate that NMDA receptors are not essential for respiratory rhythm generation or drive transmission in the neonate. More importantly, they suggest that NMDA receptors are not obligatory for the prenatal development of circuits producing respiratory rhythm.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-3077
pubmed:author
pubmed:issnType
Print
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1414-20
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9310432-Animals, pubmed-meshheading:9310432-Animals, Newborn, pubmed-meshheading:9310432-Brain Stem, pubmed-meshheading:9310432-DNA Primers, pubmed-meshheading:9310432-Female, pubmed-meshheading:9310432-Instinct, pubmed-meshheading:9310432-Medulla Oblongata, pubmed-meshheading:9310432-Membrane Potentials, pubmed-meshheading:9310432-Mice, pubmed-meshheading:9310432-Mice, Inbred C57BL, pubmed-meshheading:9310432-Mice, Knockout, pubmed-meshheading:9310432-Motor Neurons, pubmed-meshheading:9310432-Mutation, pubmed-meshheading:9310432-Nerve Net, pubmed-meshheading:9310432-Patch-Clamp Techniques, pubmed-meshheading:9310432-Receptors, AMPA, pubmed-meshheading:9310432-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:9310432-Respiratory Mechanics, pubmed-meshheading:9310432-Spinal Cord
pubmed:year
1997
pubmed:articleTitle
Functional respiratory rhythm generating networks in neonatal mice lacking NMDAR1 gene.
pubmed:affiliation
Department of Physiological Science, University of California, Los Angeles 90095-1527, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't