Linked Life Data

7908647

Source:http://linkedlifedata.com/resource/pubmed/id/7908647

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-5-9
pubmed:abstractText
To analyze the functional consequences of hypoxia on the efficacy of intracortical inhibitory mechanisms mediated by gamma-aminobutyric acid (GABA), extra- and intracellular recordings were obtained from rat primary somatosensory cortex in vitro. Hypoxia, induced by transient N2 aeration, caused a decrease in stimulus-evoked inhibitory postsynaptic potentials (IPSPs), followed by a pronounced anoxic depolarization. Upon reoxygenation, the fast (f-) and long-latency (l-) IPSP showed a positive shift in the reversal potential by 24.4 and 14.9 mV, respectively. The peak conductance of the f- and l-IPSP was reversibly reduced in the postanoxic period by 72% and 94%, respectively. Extracellular field potential recordings and application of a paired-pulse inhibition protocol confirmed the enhanced sensitivity of inhibitory synaptic transmission for transient oxygen deprivation. Intracellular recordings from morphologically or electrophysiologically identified interneurons did not reveal any enhanced susceptibility for hypoxia as compared to pyramidal cells, suggesting that inhibitory neurons are not selectively impaired in their functional properties. Intracellularly recorded spontaneous IPSPs were transiently augmented in the postanoxic period, indicating that presynaptic GABA release was not suppressed. Developmental studies in adult (older than postnatal day 28), juvenile (P14-18), and young (P5-8) neocortical slices revealed a prominent functional resistance of immature tissue for hypoxia. In comparison with adult cortex, the hypoxia-induced reduction in excitatory and inhibitory synaptic transmission was significantly smaller in immature cortex. Our data indicate a hypoxia-induced distinct reduction of postsynaptic GABAergic mechanisms, leading to the manifestation of intracortical hyperexcitability as a possible functional consequence.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0014-4819
pubmed:author
pubmed:issnType
Print
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
209-24
pubmed:dateRevised
2009-11-11
pubmed:meshHeading
pubmed-meshheading:7908647-2-Amino-5-phosphonovalerate, pubmed-meshheading:7908647-6-Cyano-7-nitroquinoxaline-2,3-dione, pubmed-meshheading:7908647-Aging, pubmed-meshheading:7908647-Animals, pubmed-meshheading:7908647-Cell Hypoxia, pubmed-meshheading:7908647-Electric Conductivity, pubmed-meshheading:7908647-Electric Stimulation, pubmed-meshheading:7908647-Evoked Potentials, pubmed-meshheading:7908647-GABA Antagonists, pubmed-meshheading:7908647-Interneurons, pubmed-meshheading:7908647-Neurons, pubmed-meshheading:7908647-Quinoxalines, pubmed-meshheading:7908647-Rats, pubmed-meshheading:7908647-Rats, Wistar, pubmed-meshheading:7908647-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:7908647-Somatosensory Cortex, pubmed-meshheading:7908647-Synaptic Transmission, pubmed-meshheading:7908647-gamma-Aminobutyric Acid
pubmed:year
1993
pubmed:articleTitle
Influence of hypoxia on excitation and GABAergic inhibition in mature and developing rat neocortex.
pubmed:affiliation
Institute of Neurophysiology, University of Cologne, Germany.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't