Linked Life Data

9065495

Source:http://linkedlifedata.com/resource/pubmed/id/9065495

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1999-2-25
pubmed:abstractText
Synchronous thalamic network activity occurring during slow wave sleep and paroxysmal discharges critically depends on the ability of thalamocortical relay cells and inhibitory neurons of the nucleus reticularis thalami (nRt) to fire bursts of action potentials. Inhibitory synaptic potentials (IPSPs) originating from nRt cells are crucial in deinactivating T-channels and thus promoting burst firing in relay cells, but the functional role of intra-nRt IPSPs is less well understood. A major factor that regulates the net effects of IPSP generation is the chloride equilibrium potential (ECl). Here we applied the perforated patch-clamp technique, using the cation-selective ionophore gramicidin to assess the reversal potential of chloride in nRt and relay cells in brain slices. We found that the reversal potential of GABA-induced membrane currents (EGABA) was significantly more hyperpolarized in relay (-81 +/- 2.6 mV), as compared with nRt cells (-71 +/- 2.5 mV). EGABA was not significantly different from the reversal potential of evoked IPSCs (EIPSC; -82 +/- 4.4 mV) in relay cells. In both relay and reticular neurons the chloride gradient was collapsed partially by the chloride cation cotransport blocker furosemide, suggesting an active chloride extrusion mechanism in thalamic neurons. Given the relatively hyperpolarized resting potentials (approximately -70 mV) reported for nRt and relay cells during in vitro thalamic oscillations, we conclude that under these conditions GABAA IPSPs lead to significant hyperpolarization in relay cells. By contrast, intra-nRt inhibition essentially would be shunting, i.e., would produce minimal membrane polarization but still could reduce the amplitude of excitatory events.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0270-6474
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2348-54
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9065495-2-Amino-5-phosphonovalerate, pubmed-meshheading:9065495-6-Cyano-7-nitroquinoxaline-2,3-dione, pubmed-meshheading:9065495-Animals, pubmed-meshheading:9065495-Chlorides, pubmed-meshheading:9065495-Excitatory Amino Acid Antagonists, pubmed-meshheading:9065495-Female, pubmed-meshheading:9065495-GABA-B Receptor Antagonists, pubmed-meshheading:9065495-Homeostasis, pubmed-meshheading:9065495-Male, pubmed-meshheading:9065495-Membrane Potentials, pubmed-meshheading:9065495-Neurons, pubmed-meshheading:9065495-Organophosphorus Compounds, pubmed-meshheading:9065495-Patch-Clamp Techniques, pubmed-meshheading:9065495-Rats, pubmed-meshheading:9065495-Rats, Sprague-Dawley, pubmed-meshheading:9065495-Synaptic Transmission, pubmed-meshheading:9065495-Thalamic Nuclei, pubmed-meshheading:9065495-Time Factors, pubmed-meshheading:9065495-gamma-Aminobutyric Acid
pubmed:year
1997
pubmed:articleTitle
Nucleus-specific chloride homeostasis in rat thalamus.
pubmed:affiliation
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't