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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-7-17
pubmed:abstractText
Exocytosis is commonly viewed as the only secretory process able to account for quantal forms of fast synaptic transmission. However, the demonstrated variability and composite properties of miniature postsynaptic signals are not easily explained by all-or-none exocytotic discharge of transmitter in solution from inside vesicles. Recent studies of endocrine secretion have shown that hormone release does not coincide with exocytosis due to its trapping in the core matrix of the granule. Thus, we tested whether the synaptic transmitter GABA could also be held in a matrix before being released. Using confocal microscopy and flow cytometry of embryonic rat hippocampal neurons, we found a GABA immunoreaction at the surface of live cell bodies and growth cones that coincided spatially and quantitatively with the binding of tetanus toxin fragment C (TTFC). TTFC binds predominantly at membrane sites containing the trisialoglycosphingolipid GT1b. Using flow cytometry, GT1b-containing liposomes preincubated in 100 nM GABA exhibited the same relationship between GABA and TTFC surface binding as found on neurons and growth cones. Embryonic neurons differentiated in culture expressed initially a tonic, and after 3-5 days, transient, postsynaptic signals mediated by GABA acting at GABA(A) receptor/Cl(-) channels. A stream of saline applied to the neuronal surface rapidly and reversibly suppressed both tonic and transient signals. A brief application of the GABAmimetic isoguvacine immediately transformed both tonic and transient GABAergic signals into tonic and transient isoguvacinergic signals. These results and those in the literature are consistent with an immediately releasable compartment of transmitter accessible from the presynaptic surface.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0887-4476
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
38-55
pubmed:dateRevised
2008-8-14
pubmed:meshHeading
pubmed-meshheading:10842350-Adsorption, pubmed-meshheading:10842350-Animals, pubmed-meshheading:10842350-Cells, Cultured, pubmed-meshheading:10842350-Chloride Channels, pubmed-meshheading:10842350-Electrophysiology, pubmed-meshheading:10842350-Exocytosis, pubmed-meshheading:10842350-Female, pubmed-meshheading:10842350-Flow Cytometry, pubmed-meshheading:10842350-GABA Agonists, pubmed-meshheading:10842350-Gangliosides, pubmed-meshheading:10842350-Isonicotinic Acids, pubmed-meshheading:10842350-Liposomes, pubmed-meshheading:10842350-Membrane Potentials, pubmed-meshheading:10842350-Membrane Proteins, pubmed-meshheading:10842350-Neurons, pubmed-meshheading:10842350-Pregnancy, pubmed-meshheading:10842350-Presynaptic Terminals, pubmed-meshheading:10842350-Rats, pubmed-meshheading:10842350-Rats, Sprague-Dawley, pubmed-meshheading:10842350-Receptors, GABA-A, pubmed-meshheading:10842350-Synaptic Transmission, pubmed-meshheading:10842350-gamma-Aminobutyric Acid
pubmed:year
2000
pubmed:articleTitle
Surface-accessible GABA supports tonic and quantal synaptic transmission.
pubmed:affiliation
Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892, USA. vautrin@codon.nih.gov
pubmed:publicationType
Journal Article