Linked Life Data

18094106

Source:http://linkedlifedata.com/resource/pubmed/id/18094106

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-2-14
pubmed:abstractText
Acid-sensing ion channels (ASICs) are H(+)-gated channels that produce transient cation currents in response to extracellular acid. ASICs are expressed in neurons throughout the brain, and ASIC1 knockout mice show behavioral impairments in learning and memory. The role of ASICs in synaptic transmission, however, is not thoroughly understood. We analyzed the involvement of ASICs in synaptic transmission using microisland cultures of hippocampal neurons from wild-type and ASIC knockout mice. There was no significant difference in single action potential (AP)-evoked excitatory postsynaptic currents (EPSCs) between wild-type and ASIC knockout neurons. However, paired-pulse ratios (PPRs) were reduced and spontaneous miniature EPSCs (mEPSCs) occurred at a higher frequency in ASIC1 knockout neurons compared with wild-type neurons. The progressive block of NMDA receptors by an open channel blocker, MK-801, was also faster in ASIC1 knockout neurons. The amplitude and decay time constant of mEPSCs, as well as the size and refilling of the readily releasable pool, were similar in ASIC1 knockout and wild-type neurons. Finally, the release probability, which was estimated directly as the ratio of AP-evoked to hypertonic sucrose-induced charge transfer, was increased in ASIC1 knockout neurons. Transfection of ASIC1a into ASIC1 knockout neurons increased the PPRs, suggesting that alterations in release probability were not the result of developmental compensation within the ASIC1 knockout mice. Together, these findings demonstrate that neurons from ASIC1 knockout mice have an increased probability of neurotransmitter release and indicate that ASIC1a can affect presynaptic mechanisms of synaptic transmission.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3077
pubmed:author
pubmed:issnType
Print
pubmed:volume
99
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
426-41
pubmed:meshHeading
pubmed-meshheading:18094106-Amiloride, pubmed-meshheading:18094106-Animals, pubmed-meshheading:18094106-Animals, Newborn, pubmed-meshheading:18094106-Cells, Cultured, pubmed-meshheading:18094106-Drug Interactions, pubmed-meshheading:18094106-Electric Stimulation, pubmed-meshheading:18094106-Excitatory Amino Acid Antagonists, pubmed-meshheading:18094106-Excitatory Postsynaptic Potentials, pubmed-meshheading:18094106-Hippocampus, pubmed-meshheading:18094106-Humans, pubmed-meshheading:18094106-Ion Channel Gating, pubmed-meshheading:18094106-Membrane Proteins, pubmed-meshheading:18094106-Mice, pubmed-meshheading:18094106-Mice, Knockout, pubmed-meshheading:18094106-Nerve Tissue Proteins, pubmed-meshheading:18094106-Neurons, pubmed-meshheading:18094106-Patch-Clamp Techniques, pubmed-meshheading:18094106-Presynaptic Terminals, pubmed-meshheading:18094106-Probability, pubmed-meshheading:18094106-Protons, pubmed-meshheading:18094106-Sodium Channel Blockers, pubmed-meshheading:18094106-Sodium Channels, pubmed-meshheading:18094106-Transfection
pubmed:year
2008
pubmed:articleTitle
Presynaptic release probability is increased in hippocampal neurons from ASIC1 knockout mice.
pubmed:affiliation
Department of Neuroscience, The Ohio State University, Columbus, OH 43210, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.