Source:http://linkedlifedata.com/resource/pubmed/id/19686797
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2009-9-28
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pubmed:abstractText |
The effects of scorpion toxin (STX) on both spontaneous and evoked glycinergic and glutamatergic postsynaptic currents were studied by using both the mechanically dissociated single SDCN neuron (synaptic bouton preparation) and the 'focal electrical stimulation technique'. In the experimental condition where Na(+) channels on postsynaptic soma membrane were blocked by intracellular perfusion of QX-314, STX increased dose-dependently the frequency of spontaneous glycinergic and glutamatergic postsynaptic currents (sIPSC and sEPSC, respectively) without affecting the amplitude, suggesting STX acts on inhibitory and excitatory presynaptic nerve terminal. Such a facilitatory effect of STX on sIPSC was stronger than that on sEPSC. On the other hand, STX significantly enhanced the averaged current amplitude and decreased the failure rate (Rf) of both evoked inhibitory and excitatory postsynaptic currents (eIPSC and eEPSC, respectively), indicating that STX increases not only the release frequency of glycine and glutamate but also the amount of their release from the both presynaptic nerve endings. These effects of STX were completely removed by adding Na(+) or Ca(2+) channel blockers, indicating that STX increases Ca(2+) influx through Ca(2+) channels triggered by activating voltage-dependent Na(+) channels on the nerve terminals. In addition, the difference of STX actions on the amplitude of spontaneous and evoked currents was discussed.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Glycine,
http://linkedlifedata.com/resource/pubmed/chemical/Scorpion Venoms,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1879-3185
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
29
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pubmed:volume |
264
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
198-204
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pubmed:meshHeading |
pubmed-meshheading:19686797-Animals,
pubmed-meshheading:19686797-Calcium Channel Blockers,
pubmed-meshheading:19686797-Calcium Channels,
pubmed-meshheading:19686797-Calcium Signaling,
pubmed-meshheading:19686797-Dose-Response Relationship, Drug,
pubmed-meshheading:19686797-Electric Stimulation,
pubmed-meshheading:19686797-Evoked Potentials,
pubmed-meshheading:19686797-Excitatory Postsynaptic Potentials,
pubmed-meshheading:19686797-Glutamic Acid,
pubmed-meshheading:19686797-Glycine,
pubmed-meshheading:19686797-Inhibitory Postsynaptic Potentials,
pubmed-meshheading:19686797-Kinetics,
pubmed-meshheading:19686797-Presynaptic Terminals,
pubmed-meshheading:19686797-Rats,
pubmed-meshheading:19686797-Rats, Wistar,
pubmed-meshheading:19686797-Scorpion Venoms,
pubmed-meshheading:19686797-Sodium Channel Blockers,
pubmed-meshheading:19686797-Sodium Channels,
pubmed-meshheading:19686797-Spinal Nerves
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pubmed:year |
2009
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pubmed:articleTitle |
Effects of scorpion toxin on excitatory and inhibitory presynaptic terminals.
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pubmed:affiliation |
Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. hakaike@kumamoto-hsu.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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