Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
33
pubmed:dateCreated
2010-8-18
pubmed:abstractText
Endogenous opioids generate analgesic signals in the periaqueductal gray (PAG). However, because cell types in the PAG are difficult to identify, its neuronal mechanism has remained poorly understood. To address this issue, we characterized PAG neurons by their electrical properties using differentially labeled GABAergic and output neurons in the PAG. We found that GABAergic neurons were mostly fast-spiking cells and could be further divided into two distinct classes: with or without low-threshold spikes (LTS) driven by T-type channels. In contrast, the PAG output neurons lacked LTS and showed heterogeneous firing patterns. To reveal the function of the LTS, we examined the mutant mice lacking the alpha1G T-type channels (alpha1G(-/-)). The mutant mice lacked LTS in the fast-spiking GABAergic neurons of the PAG and unexpectedly showed impaired opioid-dependent analgesia; a similar phenotype was reproduced in PAG-specific alpha1G-knockdown mice. Electrophysiological analyses revealed functional expression of mu-opioid receptors in the low threshold-spiking GABAergic neurons. These neurons in the mutant lacking LTS showed markedly enhanced discharge activities, which led to an augmented inhibition of output neurons. Furthermore, the impaired analgesia observed in alpha1G(-/-) mice was reversed by blocking local GABA(A) receptors. These results indicate that alpha1G T-type channels are critical for the opioidergic descending analgesia system in the PAG.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-10066243, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-11349424, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-11406339, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-11498049, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-11917119, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-11929921, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-11978817, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-12072160, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-14526084, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-14730585, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-15582369, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-15601764, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-17100846, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-1804959, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-18203662, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-19052225, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-191150, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-19604928, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-1976803, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-2263320, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-2853058, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-3064173, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-6143527, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-6505691, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-6652378, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-6737292, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-7812601, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-7817403, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-8815798, http://linkedlifedata.com/resource/pubmed/commentcorrection/20682748-963546
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1091-6490
pubmed:author
pubmed:issnType
Electronic
pubmed:day
17
pubmed:volume
107
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
14857-62
pubmed:dateRevised
2011-7-25
pubmed:meshHeading
pubmed-meshheading:20682748-Analgesics, Opioid, pubmed-meshheading:20682748-Animals, pubmed-meshheading:20682748-Bicuculline, pubmed-meshheading:20682748-Calcium Channels, T-Type, pubmed-meshheading:20682748-Female, pubmed-meshheading:20682748-GABA Antagonists, pubmed-meshheading:20682748-GABA-A Receptor Antagonists, pubmed-meshheading:20682748-Green Fluorescent Proteins, pubmed-meshheading:20682748-In Situ Hybridization, Fluorescence, pubmed-meshheading:20682748-Male, pubmed-meshheading:20682748-Membrane Potentials, pubmed-meshheading:20682748-Mice, pubmed-meshheading:20682748-Mice, Inbred C57BL, pubmed-meshheading:20682748-Mice, Inbred Strains, pubmed-meshheading:20682748-Mice, Knockout, pubmed-meshheading:20682748-Mice, Transgenic, pubmed-meshheading:20682748-Microscopy, Confocal, pubmed-meshheading:20682748-Neurons, pubmed-meshheading:20682748-Pain, pubmed-meshheading:20682748-Pain Measurement, pubmed-meshheading:20682748-Periaqueductal Gray, pubmed-meshheading:20682748-RNA Interference, pubmed-meshheading:20682748-Receptors, GABA-A
pubmed:year
2010
pubmed:articleTitle
T-type channels control the opioidergic descending analgesia at the low threshold-spiking GABAergic neurons in the periaqueductal gray.
pubmed:affiliation
Center for Neural Science, Future Fusion Technology Laboratory, Korea Institute of Science and Technology, Seoul 136-791, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't