γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice
Thalamocortical in vivo and in vitro function was studied in mice lacking P/Q-type calcium channels (CaV2.1), in which N-type calcium channels (CaV2.2) supported central synaptic transmission. Unexpectedly, in vitro patch recordings from thalamic neurons demonstrated no γ-band subthreshold oscillati...
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2007
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v104_n45_p17819_Llinas http://hdl.handle.net/20.500.12110/paper_00278424_v104_n45_p17819_Llinas |
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paper:paper_00278424_v104_n45_p17819_Llinas2023-06-08T14:54:22Z γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice 1-Octanol Calcium channel Electroencephalogram Patch clamp VSDI calcium channel L type calcium channel N type calcium channel P type calcium channel Q type mutant protein animal cell article brain cortex coma controlled study electroencephalogram in vitro study in vivo study nonhuman oscillation priority journal protein deficiency synaptic transmission thalamus nucleus Animalia Mus Thalamocortical in vivo and in vitro function was studied in mice lacking P/Q-type calcium channels (CaV2.1), in which N-type calcium channels (CaV2.2) supported central synaptic transmission. Unexpectedly, in vitro patch recordings from thalamic neurons demonstrated no γ-band subthreshold oscillation, and voltage-sensitive dye imaging demonstrated an absence of cortical γ-band-dependent columnar activation involving cortical inhibitory interneuron activity. In vivo electroencephalogram recordings showed persistent absence status and a dramatic reduction of γ-band activity. Pharmacological block of T-type calcium channels (CaV3), although not noticeably affecting normal control animals, left the knockout mice in a coma-like state. Hence, although N-type calcium channels can rescue P/Q-dependent synaptic transmission, P/Q calcium channels are essential in the generation of γ-band activity and resultant cognitive function. © 2007 by The National Academy of Sciences of the USA. 2007 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v104_n45_p17819_Llinas http://hdl.handle.net/20.500.12110/paper_00278424_v104_n45_p17819_Llinas |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
1-Octanol Calcium channel Electroencephalogram Patch clamp VSDI calcium channel L type calcium channel N type calcium channel P type calcium channel Q type mutant protein animal cell article brain cortex coma controlled study electroencephalogram in vitro study in vivo study nonhuman oscillation priority journal protein deficiency synaptic transmission thalamus nucleus Animalia Mus |
| spellingShingle |
1-Octanol Calcium channel Electroencephalogram Patch clamp VSDI calcium channel L type calcium channel N type calcium channel P type calcium channel Q type mutant protein animal cell article brain cortex coma controlled study electroencephalogram in vitro study in vivo study nonhuman oscillation priority journal protein deficiency synaptic transmission thalamus nucleus Animalia Mus γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice |
| topic_facet |
1-Octanol Calcium channel Electroencephalogram Patch clamp VSDI calcium channel L type calcium channel N type calcium channel P type calcium channel Q type mutant protein animal cell article brain cortex coma controlled study electroencephalogram in vitro study in vivo study nonhuman oscillation priority journal protein deficiency synaptic transmission thalamus nucleus Animalia Mus |
| description |
Thalamocortical in vivo and in vitro function was studied in mice lacking P/Q-type calcium channels (CaV2.1), in which N-type calcium channels (CaV2.2) supported central synaptic transmission. Unexpectedly, in vitro patch recordings from thalamic neurons demonstrated no γ-band subthreshold oscillation, and voltage-sensitive dye imaging demonstrated an absence of cortical γ-band-dependent columnar activation involving cortical inhibitory interneuron activity. In vivo electroencephalogram recordings showed persistent absence status and a dramatic reduction of γ-band activity. Pharmacological block of T-type calcium channels (CaV3), although not noticeably affecting normal control animals, left the knockout mice in a coma-like state. Hence, although N-type calcium channels can rescue P/Q-dependent synaptic transmission, P/Q calcium channels are essential in the generation of γ-band activity and resultant cognitive function. © 2007 by The National Academy of Sciences of the USA. |
| title |
γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice |
| title_short |
γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice |
| title_full |
γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice |
| title_fullStr |
γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice |
| title_full_unstemmed |
γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice |
| title_sort |
γ-band deficiency and abnormal thalamocortical activity in p/q-type channel mutant mice |
| publishDate |
2007 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v104_n45_p17819_Llinas http://hdl.handle.net/20.500.12110/paper_00278424_v104_n45_p17819_Llinas |
| _version_ |
1768542116202414080 |