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Sökning: WFRF:(Kokaia Z) > Regulation of neuro...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005369naa a2200589 4500
001oai:lup.lub.lu.se:14b27878-c8fc-44cb-b6cb-bcd80ede84c0
003SwePub
008190625s1993 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/14b27878-c8fc-44cb-b6cb-bcd80ede84c02 URI
024a https://doi.org/10.1016/0306-4522(93)90207-V2 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Bengzon, Ju Skåne University Hospital4 aut0 (Swepub:lu)neur-jbe
2451 0a Regulation of neurotrophin and trkA, trkB and trkC tyrosine kinase receptor messenger RNA expression in kindling
264 1c 1993
520 a Levels of messenger RNA for nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, and the tyrosine kinase receptors trkA, trkB and trkC have been studied using in situ hybridization in the rat brain 2 h and four weeks after kindling-induced seizures. Epileptiform activity evoked by hippocampal stimulation and exceeding 70 s lead to a concomitant and transient increase of brain- derived neurotrophic factor, nerve growth factor, trkB and trkC messenger RNA expression in dentate granule cells after both focal and generalized seizures. Brain-derived neurotrophic factor messenger RNA levels were also increased bilaterally in the CA1-CA3 regions, amygdala and the piriform, entorhinal, perirhinal, retrosplenial and temporal cortices after generalized seizures. The magnitude of the increases was similar throughout the development of kindling and in the fully kindled brain. No changes of trkA messenger RNA were observed. In amygdalar kindling, elevated brain-derived neurotrophic factor messenger RNA levels developed more rapidly in the amygdala-piriform cortex than after stimulation in the hippocampus but changes in the hippocampal formation were only seen in few animals. Intraventricular 6-hydroxydopamine or a bilateral fimbria-fornix lesion did not alter basal expression or seizure-evoked changes in messenger RNA levels for neurotrophins or trk receptors but increased the number of animals exhibiting elevated levels after the first stimulation, probably due to a prolongation of seizure activity. Both in sham-operated and fimbria-fornix-lesioned rats seizure activity caused a marked reduction of neurotrophin-3 messenger RNA levels in dentate granule cells. The results indicate that activation of the brain-derived neurotrophic factor gene, at least in dentate granule cells, is an "all-or-none" type of response and dependent on the duration but not the severity of seizures or the stage of kindling epileptogenesis. Changes in brain-derived neurotrophic factor, nerve growth factor, neurotrophin-3 and trkB and trkC were observed concomitantly in the dentate gyrus, which suggests that seizure activity sets in motion a cascade of genomic events possibly mediated via a common mechanism. Since altered messenger RNA levels outside hippocampus were detected only for brain-derived neurotrophic factor, neurotrophin and trk gene expression in these regions seems to be regulated differently.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
653 a Amygdala/physiology
653 a Animals
653 a Base Sequence
653 a Brain-Derived Neurotrophic Factor
653 a Electric Stimulation
653 a Electrodes, Implanted
653 a Hippocampus/physiology
653 a In Situ Hybridization
653 a Kindling, Neurologic/metabolism
653 a Male
653 a Molecular Sequence Data
653 a Nerve Growth Factors/biosynthesis
653 a Nerve Tissue Proteins/biosynthesis
653 a Neurotrophin 3
653 a Protein-Tyrosine Kinases/metabolism
653 a RNA, Messenger/biosynthesis
653 a Rats
653 a Rats, Sprague-Dawley
653 a Receptors, Cell Surface/biosynthesis
700a Kokaia, Zu Skåne University Hospital4 aut0 (Swepub:lu)neur-zko
700a Ernfors, Pu Karolinska Institutet4 aut
700a Kokaia, Mu Skåne University Hospital4 aut0 (Swepub:lu)neur-mko
700a Leanza, Gu Lund University,Lunds universitet,Neurologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Neurology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)med-gle
700a Nilsson, O Gu Lund University,Lunds universitet,Neurokirurgi,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Neurosurgery,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)nkir-oni
700a Persson, Hu Karolinska Institutet4 aut
700a Lindvall, Ou Skåne University Hospital4 aut0 (Swepub:lu)neur-oli
710a Karolinska Institutetb Skåne University Hospital4 org
773t Neuroscienceg 53:2, s. 433-446q 53:2<433-446x 0306-4522
856u http://dx.doi.org/10.1016/0306-4522(93)90207-Vy FULLTEXT
8564 8u https://lup.lub.lu.se/record/14b27878-c8fc-44cb-b6cb-bcd80ede84c0
8564 8u https://doi.org/10.1016/0306-4522(93)90207-V

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