Sökning: WFRF:(Kokaia Z) > Regulation of neuro...
Fältnamn | Indikatorer | Metadata |
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000 | 05369naa a2200589 4500 | |
001 | oai:lup.lub.lu.se:14b27878-c8fc-44cb-b6cb-bcd80ede84c0 | |
003 | SwePub | |
008 | 190625s1993 | |||||||||||000 ||eng| | |
024 | 7 | a https://lup.lub.lu.se/record/14b27878-c8fc-44cb-b6cb-bcd80ede84c02 URI |
024 | 7 | a https://doi.org/10.1016/0306-4522(93)90207-V2 DOI |
040 | a (SwePub)lu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a art2 swepub-publicationtype |
072 | 7 | a ref2 swepub-contenttype |
100 | 1 | a Bengzon, Ju Skåne University Hospital4 aut0 (Swepub:lu)neur-jbe |
245 | 1 0 | a Regulation of neurotrophin and trkA, trkB and trkC tyrosine kinase receptor messenger RNA expression in kindling |
264 | 1 | c 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 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe |
650 | 7 | a 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 | |
700 | 1 | a Kokaia, Zu Skåne University Hospital4 aut0 (Swepub:lu)neur-zko |
700 | 1 | a Ernfors, Pu Karolinska Institutet4 aut |
700 | 1 | a Kokaia, Mu Skåne University Hospital4 aut0 (Swepub:lu)neur-mko |
700 | 1 | a 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 |
700 | 1 | a 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 |
700 | 1 | a Persson, Hu Karolinska Institutet4 aut |
700 | 1 | a Lindvall, Ou Skåne University Hospital4 aut0 (Swepub:lu)neur-oli |
710 | 2 | a Karolinska Institutetb Skåne University Hospital4 org |
773 | 0 | t Neuroscienceg 53:2, s. 433-446q 53:2<433-446x 0306-4522 |
856 | 4 | u http://dx.doi.org/10.1016/0306-4522(93)90207-Vy FULLTEXT |
856 | 4 8 | u https://lup.lub.lu.se/record/14b27878-c8fc-44cb-b6cb-bcd80ede84c0 |
856 | 4 8 | u https://doi.org/10.1016/0306-4522(93)90207-V |
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