001     6000
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024 7 _ |2 pmid
|a pmid:19665048
024 7 _ |2 DOI
|a 10.1016/j.neuroscience.2009.07.067
024 7 _ |2 WOS
|a WOS:000271690200037
037 _ _ |a PreJuSER-6000
041 _ _ |a eng
082 _ _ |a 610
084 _ _ |2 WoS
|a Neurosciences
100 1 _ |a Haghir, H.
|b 0
|0 P:(DE-HGF)0
245 _ _ |a Patterns of neurotransmitter receptor distributions following cortical spreading depression
260 _ _ |a Amsterdam [u.a.]
|b Elsevier Science
|c 2009
300 _ _ |a 1340 - 1352
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a article
|2 DRIVER
440 _ 0 |a Neuroscience
|x 0306-4522
|0 4579
|y 4
|v 163
500 _ _ |a Record converted from VDB: 12.11.2012
520 _ _ |a Spreading depression (SD), a self-propagating depolarization of neurons and glia, is believed to play a role in different neurological disorders including migraine aura and acute brain ischaemia. Initiation and propagation of SD modulate excitability of neuronal network. A brief period of excitation heralds SD which is immediately followed first by prolonged nerve cell depression and later by an excitatory phase. The aim of the present study was to characterize local and remote transmitter receptor changes after propagation of cortical SD. Quantitative receptor autoradiography was used to asses 16 transmitter receptor types in combined striatum-hippocampus-cortex slices of the rat 1 h after induction of cortical SD. In neocortical tissues, local increases of glutamate NMDA, AMPA, and kainate receptor binding sites were observed. In addition to up-regulation of ionotropic glutamate receptors, receptor binding sites of GABA(A), muscarinic M1 and M2, adrenergic alpha(1) and alpha(2), and serotonergic 5-HT(2) receptors were increased in the hippocampus. Cortical SD also upregulated NMDA, AMPA, kainate, GABA(A), serotonergic 5-HT(2), adrenergic alpha(2) and dopaminergic D1 receptor binding sites in the striatum. These findings indicate selective changes in several receptors binding sites both in cortical and subcortical regions by SD which may explain delayed excitatory phase after SD. Mapping of receptor changes by cortical SD increases our understanding of the mechanism of SD action in associated neurological disorders.
536 _ _ |a Funktion und Dysfunktion des Nervensystems
|c P33
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588 _ _ |a Dataset connected to Web of Science, Pubmed
650 _ 2 |2 MeSH
|a Animals
650 _ 2 |2 MeSH
|a Autoradiography
650 _ 2 |2 MeSH
|a Cerebral Cortex: physiology
650 _ 2 |2 MeSH
|a Corpus Striatum: physiology
650 _ 2 |2 MeSH
|a Cortical Spreading Depression: physiology
650 _ 2 |2 MeSH
|a Hippocampus: physiology
650 _ 2 |2 MeSH
|a Microelectrodes
650 _ 2 |2 MeSH
|a Neuronal Plasticity: physiology
650 _ 2 |2 MeSH
|a Rats
650 _ 2 |2 MeSH
|a Receptors, Neurotransmitter: metabolism
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, Neurotransmitter
650 _ 7 |a J
|2 WoSType
653 2 0 |2 Author
|a migraine headache
653 2 0 |2 Author
|a stroke
653 2 0 |2 Author
|a epilepsy
653 2 0 |2 Author
|a transmitter density
653 2 0 |2 Author
|a autoradiography
700 1 _ |a Kovac, S.
|b 1
|0 P:(DE-HGF)0
700 1 _ |a Speckmann, E.-J.
|b 2
|0 P:(DE-HGF)0
700 1 _ |a Zilles, K.
|b 3
|u FZJ
|0 P:(DE-Juel1)131714
700 1 _ |a Gorji, A.
|b 4
|0 P:(DE-HGF)0
773 _ _ |a 10.1016/j.neuroscience.2009.07.067
|g Vol. 163, p. 1340 - 1352
|p 1340 - 1352
|q 163<1340 - 1352
|0 PERI:(DE-600)1498423-4
|t Neuroscience
|v 163
|y 2009
|x 0306-4522
856 7 _ |u http://dx.doi.org/10.1016/j.neuroscience.2009.07.067
909 C O |o oai:juser.fz-juelich.de:6000
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920 1 _ |0 I:(DE-82)080010_20140620
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