Home > Publications database > Pentylenetetrazole-induced seizures affect binding site densities for GABA, glutamate and adenosine receptors in the rat brain > print

001     5513
005     20180208194813.0
024 7 _ |2 pmid
|a pmid:19345722
024 7 _ |2 DOI
|a 10.1016/j.neuroscience.2009.03.068
024 7 _ |2 WOS
|a WOS:000269404600044
037 _ _ |a PreJuSER-5513
041 _ _ |a eng
082 _ _ |a 610
084 _ _ |2 WoS
|a Neurosciences
100 1 _ |a Cremer, C.M.
|b 0
|u FZJ
|0 P:(DE-Juel1)VDB71164
245 _ _ |a Pentylenetetrazole-induced seizures affect binding site densities for GABA, glutamate and adenosine receptors in the rat brain
260 _ _ |a Amsterdam [u.a.]
|b Elsevier Science
|c 2009
300 _ _ |a 490 - 499
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|0 0
|2 EndNote
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a article
|2 DRIVER
440 _ 0 |a Neuroscience
|x 0306-4522
|0 4579
|y 1
|v 163
500 _ _ |a Record converted from VDB: 12.11.2012
520 _ _ |a Pentylenetetrazole (PTZ) is a convulsant used to model epileptic seizures in rats. In the PTZ-model, altered heat shock protein 27 (HSP-27) expression highlights seizure-affected astrocytes, which play an important role in glutamate and GABA metabolism. This raises the question whether impaired neurotransmitter metabolism leads to an imbalance in neurotransmitter receptor expression. Consequently, we investigated the effects of seizures on the densities of seven different neurotransmitter receptors in rats which were repeatedly treated with PTZ (40 mg/kg) over a period of 14 days. Quantitative in vitro receptor autoradiography was used to measure the regional binding site densities of the glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate and N-methyl-D-aspartate (NMDA) receptors, the adenosine receptor type 1 (A(1)), which is part of the system controlling glutamate release, and the gamma-aminobutyric acid (GABA) receptors GABA(A) and GABA(B) as well as the GABA(A)-associated benzodiazepine (BZ) binding sites in each rat. Our results demonstrate altered receptor densities in brain regions of PTZ-treated animals, including the HSP-27 expressing foci (i.e. amygdala, piriform and entorhinal cortex, dentate gyrus). A general decrease of kainate receptor densities was observed together with an increase of NMDA binding sites in the hippocampus, the somatosensory, piriform and the entorhinal cortices. Furthermore, A(1) binding sites were decreased in the amygdala and hippocampal CA1 region (CA1), while BZ binding sites were increased in the dentate gyrus and CA1. Our data demonstrate the impact of PTZ induced seizures on the densities of kainate, NMDA, A(1) and BZ binding sites in epileptic brain. These changes are not restricted to regions showing glial impairment. Thus, an altered balance between different excitatory (NMDA) and modulatory receptors (A(1), BZ binding sites, kainate) shows a much wider regional distribution than that of glial HSP-27 expression, indicating that receptor changes are not following the glial stress responses, but may precede the HSP-27 expression.
536 _ _ |a Funktion und Dysfunktion des Nervensystems
|c P33
|2 G:(DE-HGF)
|0 G:(DE-Juel1)FUEK409
|x 0
588 _ _ |a Dataset connected to Web of Science, Pubmed
650 _ 2 |2 MeSH
|a Animals
650 _ 2 |2 MeSH
|a Binding Sites: drug effects
650 _ 2 |2 MeSH
|a Binding Sites: physiology
650 _ 2 |2 MeSH
|a Binding, Competitive: drug effects
650 _ 2 |2 MeSH
|a Binding, Competitive: physiology
650 _ 2 |2 MeSH
|a Brain: anatomy & histology
650 _ 2 |2 MeSH
|a Brain: metabolism
650 _ 2 |2 MeSH
|a Brain: physiopathology
650 _ 2 |2 MeSH
|a Convulsants: pharmacology
650 _ 2 |2 MeSH
|a Disease Models, Animal
650 _ 2 |2 MeSH
|a Epilepsy: chemically induced
650 _ 2 |2 MeSH
|a Epilepsy: metabolism
650 _ 2 |2 MeSH
|a Epilepsy: physiopathology
650 _ 2 |2 MeSH
|a HSP27 Heat-Shock Proteins: drug effects
650 _ 2 |2 MeSH
|a HSP27 Heat-Shock Proteins: metabolism
650 _ 2 |2 MeSH
|a Male
650 _ 2 |2 MeSH
|a Neuroglia: metabolism
650 _ 2 |2 MeSH
|a Pentylenetetrazole: pharmacology
650 _ 2 |2 MeSH
|a Rats
650 _ 2 |2 MeSH
|a Rats, Wistar
650 _ 2 |2 MeSH
|a Receptor, Adenosine A1: drug effects
650 _ 2 |2 MeSH
|a Receptor, Adenosine A1: metabolism
650 _ 2 |2 MeSH
|a Receptors, AMPA: drug effects
650 _ 2 |2 MeSH
|a Receptors, AMPA: metabolism
650 _ 2 |2 MeSH
|a Receptors, GABA: metabolism
650 _ 2 |2 MeSH
|a Receptors, GABA-A: drug effects
650 _ 2 |2 MeSH
|a Receptors, GABA-A: metabolism
650 _ 2 |2 MeSH
|a Receptors, GABA-B: drug effects
650 _ 2 |2 MeSH
|a Receptors, GABA-B: metabolism
650 _ 2 |2 MeSH
|a Receptors, Glutamate: metabolism
650 _ 2 |2 MeSH
|a Receptors, Kainic Acid: drug effects
650 _ 2 |2 MeSH
|a Receptors, Kainic Acid: metabolism
650 _ 2 |2 MeSH
|a Receptors, N-Methyl-D-Aspartate: drug effects
650 _ 2 |2 MeSH
|a Receptors, N-Methyl-D-Aspartate: metabolism
650 _ 2 |2 MeSH
|a Receptors, Purinergic P1: metabolism
650 _ 2 |2 MeSH
|a Stress, Physiological: physiology
650 _ 2 |2 MeSH
|a Synaptic Transmission: drug effects
650 _ 2 |2 MeSH
|a Synaptic Transmission: physiology
650 _ 7 |0 0
|2 NLM Chemicals
|a Convulsants
650 _ 7 |0 0
|2 NLM Chemicals
|a HSP27 Heat-Shock Proteins
650 _ 7 |0 0
|2 NLM Chemicals
|a Hspb1 protein, rat
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptor, Adenosine A1
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, AMPA
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, GABA
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, GABA-A
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, GABA-B
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, Glutamate
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, Kainic Acid
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, N-Methyl-D-Aspartate
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, Purinergic P1
650 _ 7 |0 54-95-5
|2 NLM Chemicals
|a Pentylenetetrazole
650 _ 7 |a J
|2 WoSType
653 2 0 |2 Author
|a epilepsy
653 2 0 |2 Author
|a animal model
653 2 0 |2 Author
|a neurotransmitter receptors
653 2 0 |2 Author
|a PTZ
700 1 _ |a Palomero-Gallagher, N.
|b 1
|u FZJ
|0 P:(DE-Juel1)VDB1208
700 1 _ |a Bidmon, H.-J.
|b 2
|0 P:(DE-HGF)0
700 1 _ |a Schleicher, A.
|b 3
|0 P:(DE-HGF)0
700 1 _ |a Speckmann, E.-J.
|b 4
|0 P:(DE-HGF)0
700 1 _ |a Zilles, K.
|b 5
|u FZJ
|0 P:(DE-Juel1)131714
773 _ _ |a 10.1016/j.neuroscience.2009.03.068
|g Vol. 163, p. 490 - 499
|p 490 - 499
|q 163<490 - 499
|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.2009.03.068
909 C O |o oai:juser.fz-juelich.de:5513
|p VDB
913 1 _ |k P33
|v Funktion und Dysfunktion des Nervensystems
|l Funktion und Dysfunktion des Nervensystems
|b Gesundheit
|0 G:(DE-Juel1)FUEK409
|x 0
914 1 _ |y 2009
915 _ _ |0 StatID:(DE-HGF)0010
|a JCR/ISI refereed
920 1 _ |0 I:(DE-Juel1)INM-2-20090406
|k INM-2
|l Molekulare Organisation des Gehirns
|g INM
|x 0
920 1 _ |0 I:(DE-82)080010_20140620
|k JARA-BRAIN
|l Jülich-Aachen Research Alliance - Translational Brain Medicine
|g JARA
|x 1
970 _ _ |a VDB:(DE-Juel1)113128
980 _ _ |a VDB
980 _ _ |a ConvertedRecord
980 _ _ |a journal
980 _ _ |a I:(DE-Juel1)INM-2-20090406
980 _ _ |a I:(DE-82)080010_20140620
980 _ _ |a UNRESTRICTED
981 _ _ |a I:(DE-Juel1)VDB1046

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