D
Deniz Kirik
Researcher at Lund University
Publications - 189
Citations - 18127
Deniz Kirik is an academic researcher from Lund University. The author has contributed to research in topics: Substantia nigra & Dopamine. The author has an hindex of 64, co-authored 182 publications receiving 16897 citations. Previous affiliations of Deniz Kirik include University of Freiburg & Centre national de la recherche scientifique.
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Neuronal replacement from endogenous precursors in the adult brain after stroke
TL;DR: It is shown that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone, and stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion.
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Parkinson-like neurodegeneration induced by targeted overexpression of alpha-synuclein in the nigrostriatal system.
Deniz Kirik,Carl Rosenblad,Corinna Burger,Cecilia Lundberg,Teit E. Johansen,Nicholas Muzyczka,Ronald J. Mandel,Anders Björklund +7 more
TL;DR: It is shown that nigral dopamine neurons are selectively vulnerable to high levels of either wild-type or mutant α-synuclein, pointing to a key role for α- Synuclein in the pathogenesis of Parkinson's disease.
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Characterization of behavioral and neurodegenerative changes following partial lesions of the nigrostriatal dopamine system induced by intrastriatal 6-hydroxydopamine in the rat
TL;DR: The results indicate that the four-site intrastriatal 6-OHDA lesion may be a relevant model of the neuropathology seen in parkinsonian patients in a manifest symptomatic stage of the disease and may be particularly useful experimentally since it leaves a significant portion of the nigrostriatal projection intact which can serve as a substrate for regeneration and functional recovery in response to growth promoting and neuroprotective agents.
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Pharmacological validation of behavioural measures of akinesia and dyskinesia in a rat model of Parkinson's disease.
Martin Lundblad,Malin Andersson,Christian Winkler,Christian Winkler,Deniz Kirik,Nils Wierup,M. A. Cenci +6 more
TL;DR: It is demonstrated that 6‐OHDA‐lesioned rats do exhibit motor deficits that share essential functional similarities with parkinsonian akinesia or dyskinesia, and can be quantified using novel and relatively simple testing procedures, whereas rotometry cannot discriminate between dyskinetic and antiakinetic effects of antiparkinsonian treatments.
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Dopamine released from 5-HT terminals is the cause of L-DOPA-induced dyskinesia in parkinsonian rats.
TL;DR: It is shown that dyskinesia induced by chronic L-DOPA treatment in rats with 6-hydroxydopamine-induced lesions of the nigrostriatal dopamine pathway is critically dependent on the integrity and function of the serotonergic system.