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Contenido archivado el 2024-05-27

Interaction between a2a and nmda receptors in parkinson 's disease

Objetivo

The Rudolf-Boehm-Institute of Pharmacology and Toxicology at the University of Leipzig seeks three post-doctoral fellows for a project regarding the co-expression of adenosine A2A and N-methyl-D-aspartate receptor (NMDA) subunits in Parkinson's disease. Whereas the antagonistic interaction between adenosine A2A and dopamine D2 receptors situated at the striatopallidal subpopulation of medium spiny neurons is generally supposed to be involved in the ethiology of Parkinson's disease there is much less knowledge on a recently described antagonistic interaction between NMDA and A2A receptors. Degeneration of dopaminergic neurons and alteration of NMDA receptors appears to be a major pathogenetic feature in Parkinson's disease. Accompanying changes in the function or expression of A2A receptors is a highly important prospective field of research. The investigations will be performed on brain tissue of Parkinson patients and controls, and in a Parkinson model in rats (6-hydroxydopamine (6-OHDA)- lesion of the substantial nigra). The expression of the NMDAR subunits (splice variants) and A2A as well as D2 receptors will be investigated immunohistochemically, by in site hybridization, and by other molecular biological methods dealing with topical aspects. The investigations will take place in the Rudolf-Boehm-Institute of Pharmacology in cooperation with the Department of Neuropathology. All logistic and modern technical facilities are available for a successful completion of the study. Applicants should be qualified in histochemistry and molecular biology and should be interested in neuroscience topics.

Ámbito científico (EuroSciVoc)

Programa(s)

Tema(s)

Datos no disponibles

Convocatoria de propuestas

Datos no disponibles

Régimen de financiación

BUR - Bursaries, grants, fellowships

Coordinador

UNIVERSITAET LEIPZIG
Aportación de la UE
Sin datos
Dirección
Haertelstrasse 16-18
04107 LEIPZIG
Alemania
Coste total
Sin datos