The effects of DHA on GDNF and NTN in a rat model of Parkinson disease
-
1
Akdeniz University School of Medicine, Department of Histology and Embryology, Türkiye
-
2
Akdeniz University School of Medicine, Türkiye
Parkinson’s disease (PD), is the second most common neurodegenerative disorder after Alzheimer’s disease. In PD, it is shown that the cell death and degenaration in substantia nigra (SN) mostly depends on age and that the reason of decrease is the concentration of the polyunsaturated fatty acid (PUFA) in the cell membrane. Supplementation of the diet with these PUFAs, may help to delay changes associated with neurodegenerative diseases such as PD. Docosahexaenoic acid (DHA) is the major PUFA in the phospholipids fraction of the brain and is required for normal cellular function. Maintaining concentrations of this PUFA is essential for enhanced cognitive, learning and memory functions. Neurodegenerative disorders, often exhibit significant declines in DHA and other PUFAs, which may in part, contribute to some of the observed declines in brain functions. Considerable effort has been devoted to the search for molecules that might exert trophic influences on midbrain dopamine neurons, and pottentially be of therapeutic value in the treatment of PD. GDNF (glial-cell-line-derived neurotrophic factor) and NTN (neurturin) are very potent trophic factors for PD. GDNF promotes recovery of the injured nigrostriatal dopamine system and improves motor functions in rodent and nonhuman primate models of PD. Both GDNF and its recently discovered congener, NTN, have been shown to exert neuroprotective effects on lesioned nigral dopamine neurons. The aim of the study is to evaluate the neuroprotective effects of GDNF and NTN by investigating their expression levels after administration of DHA to a rat model of PD. For this reason we hypothesized that DHA administered to a rat model of PD might alter GDNF, and NTN expression in SN. In this study 1-methyl-4-phenyl-1, 2, 3, 6-tetrahdropyridine (MPTP) neurotoxin that induces dopaminergic neurodegeneration was used to create a Parkinson’s model. The rats were divided into; control, DHA-treated, Parkinson-induced, Parkinson-induced + DHA-treated groups. In the DHA-treated groups, DHA was supplied daily by gavage for 4 weeks; in PD groups MPTP was microinjected bilaterally into SN. Seven days after the creation of PD, model motor activity and balance determination of the rats was investigated by the “vertical pole” and “vertical wire” tests. We used immunohistochemical technique for explaining the changes. Dopaminergic neuron numbers were clearly decreased in Parkinson induced groups but showed on increase in Parkinson induced+DHA treated groups. As a result of this, DHA administration recovered dopaminergic neurons as shown by tyrosine hydroxylase immunohistochemistry. In these two groups, GDNF and NTN immunoreaction in dopaminergic neurons were higher than that of the normal healty groups. In conclusion, the characterization of GDNF and NTN will certainly help elucidate the mechanism of GDNF action, and lead to better strategies for the use of GDNF to treat neurodegenerative diseases. While the knowledge on the therapeutic potential of neurotrophic factors such as GDNF and NTN is still contradictory, it should be known that we are only at the beginning of the story.
Conference:
10th International Conference on Cognitive Neuroscience, Bodrum, Türkiye, 1 Sep - 5 Sep, 2008.
Presentation Type:
Poster Presentation
Topic:
Animal Models of Cognition
Citation:
Tanriöver
G,
Seval
Y,
Kose
O,
Akkoyunlu
G,
Savcioglu
F,
Demir
N and
Agar
A
(2008). The effects of DHA on GDNF and NTN in a rat model of Parkinson disease.
Conference Abstract:
10th International Conference on Cognitive Neuroscience.
doi: 10.3389/conf.neuro.09.2009.01.081
Copyright:
The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers.
They are made available through the Frontiers publishing platform as a service to conference organizers and presenters.
The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated.
Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed.
For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions.
Received:
02 Dec 2008;
Published Online:
02 Dec 2008.
*
Correspondence:
Gamze Tanriöver, Akdeniz University School of Medicine, Department of Histology and Embryology, Antalya, Türkiye, gamzetanriover@yahoo.com