PMID- 21071351
OWN - NLM
STAT- MEDLINE
DCOM- 20110301
LR  - 20191210
IS  - 1897-5631 (Electronic)
IS  - 0239-8508 (Linking)
VI  - 48
IP  - 3
DP  - 2010 Sep 30
TI  - The effects of docosahexaenoic acid on glial derived neurotrophic factor and 
      neurturin in bilateral rat model of Parkinson's disease.
PG  - 434-41
LID - 10.2478/v10042-010-0047-6 [doi]
AB  - Parkinson's disease (PD) is the second most common neurodegenerative disorder 
      marked by cell death in the Substantia nigra (SN). Docosahexaenoic acid (DHA) is 
      the major polyunsaturated fatty acid (PUFA) in the phospholipid fraction of the 
      brain and is required for normal cellular function. Glial cell line derived 
      neurotrophic factor (GDNF) and neurturin (NTN) are very potent trophic factors 
      for PD. The aim of the study was to evaluate the neuroprotective effects of GDNF 
      and NTN by investigating their immunostaining levels after administration of DHA 
      in a model of PD. For this reason we hypothesized that DHA administration of PD 
      might alter GDNF, NTN expression in SN. MPTP neurotoxin that induces dopaminergic 
      neurodegeneration was used to create the experimental Parkinsonism model. Rats 
      were divided into; control, DHA-treated (DHA), MPTP-induced (MPTP), 
      MPTP-induced+DHA-treated (MPTP+DHA) groups. Dopaminergic neuron numbers were 
      clearly decreased in MPTP, but showed an increase in MPTP+DHA group. As a result 
      of this, DHA administration protected dopaminergic neurons as shown by tyrosine 
      hydroxylase immunohistochemistry. In the MPTP+DHA group, GDNF, NTN 
      immunoreactions in dopaminergic neurons were higher than that of the MPTP group. 
      In conclusion, the characterization of GDNF and NTN will certainly help elucidate 
      the mechanism of DHA action, and lead to better strategies for the use of DHA to 
      treat neurodegenerative diseases.
FAU - Tanriover, Gamze
AU  - Tanriover G
AD  - Department of Histology and Embryology, Akdeniz University School of Medicine, 
      Antalya, Turkey. ayagar@akdeniz.edu.tr
FAU - Seval-Celik, Yasemin
AU  - Seval-Celik Y
FAU - Ozsoy, Ozlem
AU  - Ozsoy O
FAU - Akkoyunlu, Gokhan
AU  - Akkoyunlu G
FAU - Savcioglu, Feyza
AU  - Savcioglu F
FAU - Hacioglu, Gulay
AU  - Hacioglu G
FAU - Demir, Necdet
AU  - Demir N
FAU - Agar, Aysel
AU  - Agar A
LA  - eng
PT  - Comparative Study
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Poland
TA  - Folia Histochem Cytobiol
JT  - Folia histochemica et cytobiologica
JID - 8502651
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Neurotoxins)
RN  - 0 (Neurturin)
RN  - 25167-62-8 (Docosahexaenoic Acids)
RN  - 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
MH  - Animals
MH  - Disease Models, Animal
MH  - Docosahexaenoic Acids/*pharmacology
MH  - Dopamine/metabolism
MH  - Glial Cell Line-Derived Neurotrophic Factor/adverse 
      effects/*metabolism/pharmacology
MH  - Immunohistochemistry
MH  - Male
MH  - Nerve Degeneration/chemically induced/pathology
MH  - Neurons/drug effects
MH  - Neuroprotective Agents/pharmacology
MH  - Neurotoxins
MH  - Neurturin/adverse effects/*metabolism/pharmacology
MH  - Parkinson Disease, Secondary/*pathology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Substantia Nigra/cytology/metabolism/pathology
MH  - Tyrosine 3-Monooxygenase/immunology/metabolism
EDAT- 2010/11/13 06:00
MHDA- 2011/03/02 06:00
CRDT- 2010/11/13 06:00
PHST- 2010/11/13 06:00 [entrez]
PHST- 2010/11/13 06:00 [pubmed]
PHST- 2011/03/02 06:00 [medline]
AID - H527N45853505537 [pii]
AID - 10.2478/v10042-010-0047-6 [doi]
PST - ppublish
SO  - Folia Histochem Cytobiol. 2010 Sep 30;48(3):434-41. doi: 
      10.2478/v10042-010-0047-6.