PMID- 23396085
OWN - NLM
STAT- MEDLINE
DCOM- 20130923
LR  - 20220316
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 237
DP  - 2013 May 1
TI  - BDNF receptor blockade hinders the beneficial effects of exercise in a rat model 
      of Parkinson's disease.
PG  - 118-29
LID - S0306-4522(13)00104-8 [pii]
LID - 10.1016/j.neuroscience.2013.01.060 [doi]
AB  - Physical exercise is known to produce beneficial effects to the nervous system. 
      In most cases, brain-derived neurotrophic factor (BDNF) is involved in such 
      effects. However, little is known on the role of BDNF in exercise-related effects 
      on Parkinson's disease (PD). The aim of this study was to investigate the effects 
      of intermittent treadmill exercise-induced behavioral and 
      histological/neurochemical changes in a rat model of unilateral PD induced by 
      striatal injection of 6-hydroxydopamine (6-OHDA), and the role of BDNF in the 
      exercise effects. Adult male Wistar rats were divided into two main groups: (1) 
      injection of K252a (a blocker of BDNF receptors), and (2) without BDNF receptor 
      blockade. These groups were then subdivided into four groups: control (CLT), 
      sedentary (SED, non-exercised with induction of PD), exercised 3x/week during 
      four weeks before and four weeks after the induction of PD (EXB+EXA), and 
      exercised 3x/week during four weeks after the induction of PD (EXA). One month 
      after 6-OHDA injections, the animals were subjected to rotational behavioral test 
      induced by apomorphine and the brains were collected for immunohistochemistry and 
      immunoblotting assays, in which we measured BDNF and tyrosine hydroxylase (TH) in 
      the substantia nigra pars compacta (SNc) and the striatum (caudate-putamen, CPu). 
      Our results showed a significant reduction of rotational asymmetry induced by 
      apomorphine in the exercised parkinsonian rats. BDNF decreased in the SNc of the 
      SED group, and exercise was able to revert that effect. Exercised groups 
      exhibited reduced damage to the dopaminergic system, detected as a decreased drop 
      of TH levels in SNc and CPu. On the other hand, BDNF blockade was capable of 
      substantially reducing TH expression postlesion, implying enhanced dopaminergic 
      cell loss. Our data revealed that physical exercise is capable of reducing the 
      damage induced by 6-OHDA, and that BDNF receptors are involved in that effect.
CI  - Copyright (c) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Real, C C
AU  - Real CC
AD  - Laboratory of Cellular Neurobiology, Department of Physiology and Biophysics, 
      University of Sao Paulo, Sao Paulo, SP 05508-000, Brazil. careal@icb.usp.br
FAU - Ferreira, A F B
AU  - Ferreira AF
FAU - Chaves-Kirsten, G P
AU  - Chaves-Kirsten GP
FAU - Torrao, A S
AU  - Torrao AS
FAU - Pires, R S
AU  - Pires RS
FAU - Britto, L R G
AU  - Britto LR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130208
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Carbazoles)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Indole Alkaloids)
RN  - 8HW4YBZ748 (Oxidopamine)
RN  - 97161-97-2 (staurosporine aglycone)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - N21FAR7B4S (Apomorphine)
SB  - IM
EIN - Neuroscience. 2013 Sep 5;247:319-20
MH  - Analysis of Variance
MH  - Animals
MH  - Apomorphine
MH  - Carbazoles/pharmacology
MH  - Corpus Striatum/drug effects/physiology
MH  - Disease Models, Animal
MH  - Enzyme Inhibitors/pharmacology
MH  - Exercise Test
MH  - Exercise Therapy/*methods
MH  - Gene Expression Regulation/drug effects
MH  - Indole Alkaloids/pharmacology
MH  - Male
MH  - Oxidopamine/toxicity
MH  - Parkinson Disease/etiology/*rehabilitation
MH  - Putamen/drug effects/physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, trkB/*metabolism
MH  - Stereotyped Behavior/drug effects
MH  - Time Factors
MH  - Tyrosine 3-Monooxygenase/metabolism
EDAT- 2013/02/12 06:00
MHDA- 2013/09/24 06:00
CRDT- 2013/02/12 06:00
PHST- 2012/12/05 00:00 [received]
PHST- 2013/01/21 00:00 [revised]
PHST- 2013/01/22 00:00 [accepted]
PHST- 2013/02/12 06:00 [entrez]
PHST- 2013/02/12 06:00 [pubmed]
PHST- 2013/09/24 06:00 [medline]
AID - S0306-4522(13)00104-8 [pii]
AID - 10.1016/j.neuroscience.2013.01.060 [doi]
PST - ppublish
SO  - Neuroscience. 2013 May 1;237:118-29. doi: 10.1016/j.neuroscience.2013.01.060. 
      Epub 2013 Feb 8.