PMID- 18479829
OWN - NLM
STAT- MEDLINE
DCOM- 20080829
LR  - 20220321
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 154
IP  - 2
DP  - 2008 Jun 23
TI  - Voluntary exercise or amphetamine treatment, but not the combination, increases 
      hippocampal brain-derived neurotrophic factor and synapsin I following cortical 
      contusion injury in rats.
PG  - 530-40
LID - 10.1016/j.neuroscience.2008.04.003 [doi]
AB  - Prior work has shown that d-amphetamine (AMPH) treatment or voluntary exercise 
      improves cognitive functions after traumatic brain injury (TBI). In addition, 
      voluntary exercise increases levels of brain-derived neurotrophic factor (BDNF). 
      The current study was conducted to determine how AMPH and exercise treatments, 
      either alone or in combination, affect molecular events that may underlie 
      recovery following controlled cortical impact (CCI) injury in rats. We also 
      determined if these treatments reduced injury-induced oxidative stress. Following 
      a CCI or sham injury, rats received AMPH (1 mg/kg/day) or saline treatment via an 
      ALZET pump and were housed with or without access to a running wheel for 7 days. 
      CCI rats ran significantly less than sham controls, but exercise level was not 
      altered by drug treatment. On day 7 the hippocampus ipsilateral to injury was 
      harvested and BDNF, synapsin I and phosphorylated (P) -synapsin I proteins were 
      quantified. Exercise or AMPH alone significantly increased BDNF protein in sham 
      and CCI rats, but this effect was lost with the combined treatment. In 
      sham-injured rats synapsin I increased significantly after AMPH or exercise, but 
      did not increase after combined treatment. Synapsin levels, including the 
      P-synapsin/total synapsin ratio, were reduced from sham controls in the 
      saline-treated CCI groups, with or without exercise. AMPH treatment significantly 
      increased the P-synapsin/total synapsin ratio after CCI, an effect that was 
      attenuated by combining AMPH with exercise. Exercise or AMPH treatment alone 
      significantly decreased hippocampal carbonyl groups on oxidized proteins in the 
      CCI rats, compared with saline-treated sedentary counterparts, but this reduction 
      in a marker of oxidative stress was not found with the combination of exercise 
      and AMPH treatment. These results indicate that, whereas exercise or AMPH 
      treatment alone may induce plasticity and reduce oxidative stress after TBI, 
      combining these treatments may cancel each other's therapeutic effects.
FAU - Griesbach, G S
AU  - Griesbach GS
AD  - Division of Neurosurgery, Department of Surgery, David Geffen School of Medicine 
      at UCLA, Box 957039, Los Angeles, CA 90095-7039, USA. ggriesbach@mednet.ucla.edu
FAU - Hovda, D A
AU  - Hovda DA
FAU - Gomez-Pinilla, F
AU  - Gomez-Pinilla F
FAU - Sutton, R L
AU  - Sutton RL
LA  - eng
GR  - R01 NS027544-10A2/NS/NINDS NIH HHS/United States
GR  - R21 NS048535/NS/NINDS NIH HHS/United States
GR  - NS048535/NS/NINDS NIH HHS/United States
GR  - R21 NS048535-02/NS/NINDS NIH HHS/United States
GR  - R01 NS050465-03/NS/NINDS NIH HHS/United States
GR  - R01 NS050465/NS/NINDS NIH HHS/United States
GR  - NS27544/NS/NINDS NIH HHS/United States
GR  - R21 NS048535-01A1/NS/NINDS NIH HHS/United States
GR  - R01 NS027544-12/NS/NINDS NIH HHS/United States
GR  - NS50465/NS/NINDS NIH HHS/United States
GR  - R01 NS027544/NS/NINDS NIH HHS/United States
GR  - R01 NS050465-04/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20080409
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Central Nervous System Stimulants)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Synapsins)
RN  - CK833KGX7E (Amphetamine)
SB  - IM
MH  - Amphetamine/*pharmacology
MH  - Animals
MH  - Blotting, Western
MH  - Brain Injuries/*metabolism/pathology
MH  - Brain-Derived Neurotrophic Factor/*biosynthesis
MH  - Central Nervous System Stimulants/*pharmacology
MH  - Hippocampus/*metabolism/pathology
MH  - Male
MH  - Motor Activity/*physiology
MH  - Nerve Tissue Proteins/metabolism
MH  - *Neuroprotective Agents
MH  - Oxidation-Reduction
MH  - Oxidative Stress/drug effects/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Synapsins/*biosynthesis
MH  - Up-Regulation/drug effects/physiology
PMC - PMC2441485
MID - NIHMS49609
EDAT- 2008/05/16 09:00
MHDA- 2008/08/30 09:00
PMCR- 2008/06/27
CRDT- 2008/05/16 09:00
PHST- 2008/01/07 00:00 [received]
PHST- 2008/04/01 00:00 [revised]
PHST- 2008/04/02 00:00 [accepted]
PHST- 2008/05/16 09:00 [pubmed]
PHST- 2008/08/30 09:00 [medline]
PHST- 2008/05/16 09:00 [entrez]
PHST- 2008/06/27 00:00 [pmc-release]
AID - S0306-4522(08)00538-1 [pii]
AID - 10.1016/j.neuroscience.2008.04.003 [doi]
PST - ppublish
SO  - Neuroscience. 2008 Jun 23;154(2):530-40. doi: 10.1016/j.neuroscience.2008.04.003. 
      Epub 2008 Apr 9.