Can exercise help repair the FASD brain?. UBC Campus, Vancouver. UBC/UVIC Campus, Victoria. Brian Christie, Division of Medical Sciences. Department of Psychology. UBC - Cellular and Physiological Sciences UVIC - Division of Medical Sciences. Studying the brain. 100 billion neurons.
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UBC Campus, Vancouver
UBC/UVIC Campus, Victoria
Division of Medical Sciences
Department of Psychology
UBC - Cellular and Physiological Sciences
UVIC - Division of Medical Sciences
100 billion neurons
Each neuron has 1000 to 10000 synapses
Do these new cells have a purpose?
Does prenatal ethanol exposure affect them?
Animals that exercise:
Can we use this knowledge to do something positive?
1. There is cell loss in the Hippocampus of offspring following prenatal ethanol exposure.
2. Hippocampal cells do not appear to be fully mature.
3. Animals (including humans) exposed to ethanol exhibit impaired learning.
4. Neurons in the brain do not communicate as well as they should.
Can exercise rescue animals from the deleterious effects of PNEE?
Ethanol exposure in the first two trimesters:
Pair-fed, No Ethanol
Ad Libitum (no diet, no alcohol)
Gestation Day 1
Female rats become
begin prenatal feeding
or ad libitum diet).
Postnatal Day 1
Special diets end.
Pups are born.
Litters are culled to 10
(5 m and 5 f).
Postnatal Day 22
Pups are weaned
and housed individually in either normal cages
or cages containing an exercise wheel
according to sex and prenatal diet.
Never drink themselves
* Note this is the equivalent of drinking in G1 and G2 only.
BehaviouralTesting in the offspring when they are adults (P50-60).
Hippocampal Long-Term Potentiation:A Biological Mechanism for Learning and Memory.
Increase in Slope
LTP Induced at Synapses in Conditioned Pathway only.
Normal adult animals show more LTP when they are allowed to exercise.
Pair-fed animals also show more LTP when they are allowed to exercise.
PNEE animals also show more LTP when they are allowed to exercise!
After exercising, PNEE animals do slightly better than normal “non-exercising” animals.
Mean # BrdU cells/hpc
Wang and Wojtowicz, 2000
Eadieet al., 2005
Redila et al., 2006
Lipid peroxidationFASD and Oxidative Stress
Impaired membrane fluidity
4HNE and MDA
Protein and DNA adducts
Altered cell signalling
Cognitive and Behavioural Problems
Average BAC Level in Ethanol exposed dams on GD15: 103g/dl
Does prenatal ethanol exposure alter the capacity of the brain to handle oxidative stress?
If the body is exposed to a toxin such as alcohol then GST can bind GSH to the toxin and create a detoxified compound that can then be excreted from the system
- Metabolism of alcohol
GR: Glutathione Reductase
GPx: Glutathione Peroxidase
GSSG: Glutathione disulfide
Ad Libitum control
** = p < 0.001
Does Omega-3 fatty acid supplementation enhance glutathione levels and reduce oxidative stress?
Solid = Regular Diet
Stripes = Omega-3
* = p < 0.05
** = p < 0.001
MDA = malondialdehyde (lipid peroxidation product)
Theta burst stimulation (TBS)
fEPSP slope (% change)
Ad Libitum control, n=17
Ad libitum control, n=17
Ethanol+ omega-3, n=17
(Serrano and Klann, 2004; Auerbach and Segal 1997; Pellmaret al., 1991)
(Almaguer-Milan et al., 2000; Steulletet al., 2006)
(Robillardet al., 2011)
(Janaky 1999; Tan and Aizermann 1993; Ogita 1995)