Department of Neurology, University of Miami School Of Medicine, Miami, Florida

The 'wobbler' mouse is considered a model of motor neuron disease.

Objective

To determine whether HBOT may protect brain mitochondria and delay the onset of motor neuron disease in this animal model.

Methods

Mitochondrial physiology in non-synaptic mitochondrial isolated from the 'motor cortex' of the mice in non-treated and in hyperbaric oxygen treated mice.

We treated mice with HBOT (2 ATA) for 60-minutes 6-days a week for 30 and 180 days consecutively for mitochondrial and neurological studies respectively.

Results

In non-synaptic mitochondrial isolated from the motor cortex, the rate of oxygen consumption for complex IV was 38% (P~0.02) higher in both the control mice and the hyperbaric treated mice than the untreated mice.

To study neurological deficits, litters were clinically examined for symptoms of motor neuron disease with the disability scale described earlier. The onset of the disease averaged 33 and 60 days in the untreated and in the hyperbaric group respectively (n=7).

Conclusions

From these studies we conclude that hyperbaric oxygen therapy greatly delays the onset of the disease in the mice study and significantly ameliorates mitochondrial dysfunction in the motor cortex of the mice study.