Positive Health Online

Abstract

FIGUEIREDO and COLLEAGUES, 1 Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814, USA; 2 Department of Neurology and Program in Neuroscience, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD, 20814, USA; 3 Department of Neurology and Program in Neuroscience, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD, 20814, USA. ann.marini@usuhs.edu studied the effects of cortical impact (CCI) injury in rodents and how treatment with alpha-linolenic acid (ALA) with for CCI prevents neuropathology and pathophysiological effects of mTBI.

Background

Approximately, 1.7 million Americans suffer a Traumatic Brain Injury (TBI) annually and TBI is a major cause of death and disability.

Methodology

The majority of the TBI cases are of the mild type and while most patients recover completely from mild TBI (mTBI) about 10% result in persistent symptoms and some result in lifelong disability. Anxiety disorders are the second most common diagnosis post-TBI. Of note, TBI-induced anxiety disorders are difficult to treat and remain a chronic condition suggesting that new therapies are needed.

Results

Previous work from our laboratory demonstrated that a mild TBI induced an anxiety-like phenotype, a key feature of the human condition, associated with loss of GABAergic interneurons and hyper excitability in the basolateral amygdala (BLA) in rodents 7 and 30 days after a controlled cortical impact (CCI) injury. We now confirm that animals display significantly increased anxiety-like behavior 30 days after CCI. The anxiety-like behavior was associated with a significant loss of GABAergic interneurons and significant reductions in the frequency and amplitude of spontaneous and miniature GABAA-receptor-mediated inhibitory postsynaptic currents (IPSCs) in the BLA. Significantly, sub chronic treatment with alpha-linolenic acid (ALA) after CCI prevents the development of anxiety-like behaviour, the loss of GABAergic interneurons, hyper excitability in the BLA and reduces the impact injury.

Conclusion

Taken together, administration of ALA after CCI is a potent therapy against the neuropathology and pathophysiological effects of mTBI in the BLA.

References

Taiza H Figueiredo  1 , Carolina L Harbert  1 , Volodymyr Pidoplichko  1 , Camila P Almeida-Suhett  1 , Hongna Pan  2 , Katia Rossetti  1 , Maria F M Braga  1 , Ann M Marini  3.  Alpha-Linolenic Acid Treatment Reduces the Contusion and Prevents the Development of Anxiety-Like Behavior Induced by a Mild Traumatic Brain Injury in Rats Mol Neurobiol;55(1):187-200. doi: 10.1007/s12035-017-0732-y. Jan 2018.