Alpha-Linolenic Acid Treatment Reduces the Contusion and Prevents the Development of Anxiety-Like Behavior Induced by a Mild Traumatic Brain Injury in Rats

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https://link.springer.com/article/10.1007/s12035-017-0732-y

• Authors
• Authors and affiliations

• Taiza H. Figueiredo
• Carolina L. Harbert
• Volodymyr Pidoplichko
• Camila P. Almeida-Suhett
• Hongna Pan
• Katia Rossetti
• Maria F. M. Braga
• Ann M. MariniEmail author

• 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
  • 2
  Email author

1. 1.Department of Anatomy, Physiology and GeneticsUniformed Services University of the Health SciencesBethesdaUSA
2. 2.Department of Neurology and Program in NeuroscienceUniformed Services University of the Health SciencesBethesdaUSA

Article

First Online:

26 August 2017

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Abstract

Approximately, 1.7 million Americans suffer a TBI annually and TBI is a major cause of death and disability. 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. 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 hyperexcitability 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 GABA_A-receptor-mediated inhibitory postsynaptic currents (IPSCs) in the BLA. Significantly, subchronic treatment with alpha-linolenic acid (ALA) after CCI prevents the development of anxiety-like behavior, the loss of GABAergic interneurons, hyperexcitability in the BLA and reduces the impact injury. Taken together, administration of ALA after CCI is a potent therapy against the neuropathology and pathophysiological effects of mTBI in the BLA.