Maria Braga, Ph.D.

Research Assistant Professor
Department of Psychiatry
F.Edward Hebert School of Medicine
Uniformed Services University of the Health Sciences

Dr. Braga is currently an Assistant Professor in the Department of Anatomy, Physiology and Genetics at the Uniformed Services University of the Heath Sciences. She received her PhD in Physiology and Pharmacology at the University of Strathclyde in Scotland in 1993. Her other positions have included Postdoctoral Fellow in the Department of Pharmacology and Experimental Therapeutics at the University of Maryland – School of Medicine, and Research Assistant Professor in the Department of Psychiatry, USUHS.

Here at USUHS, she has been conducting studies on the cellular and molecular mechanisms regulation neuronal excitability in the amygdala, and the pathophysiology of anxiety disorders and epilepsy. Neuronal excitability in the brain is determined by the balance of excitatory synaptic transmission — primarily glutamatergic- and inhibitory synaptic transmission — primarily GABAergic. This balance is maintained by a number of regulatory mechanisms, involving neurotransmitters and neuromodulators acting on their receptors on somatodendritic neuronal regions, where they modulate neuronal responses to synaptic input, or on presynaptic neuronal terminals, where they directly modulate neurotransmitter release. Physical brain insult, such as stroke or head injury, or emotional insult, such as excessive stress, can significantly disturb the balance between neuronal excitation and inhibition. Depending on the severity of this disturbance, as well as on the brain region(s) where it occurs, epilepsy, or psychiatric disorders may develop. The amygdala, a brain region in the temporal lobe, plays a key role on epileptogenesis, as well as on a host of psychiatric illnesses. Yet, there is very limited information on the mechanisms regulating neuronal excitability in the amygdala. We recently identified two important mechanisms regulating GABAergic synaptic transmission in the amygdala. These mechanisms involve a direct regulation of GABA release by presynaptic GluR5 kainate receptors and a1A adrenoceptors. We have also obtained evidence for the clinical significance of these findings. The long-term goal of her research program is to provide the basic knowledge that is crucial for the development of effective therapeutic strategies aimed at preventing or treating neurological and psychiatric disorders involving the amygdala.