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mbraga@usuhs.mil
The Research Program in the laboratory of Dr. Maria Braga (Associate Professor and Principal Investigator).
Our research is centered in a temporal lobe structure called amygdala. The amygdala plays a central role in emotional behavior, as well as in modulating cognitive functions. Accordingly, many emotional/psychiatric disorders are associated with pathophysiological changes in the amygdala. In addition to its role in affective disorders, the amygdala also plays a central role in the pathogenesis and symptomatology of epilepsy. This is mainly because neuronal circuits in the amygdala -and particularly in the basolateral nucleus of the amygdala (BLA)- are exceptionally prone to hyperexcitability, and, therefore, very susceptible to seizure-triggering and/or epileptogenic insults, such as traumatic brain injury, status epilepticus, or exposure to organophosphorous toxins. Our studies are focused on understanding the mechanisms regulating neuronal excitability in the BLA, and finding pharmacological means to exploit these mechanisms in order to prevent and/or treat certain neurological and psychiatric illnesses, namely epileptogenesis, seizure-induced brain damage, and the development of stress-related psychiatric disorders. The broad goal of our research is to provide knowledge that can serve as a basis for the development of effective therapeutic strategies aimed at preventing or treating neurological and psychiatric disorders involving the amygdala. To accomplish this goal we are currently working on the following objectives: 1) To delineate the mechanisms by which kainate receptors containing the GluR5 subunit (GluR5KRs) regulate neuronal excitability in the rodent BLA, and the role that these receptors play in epileptogenesis. 2) To determine the efficacy of the GluR5KR antagonists LY293558 and topiramate, when administered alone or in combination with the anticholinergic agent caramiphen, against Sarin-induced seizures and neuronal damage in the rat brain. 3) To determine the efficacy of the GluR5KR antagonists LY293558 and UBP302 in preventing the induction or blocking the expression of Soman-induced epileptiform activity in the rat amygdala and hippocampus, in vitro, and soman-induced seizures and neuropathology in the rat brain, in vivo. 4) To delineate the mechanisms by which Norepinephrine regulates neuronal excitability in the BLA, and determine the alterations of these mechanisms induced by stress.
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