We are also using fMRI in humans to examine the regions of the forebrain mediating stress and cardiovascular dysfunction. Our research has demonstrated that several conditions have direct implications for the rate of mortality following a stroke, including age, hypertension, and the side of the brain affected. We are investigating the specific sites in the brain and the role of various neurotransmitters and neuropeptides that might be involved in mediating these cardiac abnormalities. In particular, there are neuropeptide and catecholaminergic changes in the neurons located in the area surrounding the infarct that function to limit the spread of the damage due to ischemia. We are using both animal models of stroke and cell culture techniques to investigate the mechanisms by which these compounds can prevent neurodegeneration.
Peptide changes in the parabrachial nucleus following cervical vagal stimulation .
Cardiovascular responses to stress following middle cerebral artery occlusion in the rat. Complementary antihypertensive action of rilmenidine on the pressure natiuresis relationship and sodium preference in spontaneously hypertensive rats. Rilmenidine elevates cytosolic free calcium concentration in cerebral astrocytes. Neurotransmitters in the lateral hypothalamic area mediating insular cortex sympathetic responses. Neuropeptide Y-Y1 receptor antisense oligonceleotide increases the infaract volume after middle cerebral artery occlusion in rats.