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Efrain C. AzmitiaBiologyMolecular Neuroplasticity
Go to my homepage in Biology. Depression is associated with affective and cognitive disorders. Some of these symptoms may be due to changes in hippocampal and cortical morphology (cytoskeletal collapse) induced by loss of serotonin (5-HT). Loss of 5-HT in the adult rat brain produces decreased dendritic length, spine number and size, synapse number and reduction in neuronal and glial markers. Injection with a 5-HT1A antagonist produces similar loss of synapses and dendritic spines. The loss of neuronal and glial markers is reversed by treatment with 5-HT1A agonist. Our long-term aim is to test the hypothesis that the 5-HT1A receptor stabilizes the neuronal cytoskeleton, protects neurons from death, and induces neurogenesis. Other studies focus on the effects of 5-HT drugs on morphological reversal after 5-HT loss. Specifically, we would like to test if 5-HT1A receptor stimulation or S100b treatment will restore the cytoskeleton after exposure to colchicine, which promotes microtubule disassembly and apoptosis. Methods used in our laboratory include tissue culture, computer-assisted morphometry, immunocytochemistry, and automated computer-programmed time-lapse microscopy. We work extensively with outside collaborators, including: Patricia Whitaker at SUNY Stony Brook to study transgenic mice using behavioral and developmental techniques; Mony DeLeon at NYU Medical Center to study the blood of Alzheimer patients for protein markers of neurodegenration; and Probal Banerjee at SUNY Staten Island on dual insertion of separately inducible 5-HT receptors in single cells. These studies allow us to broaden our research program from clinical to molecular biology while remaining focused on our research program in molecular neuroplasticity and the role of 5-HT receptors and glial cells. Email: efrain.azmitia@nyu.edu Selected Publications
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