Alteration of the glutamate signaling in the nucleus tractus solitarii of Alzheimer’s disease-induced rats
Alzheimer’s disease (AD) is a neurodegenerative disease which is predominantly characterized by memory loss, but AD patients also experience problems with blood pressure and breathing control. These cardiorespiratory symptoms may be caused by alterations of brain neuron activity located in the nucleus tractus solitarii (nTS). The nTS integrates signals about changing blood pressure from baroreceptors located at the heart and blood oxygen level from chemoreceptors located in the carotid body. Hyperexcitability, an increase in neuronal activity, is one of the early events in AD pathogenesis and known to contribute to memory loss in AD patients. The aim of this study is to analyze factors influencing activity of nTS neurons using an established AD rodent model. I quantified changes in glutamate transmitter (vGlut2), number of glutamate receptors (GluR2), and glutamate recycling (Glutamate synthetase) using fluorescently labeled antibodies (immunohistochemistry).
Keywords: Alzheimer’s Disease, Glutamate Signaling, nucleus Tractus Solitarii, Cardiorespiratory Dysfunction, Immunohistochemistry
Topic(s):Biology
Biochemistry and Molecular Biology
Presentation Type: Poster Presentation
Session: 2-14
Location: SUB Activities Room
Time: 3:00