Presentation Title

MITOCHONDRIAL REGULATION OF CALCIUM AND ELECTRICAL SIGNALING IN THE CARDIOVASCULAR AND NERVOUS SYSTEMS WITH ADVANCING AGE

Presenter Information

Briana Hickey, CSUSBFollow

Start Date

November 2016

End Date

November 2016

Location

HUB 302-31

Type of Presentation

Poster

Abstract

Old age (i.e., >60 years) is the key risk factor for the development of cardiovascular disease and cognitive decline. Despite the well-known cooperation between components of cerebral perfusion and neuronal activity, such functions are not commonly integrated for investigation. Furthermore, we now recognize the vulnerability of the regulation of calcium homeostasis and alterations in cellular membrane potential (Vm) with advancing age, whereby mitochondria play a central role. Thus, we are testing the hypothesis that the mitochondrial calcium uniporter (MCU) may regulate the interface between calcium homeostasis and regulation of cellular membrane potential (Vm) throughout cardiovascular and neuronal systems with advancing age. Regions of intact cortex, hippocampus, superior cervical ganglia, heart, cerebral arteries, and endothelial “tubes” are freshly isolated from C57BL/6 mice (age: 4 to 26 months, male and female). Molecular analyses include protein measurements of the MCU via Western Blot and immunofluorescence. Physiological assessments (+/- pharmacological stimulation and block of MCU) include simultaneous photometric measurements of calcium/reactive oxygen species and sharp electrode determinations of intracellular membrane potential and cell-to-cell coupling through gap junctions in freshly isolated and intact tissues. Also, we will examine mouse models of Alzheimer’s Disease (e.g., 3xTg-AD, 5XFAD; fully develop pathology by middle age) and mitochondrial-targeted catalase mice (mCAT; readily decompose cellular hydrogen peroxide & live ≈5 months longer vs. normal C57BL/6) as negative and positive controls for healthy aging respectively. Resolving interactions between cardiovascular and neuronal function in the context of mitochondrial calcium signaling will enable our efforts to ameliorate neurodegeneration and a diminished quality of life with aging.

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Nov 12th, 1:00 PM Nov 12th, 2:00 PM

MITOCHONDRIAL REGULATION OF CALCIUM AND ELECTRICAL SIGNALING IN THE CARDIOVASCULAR AND NERVOUS SYSTEMS WITH ADVANCING AGE

HUB 302-31

Old age (i.e., >60 years) is the key risk factor for the development of cardiovascular disease and cognitive decline. Despite the well-known cooperation between components of cerebral perfusion and neuronal activity, such functions are not commonly integrated for investigation. Furthermore, we now recognize the vulnerability of the regulation of calcium homeostasis and alterations in cellular membrane potential (Vm) with advancing age, whereby mitochondria play a central role. Thus, we are testing the hypothesis that the mitochondrial calcium uniporter (MCU) may regulate the interface between calcium homeostasis and regulation of cellular membrane potential (Vm) throughout cardiovascular and neuronal systems with advancing age. Regions of intact cortex, hippocampus, superior cervical ganglia, heart, cerebral arteries, and endothelial “tubes” are freshly isolated from C57BL/6 mice (age: 4 to 26 months, male and female). Molecular analyses include protein measurements of the MCU via Western Blot and immunofluorescence. Physiological assessments (+/- pharmacological stimulation and block of MCU) include simultaneous photometric measurements of calcium/reactive oxygen species and sharp electrode determinations of intracellular membrane potential and cell-to-cell coupling through gap junctions in freshly isolated and intact tissues. Also, we will examine mouse models of Alzheimer’s Disease (e.g., 3xTg-AD, 5XFAD; fully develop pathology by middle age) and mitochondrial-targeted catalase mice (mCAT; readily decompose cellular hydrogen peroxide & live ≈5 months longer vs. normal C57BL/6) as negative and positive controls for healthy aging respectively. Resolving interactions between cardiovascular and neuronal function in the context of mitochondrial calcium signaling will enable our efforts to ameliorate neurodegeneration and a diminished quality of life with aging.