Postdoctoral Research Position Available
Calcium Channel Regulation, Neuroplasticity, Spatial Learning, and Memory
William A. Catterall, Department of Pharmacology and Neuroscience Program
University of Washington, Seattle, WA 98195-7280 USA
Calcium influx through voltage-gated calcium channels in presynaptic nerve terminals initiates synaptic transmission. Regulation of these presynaptic calcium channels modulates synaptic plasticity, spatial learning, and memory. Cav2.1 channels that conduct P/Q-type calcium currents in nerve terminals form a large signaling complex, which includes SNARE proteins, protein kinases and phosphatases, calmodulin, and calmodulin-like neural calcium sensor proteins. We study the regulation of Cav2.1 channels by this presynaptic signaling complex in transfected cells and cultured neurons in vitro and in mutant mouse lines with specific mutations that alter calcium channel regulation in vivo. The functional impacts of mutations that alter calcium channel regulation are determined by in vitro electrophysiological studies of dissociated neurons and brain slices and by in vivo electrophysiology, including measurements of sharp-wave ripples, place cell formation, and other functional read-outs of neuronal circuits. In addition, the behavioral impacts of calcium channel mutations are determined by analysis of spatial learning and memory, including the Barnes Maze, context-dependent fear conditioning, and social interaction. The overall goal of these studies is to understand how calcium channel regulation of synaptic transmission controls learning and memory at the molecular, cellular, circuit and behavioral levels.
We seek enthusiastic well-trained neuroscientists who are excited about the opportunity to analyze the role of calcium channel regulation in spatial learning and memory from molecules to the brain.
Salary: $60,000 to $70,000 depending on experience.
University of Washington fringe benefits, including health care coverage and a retirement plan.
PhD or equivalent in neuroscience, physiology, pharmacology, or a related discipline.
Experience in molecular biology, cell biology, and electrophysiology using patch clamp and brain slices is required. Experience in mouse genetics and behavior is valuable.
Djillani D, Bazinet J, Catterall WA (2021) Synaptotagmin-7 potentiates facilitation of Cav2.1 channels. Soc. Neurosci Abst.
Nanou E, Catterall WA. (2018) Calcium channels, synaptic plasticity, and neuropsychiatric disease. Neuron 98:466-481.
Nanou E, Lee A, Catterall WA. (2018) Control of excitation/inhibition balance in a hippocampal circuit by calcium sensor protein regulation of presynaptic calcium channels. J Neurosci. 38:4430-4440.
Nanou E, Scheuer T, Catterall WA. (2016) Calcium sensor regulation of the Cav2.1 channel contributes to long-term potentiation and spatial learning. PNAS 113:13209-13214.
Nanou E, Sullivan JM, Scheuer T, Catterall WA. (2016) Calcium sensor regulation of the Cav2.1 channel contributes to short-term synaptic plasticity in hippocampal neurons. PNAS 113:1062-1067.
Nanou E, Yan J, Whitehead NP, Kim MJ, Froehner SC, Scheuer T, Catterall WA. (2016) Altered short-term synaptic plasticity and reduced muscle strength in mice with impaired regulation of presynaptic Cav2.1 channels. PNAS 113:1068-73.
University of Washington is an affirmative action, equal opportunity employer. All qualified applicants will receive consideration without regard to race, color, religion, sex, sexual orientation, gender identity, gender expression, national origin, age, protected veteran or disabled status, or genetic information.