Robert Raike

Ph.D. 2004

Thesis Title:

A Potential Mouse Model of Episodic Ataxia Type 2

Current Position:

  • Director, Neuromodulation Research and Technology at Medtronic Neuromodulation, Medtronic, Inc.

Former Position(s):

  • Technology Strategy and Business Development, Neuromodulation, Medtronic, Inc.
  • Senior Principal Scientist / DBS Chief Scientist, Neuromodulation, Medtronic, Inc.
  • Principal Scientist, Neuromodulation, Medtronic, Inc.
  • Postdoctoral Fellow, Department of Pharmacology and Neurology, Emory University School of Medicine

Major Advisor(s):

Christopher Gomez

Selected Publications:

  • Raike RS, Kordasiewicz HB, Thompson RM, Gomez CM. Dominant-negative suppression of Cav2.1 currents by alpha1 2.1 truncations requires the conserved interaction domain for beta subunits. Mol Cell Neurosci. 2007;34(2):168-177.
  • Subramony SH, Schott K, Raike RS, Callahan J, Langford LR, Christova PS, Anderson JH, Gomez CM. Novel CACNA1A mutation causes febrile episodic ataxia with interictal ocular motor and posture abnormalities. Ann Neurol. 2003;4(6):725-31.
  • Restituito S, Thompson RM, Eliet J, Raike RS, Riedl M, Charnet P, Gomez CM. The polyglutamine expansion in spinocerebellar ataxia type 6 causes a beta subunit-specific enhanced activation of P/Q-type calcium channels in Xenopus oocytes. J Neurosci. 2000;20(17): 6394-403.
Robert Raike