David Prince

Administrative Appointments

• Chairman, Department of Neurology and Neurological Sciences, Stanford Univ. School of Medicine (1970 - 1989)

Honors and Awards

• Special Lecturer, Society for Neuroscience (2008)
• Lothman Lecturer, University of Virginia (2007)
• The Larry Benardo Research and Education Fund Lecturer ., SUNY Downstate Medical Center, New York (2006)
• Servier Lecturer, University of Montreal (2002)
• Bronte Lecturer, University of California, Davis (2001)

Professional Education

Postdoctoral Advisees

Leonardo Faria , Yunyong Ma , Daniel Takahashi

Graduate & Fellowship Program Affiliations

• Neurology and Neurol Sciences
• Neurosciences

Web Site Links

• Prince Lab Site

Research Interests

My work deals with regulation of excitability in neurons of mammalian cerebral cortex and thalamus and mechanisms underlying development of epilepsy. Long-term goals are to understand how injury produces changes in structure and function of neurons and neuronal networks that lead to hyperexcitability and epileptogenesis, and approaches to prevention of epilepsy after cortical injury. Areas of interest include regulation of voltage dependent membrane properties, neuropharmacology of transmitters and modulators including neuropeptides, synaptic mechanisms, and intrinsic properties of single, anatomically identified neurons. Techniques include use of in vivo mammalian preparations as well as in vitro slices and acutely dissociated neurons for recordings of synaptic activities and membrane properties, using patch-clamp techniques to study whole cell currents and membrane channels. Electrophysiological approaches are combined with intracellular labeling and immunocytochemistry to identify types of neurons and responses to injury.

Current studies include:
i) Reorganization of neocortical neuronal synaptic activities,and intrinsic neuronal properties after cortical trauma.
ii) Electrophysiologic and neuroanatomic studies of axonal sprouting following chronic neocortical injury.
iii) Anatomy and pathophysiology of neocortical developmental malformations.
iv) Effects of neuropeptides and GABAergic inhibition on intrinsic, synaptic and network properties of thalamic neurons; and generation of normal and pathophysiologic rhythms.
v) Modulation of neocortical inhibitory interneuronal activities by neurotransmitters and injury.

Publications

• Epilepsy following cortical injury: cellular and molecular mechanisms as targets for potential prophylaxis. Prince DA, Parada I, Scalise K, Graber K, Jin X, Shen F. Epilepsia. 2009: 50 Suppl 2 30-40
• Surviving hilar somatostatin interneurons enlarge, sprout axons, and form new synapses with granule cells in a mouse model of temporal lobe epilepsy. Zhang W, Yamawaki R, Wen X, Uhl J, Diaz J, Prince DA, Buckmaster PS. J Neurosci. 2009; 29 (45): 14247-56
• The endocannabinoid 2-arachidonoylglycerol is responsible for the slow self-inhibition in neocortical interneurons. Marinelli S, Pacioni S, Bisogno T, Di Marzo V, Prince DA, Huguenard JR, Bacci A. J Neurosci. 2008; 28 (50): 13532-41
• Modulation of epileptiform activity by glutamine and system A transport in a model of post-traumatic epilepsy. Tani H, Bandrowski AE, Parada I, Wynn M, Huguenard JR, Prince DA, Reimer RJ. Neurobiol Dis. 2007; 25 (2): 230-8
• Enhanced excitatory synaptic connectivity in layer v pyramidal neurons of chronically injured epileptogenic neocortex in rats. Jin X, Prince DA, Huguenard JR. J Neurosci. 2006; 26 (18): 4891-900