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David A. Prince, M.D.

Affiliations: 
Stanford University, Palo Alto, CA 
Area:
Epilepsy
Website:
http://med.stanford.edu/profiles/David_Prince/
Google:
"David Prince"
Bio:

M.D. 1956, University of Pennsylvania

Mean distance: 11.62 (cluster 6)
 
Cross-listing: Neuropathology Tree

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Parents

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Children

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Yunxiang Chu research assistant 2004-2008 Stanford
Michael J. Gutnick grad student 1968-1972 Stanford
Jeffrey L. Noebels grad student 1973-1977 Stanford Medical School
Scott M. Thompson grad student 1986 Stanford
Alberto Bacci post-doc European Brain Research Institute
Tom Brown post-doc Stanford Medical School
Douglas A. Coulter post-doc Stanford
Robert Fisher post-doc Johns Hopkins
Kevin D. Graber post-doc Stanford
John R. Huguenard post-doc Stanford
Xiaoming Jin post-doc Stanford
Arnold R. Kriegstein post-doc UCSF
David A. McCormick post-doc Stanford
Timothy A. Pedley post-doc Columbia
Qian-Quan Sun post-doc Stanford
Robert KS Wong post-doc Stanford
D. Koji Takahashi post-doc 2009- University of Utah
Feng Gu post-doc 2013- Stanford
Phillip A. Schwartzkroin post-doc 1978 Stanford
Barry W. Connors post-doc 1980-1982 Stanford
Heiko J. Luhmann post-doc 1987-1990 Stanford University Medical School
Charles L. Cox post-doc 1993-1996 Stanford
Kimberle M. Jacobs post-doc 2001 Stanford
Viktor N. Kharazia post-doc 1997-2002 Stanford Medical School
Anita E. Bandrowski post-doc 2000-2004 Stanford University Medical Center
Sonal Goswami post-doc 2014-2015 Stanford Medical School

Collaborators

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Irving Wagman collaborator UC Davis
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Publications

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Shu H, Parada I, Delgado A, et al. (2024) Increased excitatory connectivity and epileptiform activity in thrombospondin1/2 knockout mice following cortical trauma. Neurobiology of Disease. 200: 106634
Bagley JR, Tan Y, Zhu W, et al. (2023) Neuron Navigator 1 (Nav1) regulates the response to cocaine in mice. Communications Biology. 6: 1053
Gu F, Parada I, Yang T, et al. (2022) Chronic partial TrkB activation reduces seizures and mortality in a mouse model of Dravet syndrome. Proceedings of the National Academy of Sciences of the United States of America. 119
Gu F, Parada I, Yang T, et al. (2020) Partial Activation of TrkB Receptors Corrects Interneuronal Calcium Channel Dysfunction and Reduces Epileptogenic Activity in Neocortex following Injury. Cerebral Cortex (New York, N.Y. : 1991)
Perez-Ramirez MB, Gu F, Prince DA. (2020) Prolonged prophylactic effects of gabapentin on status epilepticus-induced neocortical injury. Neurobiology of Disease. 104949
Klein P, Friedman A, Hameed MQ, et al. (2020) Repurposed molecules for antiepileptogenesis: Missing an opportunity to prevent epilepsy? Epilepsia. 61: 359-386
Gu F, Parada I, Yang T, et al. (2018) Partial TrkB receptor activation suppresses cortical epileptogenesis through actions on parvalbumin interneurons. Neurobiology of Disease
Takahashi DK, Jin S, Prince DA. (2017) Gabapentin Prevents Progressive Increases in Excitatory Connectivity and Epileptogenesis Following Neocortical Trauma. Cerebral Cortex (New York, N.Y. : 1991). 1-16
Gu F, Parada I, Shen F, et al. (2017) Structural alterations in fast-spiking GABAergic interneurons in a model of posttraumatic neocortical epileptogenesis. Neurobiology of Disease
Kim SY, Senatorov VV, Morrissey CS, et al. (2017) TGFβ signaling is associated with changes in inflammatory gene expression and perineuronal net degradation around inhibitory neurons following various neurological insults. Scientific Reports. 7: 7711
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