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Wade G. Regehr
Researcher at Harvard University
Publications - 173
Citations - 23236
Wade G. Regehr is an academic researcher from Harvard University. The author has contributed to research in topics: Neurotransmission & Synapse. The author has an hindex of 74, co-authored 166 publications receiving 21091 citations. Previous affiliations of Wade G. Regehr include University of Pennsylvania & Bell Labs.
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Journal ArticleDOI
Short-Term Synaptic Plasticity
Robert S. Zucker,Wade G. Regehr +1 more
TL;DR: The evidence for this hypothesis, and the origins of the different kinetic phases of synaptic enhancement, as well as the interpretation of statistical changes in transmitter release and roles played by other factors such as alterations in presynaptic Ca(2+) influx or postsynaptic levels of [Ca(2+)]i are discussed.
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Retrograde Inhibition of Presynaptic Calcium Influx by Endogenous Cannabinoids at Excitatory Synapses onto Purkinje Cells
TL;DR: It is suggested that Purkinje cells release endogenous cannabinoids in response to elevated calcium, thereby inhibiting presynaptic calcium entry and suppressing transmitter release, and suggesting a widespread role for endogenous cannabinoid in retrograde synaptic inhibition.
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Autistic-like behaviour and cerebellar dysfunction in Purkinje cell Tsc1 mutant mice
Peter T. Tsai,Court Hull,YunXiang Chu,Emily Greene-Colozzi,Abbey R. Sadowski,Jarrett M. Leech,Jason Steinberg,Jacqueline N. Crawley,Wade G. Regehr,Mustafa Sahin +9 more
TL;DR: It is shown that both heterozygous and homozygous loss of Tsc1 in mouse cerebellar PCs results in autistic-like behaviours, including abnormal social interaction, repetitive behaviour and vocalizations, in addition to decreased PC excitability.
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Calcium control of transmitter release at a cerebellar synapse
TL;DR: It is concluded that multiple types of Ca2+ channels synergistically control individual release sites and omega-Aga-IVA-sensitive channels are more effective at triggering release.
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Interplay between facilitation, depression, and residual calcium at three presynaptic terminals.
TL;DR: The interplay of facilitation and depression dictates synaptic strength and variability during repetitive activation, and the resulting synaptic plasticity transforms the timing of presynaptic spikes into varying postsynaptic response amplitudes.