Wade G. Regehr

Assessing the role of calcium-induced calcium release in short-term presynaptic plasticity at excitatory central synapses.

Contributions of receptor desensitization and saturation to plasticity at the retinogeniculate synapse.

Retrograde signaling by endocannabinoids.

Inhibition of interneuron firing extends the spread of endocannabinoid signaling in the cerebellum.

Quantal events shape cerebellar interneuron firing.

Interaction of postsynaptic receptor saturation with presynaptic mechanisms produces a reliable synapse.

Ultrastructural contributions to desensitization at cerebellar mossy fiber to granule cell synapses.

Presynaptic modulation of the retinogeniculate synapse.

Calcium dependence of retrograde inhibition by endocannabinoids at synapses onto Purkinje cells.

"Resistant" channels reluctantly reveal their roles.

Brief presynaptic bursts evoke synapse-specific retrograde inhibition mediated by endogenous cannabinoids.

Retinogeniculate synaptic properties controlling spike number and timing in relay neurons.

Structural contributions to short-term synaptic plasticity.

Endocannabinoids inhibit transmission at granule cell to Purkinje cell synapses by modulating three types of presynaptic calcium channels.

Presynaptic calcium measurements at physiological temperatures using a new class of dextran-conjugated indicators.

Variance-mean analysis in the presence of a rapid antagonist indicates vesicle depletion underlies depression at the climbing fiber synapse.

Short-term synaptic plasticity: a comparison of two synapses.

Associative short-term synaptic plasticity mediated by endocannabinoids.

Timing and specificity of feed-forward inhibition within the LGN.

Conventional synapses for unconventional cells.

Endocannabinoids control the induction of cerebellar LTD.

The influence of multivesicular release and postsynaptic receptor saturation on transmission at granule cell to Purkinje cell synapses.

Sustained elevation of dendritic calcium evokes widespread endocannabinoid release and suppression of synapses onto cerebellar Purkinje cells.

Brief bursts of parallel fiber activity trigger calcium signals in bergmann glia.

Retrograde endocannabinoid signaling in the cerebellar cortex.

Local interneurons regulate synaptic strength by retrograde release of endocannabinoids.

Fast vesicle replenishment and rapid recovery from desensitization at a single synaptic release site.

Differential expression of posttetanic potentiation and retrograde signaling mediate target-dependent short-term synaptic plasticity.

Reliability and heterogeneity of calcium signaling at single presynaptic boutons of cerebellar granule cells.

Timing dependence of the induction of cerebellar LTD.

Active dendritic conductances dynamically regulate GABA release from thalamic interneurons.

Serotonin evokes endocannabinoid release and retrogradely suppresses excitatory synapses.

Noradrenergic control of associative synaptic plasticity by selective modulation of instructive signals.

Inhibitory regulation of electrically coupled neurons in the inferior olive is mediated by asynchronous release of GABA.

Somatic spikes regulate dendritic signaling in small neurons in the absence of backpropagating action potentials.

Activity-dependent regulation of synapses by retrograde messengers.

Linking genetically defined neurons to behavior through a broadly applicable silencing allele.

Dynamics of fast and slow inhibition from cerebellar golgi cells allow flexible control of synaptic integration.

Identification of the synthetic pathway producing the endocannabinoid that mediates the bulk of retrograde signaling in the brain.

Cholinergic activation of M2 receptors leads to context-dependent modulation of feedforward inhibition in the visual thalamus.

Presynaptic CB1 receptors regulate synaptic plasticity at cerebellar parallel fiber synapses.

Short-term forms of presynaptic plasticity.

Calcium microdomains near R-type calcium channels control the induction of presynaptic long-term potentiation at parallel fiber to purkinje cell synapses.

Calcium-dependent isoforms of protein kinase C mediate posttetanic potentiation at the calyx of Held.

Identification of an inhibitory circuit that regulates cerebellar Golgi cell activity.

Short-term presynaptic plasticity.

Autistic-like behaviour and cerebellar dysfunction in Purkinje cell Tsc1 mutant mice.

Adaptive regulation maintains posttetanic potentiation at cerebellar granule cell synapses in the absence of calcium-dependent PKC.

Calcium-dependent isoforms of protein kinase C mediate glycine-induced synaptic enhancement at the calyx of Held.

Metabotropic glutamate receptors drive global persistent inhibition in the visual thalamus.

Presynaptic calcium influx controls neurotransmitter release in part by regulating the effective size of the readily releasable pool.

Hyperpolarization induces a long-term increase in the spontaneous firing rate of cerebellar Golgi cells.

Normalization of input patterns in an associative network.

Molecular mechanisms for synchronous, asynchronous, and spontaneous neurotransmitter release.

Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity.

Achieving high-frequency optical control of synaptic transmission.

The substantia nigra conveys target-dependent excitatory and inhibitory outputs from the basal ganglia to the thalamus.

Promoter decommissioning by the NuRD chromatin remodeling complex triggers synaptic connectivity in the mammalian brain.

Protein kinase C is a calcium sensor for presynaptic short-term plasticity.

Cell type-specific manipulation with GFP-dependent Cre recombinase.

Active Dendrites and Differential Distribution of Calcium Channels Enable Functional Compartmentalization of Golgi Cells.

The calcium sensor synaptotagmin 7 is required for synaptic facilitation.

Determining synaptic parameters using high-frequency activation.

Calcium-Dependent Protein Kinase C Is Not Required for Post-Tetanic Potentiation at the Hippocampal CA3 to CA1 Synapse.

Purkinje Cell Collaterals Enable Output Signals from the Cerebellar Cortex to Feed Back to Purkinje Cells and Interneurons.

Purkinje Cells Directly Inhibit Granule Cells in Specialized Regions of the Cerebellar Cortex.

Synaptic Specializations Support Frequency-Independent Purkinje Cell Output from the Cerebellar Cortex.

The readily releasable pool of synaptic vesicles.

The Mechanisms and Functions of Synaptic Facilitation.

Synaptotagmin 7 confers frequency invariance onto specialized depressing synapses.

Silk Fibroin Films Facilitate Single-Step Targeted Expression of Optogenetic Proteins.

Synaptotagmin 7 Mediates Both Facilitation and Asynchronous Release at Granule Cell Synapses.

Ephaptic Coupling Promotes Synchronous Firing of Cerebellar Purkinje Cells.

Neuronal Regulation of Fast Synaptotagmin Isoforms Controls the Relative Contributions of Synchronous and Asynchronous Release.