David L. Sulzer

This study develops a method to derive and maintain specific subtypes of human midbrain dopaminergic neurons in vitro, revealing their functional and molecular characteristics and potential vulnerability in disease.

This study presents cryo-EM structures of SV2C and its ligands, revealing structural differences that explain ligand selectivity and impact dopamine release.

This study examines how ADGRL3 knockout affects dopamine release in mice, finding increased ex vivo release and reduced in vivo task-induced signals in the nucleus accumbens.

This study identifies a mechanism by which α-synuclein and γ-tubulin cooperatively regulate activity-evoked presynaptic microtubule nucleation to control dopamine release.

This study investigates how ibogaine and its metabolite noribogaine modulate monoamine transporters, revealing their unique pharmacological profile and explaining their therapeutic effects.

This study shows that electroconvulsive therapy (ECT) improves motor function in Parkinsonian mice by promoting dopaminergic axon regeneration and restoring striatal circuitry.

The paper analyzes T-cell responses and glial pathology in Parkinson's disease substantia nigra using single nucleus RNA sequencing and spatial transcriptomics, revealing CD8+ T-cell characteristics and altered cellular interactions.

The paper examines T cell responses to PINK1 and α-synuclein in prodromal Parkinson's disease, finding elevated reactivity comparable to clinically diagnosed PD.

The paper investigates T cell subsets in Parkinson's disease patients reactive to α-synuclein, finding reduced Granulysin+ CD4 cytotoxic TEM cells and altered CELSR2 expression.

The paper shows that sound-safety association enhances striatal neuron responses to learned sounds through postsynaptic changes in direct pathway SPNs.

The paper creates a brain-wide map of mitochondrial phenotypes by combining physical voxelization with biochemical profiling, revealing regional differences in mitochondrial density and function.

The paper investigates how tonic activity patterns affect dopamine release in striatal brain slices, finding that tonic stimulation alters DA release kinetics to resemble in vivo conditions.

The paper identifies PINK1 as an autoantigen targeted by T cells in Parkinson's disease, with reactivity predominantly observed in male patients.

This study investigates dopamine neurotransmission in an eIF4E Tg mouse model of ASD, finding impaired striatal dopamine release and behavioral inflexibility due to defective nicotinic receptor signaling.

The paper investigates how dopamine modulates GABA release from striatonigral synapses via 5-HT1B receptors, revealing a serotonergic mechanism relevant to Parkinson's disease treatments.

This study shows that immunizing HLA-DRB1*15:01 mice with the alpha-synuclein epitope -syn32-46 causes intestinal inflammation, neuron loss, and constipation, mimicking prodromal Parkinson's disease features.

The paper shows IFN-γ induces MHC-I expression in ventral midbrain neurons and glia, but with lower amplitude in neurons, and MHC-II is restricted to microglia.

This study shows that auxilin deficiency causes Parkinson's disease by disrupting dopamine transporter function and synaptic vesicle sorting, leading to dopamine homeostasis disruption and neurodegeneration.

The paper presents three computational models to analyze fast-scan cyclic voltammetry data from mice, quantifying presynaptic dopamine kinetics and the role of synucleins in neurotransmission.

The paper uses subcellular proteomics to show Parkinson's disease-linked genes are enriched in axons of dopaminergic neurons in the mouse brain.

The paper investigates mRNA localization and translation in midbrain dopaminergic neurons, finding no axonal localization but dendritic ribosomes and mRNAs related to dopamine synthesis and release.

The paper shows that decreased DMS direct pathway neuronal activity, dependent on dopamine, is required for motor coordination learning, while DLS activity remains stable and correlates with skill maintenance.

This study examines the postnatal maturation of striatal cholinergic interneurons and their interaction with dopamine release in mice, showing age-related changes in activity and neurotransmission.

This study investigates how dopamine loss and chronic L-DOPA treatment affect striatal cholinergic interneuron firing rates and ion channel activity, revealing specific molecular adaptations.

This study shows α-synuclein enhances dopamine release during burst firing in substantia nigra neurons in vivo, independent of β- and γ-synucleins or presynaptic calcium.

This study identifies CalDAG-GEFI mutations causing psychomotor symptoms and bleeding in multiple species, revealing conserved signaling deficits in striatal function.

This study uses ribosome profiling to show that Fmr1 loss in mice affects translation elongation and initiation, with reduced pausing and altered mRNA binding.

The paper shows that mTOR suppresses autophagy in the striatum during postnatal development, with autophagic flux reaching adult levels by P28.

This study shows that reducing glutamate cotransmission in dopamine neurons affects amphetamine sensitization and latent inhibition, contributing to schizophrenia resilience.