David Weinshenker

This study shows that pathogenic tau in the locus coeruleus causes hyperactivity and neuropsychiatric symptoms similar to early Alzheimer's disease in mice.

This study identifies the physiological and behavioral conditions that trigger dopamine release from locus coeruleus axons, showing modality-dependent release constraints.

This study investigates the impact of early locus coeruleus lesions in TgF344-AD rats and finds that LC lesions and AD genotype rarely interact to worsen deficits or neuropathology.

This study examines sex-dependent changes in energy homeostasis and amyloid levels in TgF344-AD rats, finding differences in weight gain, thermogenic function, and glucose regulation between males and females.

The paper investigates the role of tau in VTA dopamine neuron dysfunction in Alzheimer's disease models, finding that tau induces hyperexcitability but impairs burst firing.

This study analyzes LC neuron firing patterns across species and biological factors, revealing diverse activity patterns and subregions enriched for specific factors and disease models.

This study shows that RGS14 suppresses cocaine-induced behavioral changes in female mice by modulating emotional-motivational circuits.

This study identifies entorhinal cortex PV interneuron vulnerability to hAPP as a driver of hyperexcitability and tau pathology in Alzheimer's Disease.

This study shows that dopamine β-hydroxylase knockout in mice alters innate responses to predator odor, with reduced defensive burying and increased grooming, suggesting NE and DA balance regulates behavioral responses.

This study investigates how optogenetic stimulation of the locus coeruleus affects global spatiotemporal patterns in rats using resting-state fMRI.

This study shows that tyrosinase-induced neuromelanin accumulation in mouse locus coeruleus neurons causes hyperactivity, transcriptional changes, and degeneration, mimicking early stages of Alzheimer's and Parkinson's disease.

This study shows RGS14 protects hippocampal neurons from seizure-induced mitochondrial oxidative stress and pathology by modulating excitability and signaling.

This study uses DSP-4 to model early LC-NE system changes in AD and PD, showing axon damage, neuroinflammation, and behavioral changes without LC cell death.

This study examines age-related changes in locus coeruleus firing in a transgenic rat model of Alzheimer's disease, finding age-dependent hypoactivity and hyperactivity in response to stimuli.

The paper investigates the effect of genetic NE loss on adult hippocampal neurogenesis and finds no difference in progenitor proliferation or survival in Dbh-/- mice, contrasting with pharmacological NE depletion.

The paper investigates how norepinephrine and dopamine influence distinct repetitive behaviors in mice exposed to novel odorants, showing differential effects on digging and grooming.

This study investigates the effects of hyperphosphorylated tau on AD-like neuropathology and behavior in a rat model using viral delivery of human tau.

This study examines how the D3R antagonist PG01037 affects morphine-induced behaviors in mice, finding it reduces hyperlocomotion and antinociception but not locomotor sensitization or catalepsy.

This study investigates how RGS14 affects locomotor behavior and ERK signaling in response to environmental novelty and cocaine in specific limbic regions.

This study investigates the molecular effects of the 3q29 deletion on the human neural transcriptome, identifying convergent and distributed impacts across gene clusters and pathways related to psychiatric disorders.

This study investigates the distinct roles of norepinephrine and galanin in stress-induced anxiety-like behavior using genetic and pharmacological approaches in mice.

This study investigates the role of galanin and GalR1 in the locus coeruleus during opioid withdrawal using in situ hybridization and genetic models, finding no significant behavioral impact of NE-Gal on withdrawal symptoms.

This study evaluates 32 individuals with 3q29 deletion syndrome to identify common medical and neurodevelopmental features and provides clinical care recommendations.

The paper identifies genetic variants in RGS14 that disrupt nuclear shuttling and impair LTP regulation in hippocampal neurons, with variant LR causing nuclear accumulation and loss of function.

This study shows that the 3q29 deletion causes sex-specific metabolic changes in mice, which are not linked to behavioral issues, and that a high-fat diet can improve weight in females without worsening behavior.

This study shows chronic exercise and genetic overexpression of galanin in noradrenergic neurons increase stress resilience in mice by enhancing galanin expression in the locus coeruleus.

This study develops a transgenic mouse model expressing human alpha-synuclein in noradrenergic neurons, revealing LC pathology and non-motor PD features.

This study investigates the role of central norepinephrine in novelty-induced behaviors, finding that NE signaling is essential for both neophilic and neophobic responses.

The paper investigates the role of norepinephrine in stress-induced repetitive behaviors in OCD models, finding that NE deficiency reduces compulsive behaviors and that restoring NE rescues these behaviors.

This study shows that eliminating galanin in noradrenergic neurons reduces galanin in specific brain regions and alters coping behaviors without affecting norepinephrine levels.