Diane Lane

ORCID: 0000-0001-7313-557X
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neurotransmitter Receptor Influence on Behavior
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Pain Mechanisms and Treatments
  • Barrier Structure and Function Studies
  • Stress Responses and Cortisol
  • Neuropeptides and Animal Physiology
  • Cannabis and Cannabinoid Research
  • Receptor Mechanisms and Signaling
  • Neurological Disease Mechanisms and Treatments
  • Memory and Neural Mechanisms
  • Immune Response and Inflammation
  • Heart Rate Variability and Autonomic Control
  • Immune cells in cancer
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Parkinson's Disease Mechanisms and Treatments
  • Ferroptosis and cancer prognosis
  • Lysosomal Storage Disorders Research
  • Fatty Acid Research and Health
  • Carcinogens and Genotoxicity Assessment
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Animal Ecology and Behavior Studies
  • Eicosanoids and Hypertension Pharmacology
  • Clostridium difficile and Clostridium perfringens research
  • Environmental Toxicology and Ecotoxicology

Cornell University
2010-2022

Weill Cornell Medicine
2016-2022

MIND Research Institute
2013-2022

Washington State University Vancouver
2003-2005

Washington State University
2004

Louisiana State University
1997

Ontario Neurotrauma Foundation
1997

University Medical Center New Orleans
1997

Max Planck Institute for Biophysical Chemistry
1979

National Institutes of Health
1976

Hypertension is a leading risk factor for dementia, but the mechanisms underlying its damaging effects on brain are poorly understood. Due to lack of energy reserves, relies continuous delivery blood flow active regions in accordance with their dynamic metabolic needs. disrupts these vital regulatory mechanisms, neuronal dysfunction and damage cognitive impairment. Elucidating cellular bases impairments essential developing new therapies. Perivascular macrophages (PVMs) represent distinct...

10.1172/jci86950 article EN Journal of Clinical Investigation 2016-11-13

Hypertension is a leading cause of stroke and dementia, effects attributed to disrupting delivery blood flow the brain. also alters blood-brain barrier (BBB), critical component brain health. Although endothelial cells are ultimately responsible for BBB, development maintenance properties depend on interaction with other vascular-associated cells. However, it remains unclear if BBB disruption in hypertension requires cooperative Perivascular macrophages (PVM), innate immune closely...

10.1161/hypertensionaha.120.15581 article EN Hypertension 2020-07-13

Background and Purpose- Commensal gut bacteria have a profound impact on stroke pathophysiology. Here, we investigated whether modification of the microbiota influences acute long-term outcome in mice subjected to stroke. Methods- C57BL/6 male received cocktail antibiotics or single antibiotic. After 4 weeks, fecal bacterial density 16S rRNA gene was quantitated by qPCR, phylogenetic classification obtained sequencing. Infarct volume hemispheric loss were measured 3 days 5 weeks after middle...

10.1161/strokeaha.120.029262 article EN Stroke 2020-05-14

Abstract Considerable evidence supports the release of pathogenic aggregates neuronal protein α-Synuclein (αSyn) into extracellular space. While this is proposed to instigate neuron-to-neuron transmission and spread αSyn pathology in synucleinopathies including Parkinson’s disease, molecular-cellular mechanism(s) remain unclear. To study this, we generated a new mouse model specifically immunoisolate lysosomes, established long-term culture where are produced within neurons without addition...

10.1038/s41467-022-32625-1 article EN cc-by Nature Communications 2022-08-22

Loss-of-function mutations of progranulin (PGRN) have been linked to frontotemporal dementia, but little is known about the effects PGRN deficiency on brain in health and disease. has implicated neurovascular development, inflammation, Wnt signaling, a pathway involved formation blood–brain barrier (BBB). Because BBB alterations inflammation contribute ischemic injury, we examined role damage produced by ischemia-reperfusion. +/− −/− mice underwent middle cerebral artery occlusion (MCAO)...

10.1523/jneurosci.4318-13.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-12-11

Exposure to low-dose lipopolysaccharide (LPS) before cerebral ischemia is neuroprotective in stroke models, a phenomenon termed preconditioning (PC). Although it well established that LPS-PC induces central and peripheral immune responses, the cellular mechanisms modulating ischemic injury remain unclear. Here, we investigated role of cells brain protection afforded by PC tested whether monocytes may be reprogrammed ex vivo LPS exposure, thus inflammatory after male mice. We found systemic...

10.1523/jneurosci.0324-18.2018 article EN Journal of Neuroscience 2018-06-26

Lipid second messengers such as arachidonic acid and its metabolites diacylglycerols (DAGs) are affected in brain injury. Therefore, changes the pool size fatty composition of free acids (FFAs) DAGs were analyzed different rat areas 4 35 days after traumatic Cortical impact injury low-grade severity was applied right frontal somatosensory cortex. Four injury, FFAs increased by three- twofold, respectively, injured cortex to a lesser extent contralateral compared with sham-operated animals....

10.1046/j.1471-4159.1997.69010199.x article EN Journal of Neurochemistry 1997-07-01

Opiate addiction is characterized by progressive increases in drug intake over time suggesting maladaptive changes motivational and reward systems. These behaviors are mediated dopaminergic neurons originating from the ventral tegmental area (VTA), long-term of these attributed to increased postsynaptic glutamatergic activation. Indeed, chronic morphine administration known increase AMPA receptor glutamate 1 (GluR1) subunit VTA. However, there no ultrastructural evidence that affects...

10.1523/jneurosci.2151-08.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-09-24

Cannabinoid-type 1 (CB1) receptors are implicated in μ-opioid receptor (μ-OR)-dependent reward ascribed partially to mesolimbic dopamine release the nucleus accumbens (Acb) shell. Thus, CB1 gene deletion may preferentially alter availability of μ-ORs and/or innervation this brain region, which is functionally distinct from motor-associated Acb core. To test hypothesis, we examined electron microscopic immunolabeling μ-OR and dopamine-synthesizing enzyme, tyrosine hydroxylase (TH) shell, core...

10.1002/syn.20807 article EN Synapse 2010-04-23

The nucleus accumbens (Acb) shell and caudate-putamen (CPu) are respectively implicated in the motivational motor effects of dopamine, which mediated part through dopamine D₂-like receptors (D₂Rs) modulated by activation cannabinoid-1 receptor (CB₁R). D(₂/D3) agonist, quinpirole elicits internalization D₂Rs isolated cells; however, dendritic axonal targeting may be highly influenced circuit-dependent changes vivo potentially endogenous CB₁R activation.We sought to determine whether alters...

10.1007/s00213-011-2553-4 article EN cc-by-nc Psychopharmacology 2011-12-07

Abstract Alpha-synuclein (α-syn) is an abundant neuroprotein elevated in cocaine addicts, linked to drug craving, and recruited axon terminals undergoing glutamatergic plasticity - a proposed mechanism for substance abuse. However, little known about normal α-syn function or how it contributes We show that critical preference of hedonic stimuli the cognitive flexibility needed change behavioral strategies, functions are altered with Electron microscopic analysis reveals changes targeting...

10.1038/s42003-019-0651-8 article EN cc-by Communications Biology 2019-11-15
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