Sydney Lamerand

ORCID: 0000-0002-2486-5514
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About
Contact & Profiles
Research Areas
  • Pain Mechanisms and Treatments
  • Cell death mechanisms and regulation
  • Autophagy in Disease and Therapy
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Pain Management and Opioid Use
  • Peripheral Neuropathies and Disorders
  • Neuropeptides and Animal Physiology
  • RNA regulation and disease
  • Mitochondrial Function and Pathology
  • Sphingolipid Metabolism and Signaling
  • Circadian rhythm and melatonin
  • Sleep and Wakefulness Research
  • RNA Interference and Gene Delivery
  • Memory and Neural Mechanisms
  • Botulinum Toxin and Related Neurological Disorders
  • Neuroscience and Neuropharmacology Research
  • Alzheimer's disease research and treatments

University of Pittsburgh
2021

Center for Neurosciences
2021

Northwestern University
2020

Illinois Institute of Technology
2017-2018

Abstract Tissue injury induces a long‐lasting latent sensitization (LS) of spinal nociceptive signaling that is kept in remission by an opposing µ‐opioid receptor (MOR) constitutive activity. To test the hypothesis supraspinal sites become engaged, we induced hindpaw inflammation, waited 3 weeks for mechanical hypersensitivity to resolve, and then injected opioid inhibitors naltrexone, CTOP or β‐funaltrexamine subcutaneously, and/or into cerebral ventricles. Intracerebroventricular injection...

10.1002/jnr.24846 article EN Journal of Neuroscience Research 2021-05-06

Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid that mediates wide spectrum of biological processes including apoptosis, immune response and inflammation. Here, we sought to understand how S1P signaling affects neuronal excitability in the central amygdala (CeA), which brain region associated with fear learning, aversive memory, affective dimension pain. Because G-protein coupled receptor 1 (S1PR

10.1016/j.neuropharm.2021.108885 article EN cc-by-nc-nd Neuropharmacology 2021-11-16

10.1016/j.jpain.2023.02.131 article EN publisher-specific-oa Journal of Pain 2023-04-01

BaxΔ2 is a unique functional Bax isoform resulted from the combination of mononucleotide deletion and an alternative splicing in N‐terminus. The rest sequence same between Baxα BaxΔ2. However, unable to target mitochondria due loss helix α1, encoded by exon 2. Instead, it forms cytosolic aggregates activate caspase 8‐dependent death pathway. domains involved aggregation cytotoxicity remained elusive. Using computational modeling with biochemical cellular analysis, we show here that drastic...

10.1096/fasebj.31.1_supplement.774.9 article EN The FASEB Journal 2017-04-01

Abstract BaxΔ2 is a pro-apoptotic protein originally discovered in colon cancer patients with high microsatellite instability. Unlike most Bax family members, mediates cell death through non-mitochondrial caspase 8-dependent pathway. In the scope of analyzing distribution expression human tissues, we examined panel brain samples. Here, report 4 cerebellar cases which subjects had no neurological disorder or disease documented. We found positive cells scattered all areas cerebellum, but...

10.1101/245910 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-02-02
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