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Geoffroy Laumet, Ph.D.

Interdisciplinary Science & Technology building (ISTB)
766 Service Rd, East Lansing, MI
Office#5018
Laboratory#5011

PubMed search for Dr. Laumet
https://pubmed.ncbi.nlm.nih.gov/?term=Laumet+G+[Author]

Neurobiology of chronic pain

Dr. Laumet’s lab is focused on understanding the neurobiology of chronic pain. Chronic pain is not simply a continuation of acute pain, the transition from acute to chronic pain requires persisting adaptations that govern the long-lasting plasticity of the nervous system. Improving our understanding of how pain transitions from acute to chronic will facilitate the development of novel disease-modifying drugs. Thereby improving the quality of life of those who suffer from chronic pain. Today, chronic pain affects between 11%–40% of North Americans. Chronic pain drastically impacts the quality of life, is frequently associated with mood disorders and is an expensive public health condition. Our inability to manage chronic pain gave birth to the opioid crisis.

Neurons do not work in isolation; they are constantly interacting with non-neuronal cells. Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells play active roles in the pathogenesis and resolution of pain. We are particularly interested by the contribution of non-neuronal cells to the transition from acute to chronic pain.

Neuro-immune interactions in chronic pain. Activated immune cells release pro-inflammatory factors which sensitize neurons leading to increased pain signaling. Less studied, but likely equally important is the role of anti-inflammatory immune cells in the remission of pain. We are currently investigating the role of the anti-inflammatory cytokine interleukin-10 and its relationship with opioid system in the remission and relapse of neuropathic and postoperative pain.

Head and Neck Cancer Pain. A second project in the laboratory is the interaction between cancer cells and neurons in a mouse model of Head and Neck Cancer (HNC). HNC is one of the most painful cancers and pain is a predictor of survival. Cancer cells activate “pain-sensing” neurons and induce de novo axon elongation. We are investigating how, and why, cancer cells communicate to “pain-sensing” neurons.

Experimental approaches. In our laboratory, we use mouse models to decipher the molecular and cellular mechanisms underlying the transition from acute to chronic pain. We model pain states induced by injury, surgery, cancer, inflammation, or chemotherapy treatment to investigate how these insults disturb the interaction between neurons and immune cells and the plasticity of the somatosensory system. To address the contribution of neuro-immune and onco-neuron interactions to chronic pain, we combine molecular, biochemistry, immunostaining, pharmacology, genetically modified mice, viral gene therapy, cell transfer and animal behavior in experimental models of chronic pain.

Current lab members:

Joseph Folger, PhD, Kufreobong Inyang, PhD and Geoffroy Laumet, PhD.

Selected publications

Laumet G, Bavencoffe A, Edralin JD, Huo XJ, Walters E, Dantzer R, Heijnen CJ amd Kavelaars A. Interleukin-10 resolves pain hypersensitivity induced by cisplatin by reversing sensory neuron hyperexcitability. Pain. 2020.

Laumet G, Ma J, Robison AJ, Kumari S, Heijnen CJ, Kavelaars A. T cells as an emerging target for chronic pain therapy. Front. Mol. Neurosci. doi: 10.3389/fnmol.2019.00216. doi:10.3389/fnmol.2019.00216.

Laumet G, Edralin JD, Dantzer R, Heijnen CJ and Kavelaars A. Cisplatin educates CD8+ T cells to prevent and resolve chemotherapy-induced peripheral neuropathy in mice. PAIN. 2019 Jun;160(6):1459-1468.

Laumet G, Edralin JD, Chiang ACA, Dantzer R, Heijnen CJ and Kavelaars A. Resolution of inflammation-induced depression requires T lymphocytes and endogenous brain IL-10 signaling. Neuropsychopharmacology. 2018 Dec;43(13):2597-2605.

Laumet G*, Zhou W*, Dantzer R, Edralin JD, Huo XJ, Budac DP, Mao-Ying QL, O’Connor J, Lee AW, Heijnen CJ and Kavelaars A. Upregulation of Neuronal Kynurenine 3-Monooxygenase (KMO) Mediates Depression-like Behavior in a Mouse Model of Neuropathic Pain. Brain, Behavior, and Immunity 2017 Jul 11. pii: S0889-1591(17)30215-5. * Equal contribution.

Laumet G, Garriga J, Chen SR, Zhang Y, Smith TS, Li DP, Jelinek J, Cesaroni M, Issa JP, and Pan HL. G9a is essential for epigenetic silencing of K+ channel genes and acute-to-chronic transition.
Nature Neuroscience 2015 Dec;18(12):1746-55

 

Picture of dorsal root ganglion


Picture of a dorsal root ganglion (where cluster the cell body of “pain-sensing” neurons). Viral gene transfer was used to induce the expression of Green Fluorescent Protein (GFP) in in these neurons. Image collected by Dr. Kufreobong Inyang.

Main Office

Department of Physiology
 Biomedical Physical Sciences (BPS) Building
567 Wilson Rd Rm 2201

Main Phone: 517-884-5000
Office Fax: 517-432-1967


Department Chair

C. Lee Cox
Dr. C. Lee Cox

BPS Building Rm 2201E

Phone: 517-884-5050
Fax: 517-432-1967
 coxclee@msu.edu


Graduate Office

Department of Physiology
BPS Building Rm 2205

Phone: 517-884-5075
Fax: 517-432-1967