Michael D. Burton (@mdburton) — Bluesky Profile

3 months ago

Me, Cheryl, Anne-Marie and Michael giving talks

Ewan, Anne-Marie, Cheryl and Michael having a much deserved post-symposium dinner!

Had a great time at our @sfn.org #PainResearch symposium yesterday, talks covering a whole range of pain states & roles of non-neuronal cells, review article for more reading: www.jneurosci.org/content/45/4... Thanks to @cherylstucky.bsky.social, @mdburton.bsky.social & Anne-Marie Heegaard!

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4 months ago

Figure 1. Non-neuronal–neuron communication in the skin. (1) Non-neuronal cells and extracellular matrix in the skin. (2) When in ammatory events such as IL-6, ATP, and protease
production from injury or infection are introduced, it causes an activation of cells, a disruption in extracellular matrix, and damage to sensory neurons. (3) During in ammatory cascades,
injured or sensitized neurons potentiate pain and the development of a chronic pain state.

Figure 2. Cell–cell interactions in joint pain. Numerous pathogenic changes occur within the OA joint and other musculoskeletal conditions that can contribute to pain, including cartilage
degradation, synovitis, and bone remodeling (1). Within the joint evidence has established the role of some key non-neuronal cell types that contribute to pain (2) and some of the signaling
nociceptor activation and sensitization mechanisms involved (3). There is also growing evidence for cell–cell interactions within the DRG that contribute to pain (4). See text for more details.

Figure 3. Keratinocytes contribute to normal touch and chemotherapy-induced mechanical sensitivity through PIEZO1. Keratinocytes in the most super cial layer of the skin respond to
mechanical forces via their expression of PIEZO1 channels and activated keratinocytes release ATP which signals to P2X4 channels on cutaneous sensory nerve endings. After a patient is treated
with the chemotherapeutic paclitaxel, keratinocyte PIEZO1 is sensitized; the keratinocytes release more ATP and additional mediators, resulting in greater action potential signaling in sensory
neurons that is sent to the spinal cord and brain through touch and pain pathways.

With the annual @sfn.org meeting coming up, I'm looking forward to Saturday's symposium with @cherylstucky.bsky.social , @mdburton.bsky.social & Anne-Marie Heegaard on non-neuronal cells in #PainResearch

Here's our accompanying review!
www.jneurosci.org/content/45/4...

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7 months ago

Looking forward to some exciting #PainResearch / #Neuroskyence in our Symposium: "Not just neurons: pain is orchestrated in partnership with many non-neuronal cells"

@cherylstucky.bsky.social / @mdburton.bsky.social / Anne-Marie Heegaard

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8 months ago

Congratulations!

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11 months ago

TLR4+ Dermal fibroblasts induce acute and transitional pain states The prominence of non-neuronal cells driving pain states has gained attention in recent years. Fibroblasts, a major stromal cell, perform essential functions during inflammation, tissue remodeling, an...

Excited to share a new preprint that discovered how skin fibroblasts are active participants in acute & long-term pain states & not just bystanders. We know this research, partly funded by the NIH will drive the development of new pain drugs. @elsanchez09.bsky.social
www.biorxiv.org/content/10.1...

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1 year ago

Big facts

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1 year ago

This #BlackHistoryMonth, Banbury recognizes meeting participants for their significant contributions to the biosciences & society.

We begin with @mdburton.bsky.social, Assoc. Prof. at @utdallas.bsky.social. We were happy to have him back at Banbury in 2024. (1/4)

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1 year ago

Proud to watch Shevon Alexandar defend her dissertation this past week. What an awesome part of the job to watch young scientists grow and apply their potential. She marks the 5th PhD student to graduate from the Burton Lab. She's moving on to a postdoc at @tulaneu.bsky.social @utdallas.bsky.social

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