FIVE SPEAKERS TO IGNITE YOUR SENSES.
THREE DAYS TO LEARN, CONNECT AND
ONE UNIQUE EXPLAIN PAIN EVENT.
EP3 2016 is expanding the international flavour, adding another speaker and delivering the most diverse EP3 line up yet – combining neuroimmunology, psychology, sensory processing research, education psychology, conceptual change science, brains, bodies, space and clinical pain science.
This is the third in a series of posts highlighting the rock star line up at next years EP3 event. Today we shine the spotlight on Professor Mark Hutchinson:
WTF is Nanoscale Biophotonics
Let’s face it, Mark is a bit of an overachiever – he trained as a pharmacologist, has a PhD in medicine and is also trained as an immunologist. He has an amazing list of awards and achievements, and an even longer list of publications in the peer reviewed literature. Mark has trained and worked with some of the biggest heavy hitters in the field of psychoneuroimmunology and has brought his passion, energy, wealth of knowledge and expertise back to Adelaide where he is now the director of the ARC Centre of Excellence for Nanoscale BioPhotonics.
Some of you might be wondering what Nanoscale BioPhotonics is… Put simply, it’s taking a group of researchers with backgrounds in physics, chemistry, biology, material science and engineering and locking them up until they manipulate and mix nanoscale materials to develop new technologies that enable the probing and investigation of individual cells within living organisms.
Here’s a short video featuring Mark to explain this further
A consummate communicator
To hear Mark present is to listen to an accomplished, entertaining and skilful orator. Mark has presented keynotes and hosted sessions at PainAdelaide and regularly presents talks to the public, where his ability to engage audiences is matched by his capacity to distill complex ideas into meaningful, and easily digestible messages.
Mark recently spoke at The Art of Pain event in Adelaide, and the good people at University of South Australia uploaded the whole thing for your viewing pleasure:
A prolific publisher
Mark’s contribution to the literature has been extensive, with papers covering the basic science of glia, neuro-immune interactions, opioids and addiction, as well as clinically relevant papers that translate the basic science work into potential directions for treatment. Below is a just small selection of open access papers from Mark and co-authors.
Toll-Like Receptors in Chronic Pain
Proinflammatory central immune signaling contributes significantly to the initiation and maintenance of heightened pain states. Recent discoveries have implicated the innate immune system, pattern recognition Toll-like receptors in triggering these proinflammatory central immune signaling events. These exciting developments have been complemented by the discovery of neuronal expression of Toll-like receptors, suggesting pain pathways can be activated directly by the detection of pathogen associated molecular patterns or danger associated molecular patterns.
A great place to start, this review provides an excellent overview of neuroimmune interactions in chronic pain, including activation of microglia and astrocytes, and an introduction to Toll Like Receptors which, I have on good authority, is one of Mark’s favourite topics. However I can’t mention this paper and not call out the “pain pathways” clanger…
Why is Neuroimmunopharmacology crucial for the future of addiction research?
A major development in drug addiction research in recent years has been the discovery that immune signaling within the central nervous system contributes significantly to mesolimbic dopamine reward signaling induced by drugs of abuse, and hence is involved in the presentation of reward behaviours…It is hoped that by combining the collective wisdom of neuroscience, immunology and pharmacology, into Neuroimmunopharmacology, we may more fully understanding the neuronal and immune complexities of how drugs of abuse, such as opioids, create their rewarding and addiction states. Such discoveries will point us in the direction such that one day soon we might successfully intervene to successfully treat drug addiction.
This paper contains a great summary of immune-to-brain signalling in the context of illness induced behavioural change. Building on the discoveries of immune induced behavioural change and a wealth of research in neuro-immune interactions, the authors propose the hypothesis that proinflammatory central immune signalling contributes significantly to the facilitation of reward signalling within the brain in response to opioid exposure, and the resulting presentation of reward behaviour in drug abuse. Given the role of pro-inflammatory cytokines in some chronic pain states, and the ongoing use of opioid medications to try to treat these pain states, this work has vital implications for the treatment of both addiction and pain and hints at the possibility of intriguing commonalities.
Glia as the “bad guys”: Implications for improving clinical pain control and the clinical utility of opioids
Within the past decade, there has been increasing recognition that glia are far more than simply “housekeepers” for neurons. This review explores two recently recognized roles of glia (microglia and astrocytes) in: (a) creating and maintaining enhanced pain states such as neuropathic pain, and (b) compromising the efficacy of morphine and other opioids for pain control. While glia have little-to-no role in pain under basal conditions, pain is amplified when glia become activated, inducing the release of proinflammatory products, especially proinflammatory cytokines
An earlier paper, but an excellent overview of the role of glia in persistent pain states. Includes this stop-and-pause-to-think idea, “After resolution of challenge, microglia can either return to their basal state or may enter a “primed” state for prolonged periods of time…Evidence to date from animal models suggests that prior microglial activation can leave these cells primed, such that a later pain-evoking stimulus produces both enhanced spinal proinflammatory cytokine production and enhanced pain”
Toll-like receptor 4: innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder
Major depressive disorder (MDD) poses one of the highest disease burdens worldwide. Yet, current treatments targeting serotonergic and noradrenaline reuptake systems are insufficient to provide long-term relief from depressive symptoms in most patients, indicating the need for new treatment targets. Having the ability to influence behavior similar to depressive symptoms, as well as communicate with neuronal and neuroendocrine systems, the innate immune system is a strong candidate for MDD treatments.
It’s those TLRs again, and more possible links in the substrate and commonality of pain and other ‘output systems’ such as the neuroimmune and neuroendocrine systems.
Secure your place for EP3 2016 now
Register and pay online here
Prefer to register with good ol’ fashion pen and paper? You can do that too – here.
Lodge your interest and be kept up to date (but remember, this won’t secure you a place, you need to pay to do that!) here.
One more thing…
Described as ‘probably the best little pain meeting in the world’, PainAdelaide will be held on April 4, the day following EP3. PainAdelaide tickets won’t be publicly available for purchase until later this year (and always sell out quickly) so this way you can be ahead of the field and lock in your place.
For an amazing four day experience we are pleased to offer special ‘pre-sale’ tickets for EP3 and PainAdelaide 2016 – a great deal for our overseas guests in particular!
Just select the EP3 and PainAdelaide Package in any of the payment methods above.
Looking forward to seeing you in gorgeous Glenelg in April 2016.