Dear CNAP member,
We are delighted to present to you the programme for the next round table discussion, which will take place on March 14, 2018 at 12:30 - 15:00, FRB7A/4.108.
As you already know, we will this time focus on the theme “Individual differences in nociception and pain sensitivity I: Focus on genetic-driven cellular-molecular mechanisms”.
Genetic studies conducted in the last two decades have been invaluable in elucidating molecular mechanisms underlying chronic pain conditions. Investigations highlight the importance of genes involved in neurotransmission in both ascending nociceptive and descending inhibitory signaling. Given that chronic pain conditions are heterogeneous in nature, driven by different pathways of vulnerability that include differential molecular genetic contribution, genetic studies hold promise to identify key molecular markers of susceptibility and targets for personalized treatment of chronic pain. As in other fields, two main strategies have been adopted: one is to study rare familial pain conditions with Mendelian inheritance patterns, the other to use either candidate-gene or genome-wide association studies (GWASs) to identify polymorphisms. In this round table discussion we want to discuss examples of both to gain a deeper mechanistic understanding of individual differences in nociception and pain sensitivity and potentially identifying new therapeutic approaches.
Classical papers on individual differences in nociception and pain sensitivity with a focus on genetic-driven cellular-molecular mechanisms:
Devon 2014: How Do Pain Genes Affect Pain Experience?
James 2013: Human pain and genetics: some basics
These papers are meant to serve as an introduction to/brush-up on the topic.
Programme
12.30 General presentation of the topic by Parisa
13.00 Presentation of Sakai et al. 2016: MicroRNA cluster miR-17-92 regulates multiple functionally relaled voltage-gated potassium channels in chronic neuropathic pain by Rocco
13.15 Presentation of Dib-Hajj 2005: Gain-of-function mutation in Na 1.7 in familial erythromelalgia induces bursting of sensory neurons by Jenny
13.30 Break
13.45 Presentation of Park et al. 2014: Extracellular MicroRNAs Activate Nociceptor Neurons to Elicit Pain via TLR7 and TRPA1 by Daniele
14.00 Group Activity
14.30 Easter celebration
15.00 Thank you for today!
We look forward to the discussions, and hope that together we all achieve a deeper understanding of the classical pain concepts.
Kind regards on behalf of the CNAP round table committee,
Laura, Shellie, Parisa, Carsten, and Thomas