Mechanisms of Pain Revealed by Latent Sensitisation Models

Session Title: Mechanisms of Pain Revealed by Latent Sensitisation Models

Topic: BASIC SCIENCE

Description: In rodents and humans, hyperalgesic priming of nociceptive neurons can be induced by injury, inflammation or stress that cause measurable acute hypersensitivity. These salient events underpin latent sensitisation where the acute pain episode confers a long-lasting vulnerability to developing an exaggerated sensitivity to subsequent noxious stimuli, with an increased magnitude and/or duration of hypersensitivity. Preclinical models of latent sensitisation offer the ability to (1) Study the transition from acute-to-chronic pain, (2) Reproduce the episodic nature of pain, (3) Model the response of the nociceptive system to repeated noxious stimuli.

The priming stimulus used in latent sensitisation models determines both the magnitude and duration of latent hypersensitivity following subsequent insults. The response to a subsequent insult is often greater in intensity and longer in duration (extending from hours to weeks) compared to what is observed in unprimed conditions. It is now well established that priming events can modulate response profiles of sensory neurons and induce reorganization of the transcriptional landscape of nociceptors – phenomena that contribute to the increased susceptibility of nociceptor sensitisation to subsequent subthreshold stimuli. Latent sensitisation has also been shown to underlie nociceptive responsiveness to stimuli that would normally produce analgesia.

This session will review how various preclinical models of latent sensitisation have provided important mechanistic insights into aberrant nociceptor activity and altered central nervous system circuitry underlying the transition from acute to chronic pain. The session also proudly highlights data generated across three continents and contributed by researchers ranging from early-career scientists to established investigators. The speakers will describe different experimental hyperalgesic priming paradigms in rodent models where distinct priming stimuli can produce acute nociceptive pain and enable latent sensitisation of nociceptive neurons. The talks will encompass in vivo and in vitro assessments of nociceptor activity, omics-based profiling of primed nociceptors, and central nervous system engrams that maintain latent hypersensitivity. The following datasets arising from latent sensitisation studies will be addressed:

• Dissecting the roles of amygdaloid and thalamic nuclei in the development of allostatic load and stress- and anxiety-related nociceptive behaviours in acute and persistent muscle pain
• Elucidating the contributions of endogenous systems, including peripheral opioid receptor activity and macrophage colony-stimulating factors, in acute and persistent post-operative pain
• Employing TRAP-seq (Translating Ribosome Affinity Purification sequencing) with Cre-mediated tagging of peripheral and central nervous system neurons to define the translatome of neuronal engrams of latent sensitisation

In this session, attendees will gain an integrated understanding of the cellular and molecular mechanisms underlying the transition from acute to chronic pain states. The workshop aims to facilitate knowledge transfer from the presenting researchers who are experienced in the technical application of latent sensitisation models, enabling attendees to:

• Learn how different exteroceptive and interoceptive events can prime nociceptive neurons to develop latent sensitization
• Understand how key endogenous opioid systems and innate immune cell functions contribute to modulation of latent sensitivity.
• Explore how translational reorganization in nociceptive neurons is linked to the development of latent sensitivity and maintenance of negative affect

Speakers

Cheng-Chang Lien National Yang Ming Chiao Tung University
Taiwan

Dr. Cheng-Chang Lien is the Dean of the College of Life Sciences at National Yang Ming Chiao Tung University (NYCU). He earned his MD from China Medical University in 1997. He completed his PhD under the mentorship of Dr. Peter Jonas at the University of Freiburg, Germany, in 2003, graduating summa cum laude.

Following a brief postdoctoral period in Dr. Mu-Ming Poo’s laboratory at the University of California, Berkeley, he joined the Institute of Neuroscience at National Yang-Ming University (NYMU) as a faculty member in 2006. He was promoted to Professor in 2015 and served as Director of the Institute from 2017 to 2021. His research focuses on the structure and function of brain circuits and their roles in health and disease.

Dr. Lien’s scientific contributions have been widely recognized both nationally and internationally. He holds the highest faculty rank and was honored as a Distinguished Professor and an Alexander von Humboldt Fellow. Among the numerous accolades he has received are the NSTC (formerly MOST) Outstanding Research Award (2024, 2016)—the most prestigious research prize in Taiwan—the TienTe Lee Young Scientist Research Award (2016), the NHRI Award for Integrated Research Grants in Health and Medical Sciences (2015, 2025), and the NYMU Academic Excellence Awards (2011–2019).

Internationally, his research excellence has been acknowledged through awards such as the DAAD Scholarship (1998–2004), the Alexander von Humboldt Research Fellowship (2016–2018), and the NeuroCure Fellowship (2015–2016) in Berlin, Germany. In 2026, he was elected as an IUPS Academy Fellow.

Dr. Lien is also an active contributor to the scientific community. He serves on the editorial boards of journals, including Frontiers in Cellular Neuroscience and Scientific Reports, and acts as an external reviewer for several prestigious funding agencies, such as the French National Research Agency (ANR), the Danish Research Council (in coordination with the NIH BRAIN Initiative), the National Health Research Institutes (NHRI), and the European Research Council (ERC).

Ishwarya Sankaranarayanan University of Texas at Dallas
United States

Dr. Ishwarya Sankaranarayanan is a postdoctoral researcher in the Pain Neurobiology Research Group at the University of Texas at Dallas. She earned her Master's degree from the University of Southern California and her Ph.D. from UT Dallas, where she now continues her research. Her work focuses on the molecular mechanisms underlying diabetic peripheral neuropathy (DPN) and other neuropathic pain conditions, using single-cell and other transcriptomic approaches to uncover how sensory neurons change at the molecular level in chronic pain states. At IASP, she will present her work identifying persistent changes in nociceptor translatomes that drive hyperalgesic priming, revealing GPR88 and Meteorin as key regulators of this pain plasticity.

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