About

Linda Watkins is a Distinguished Professor in the Department of Psychology and Neuroscience at the University of Colorado Boulder. She specializes in behavioral neuroscience with research interests that include pain modulation systems, immune and glial regulation of neuronal function, immune-to-brain communication, and glial regulation of pain, opioid analgesia, drugs of abuse, learning and memory, and neuronal excitability. Her work also focuses on stress-induced regulation of brain and behavior and explores novel approaches to controlling chronic pain. Dr. Watkins earned her PhD from the Medical College of Virginia in 1980. She is associated with the Center for Neuroscience and is actively involved in research aimed at understanding and developing treatments for pain and related neurological conditions.

Research topics

• Medicine
• Internal medicine
• Immunology
• Biology
• Anesthesia
• Psychiatry
• Physical therapy
• Psychology
• Pharmacology
• Pathology
• Neuroscience
• Cell biology

Selected publications

• Pain and the immune system

  Musculoskeletal Science and Practice · 2026-01-31 · 2 citations

  article
  PublisherDOI

• Reordering neuroimmune signaling to prevent and resolve chronic pain

  Pain · 2025-10-14 · 2 citations

  reviewSenior author

  ABSTRACT: Chronic pain is subserved by interactions between the immune and nervous systems. There has been an historical emphasis on the disordered pro-inflammatory mechanisms that maintain chronic pain. This narrative review will highlight the adaptive benefit of initial pro-inflammatory signaling for the long-term trajectory of pain, as well as pro-resolving mechanisms that can prevent pain from becoming chronic. Importantly, there is potential for these insights to be harnessed for safe, nonaddictive, disease-modifying treatment of pain.

  PublisherDOI

• Activation of sphingosine-1-phosphate receptor subtype 1 in the central nervous system contributes to morphine-induced hyperalgesia and antinociceptive tolerance in rodents: erratum

  Pain · 2025-04-16

  erratum
  PublisherDOI

• Caudal Granular Insular Cortex to Somatosensory Cortex I: A Critical Pathway for the Transition of Acute to Chronic Pain

  Journal of Neuroscience · 2025-12-16 · 1 citations

  articleOpen accessSenior author

  Allodynia (perceiving touch as painful) is an enduring symptom of neuropathic pain. While acute pain is initiated by afferent signaling from the periphery to spinal cord, pain chronification recruits ongoing activity in supraspinal sites. One such site that has been proposed to be important in pain chronification is the caudal granular insular cortex (CGIC). The present studies of allodynia in response to sciatic nerve injury in male and female rats focus on the role of CGIC in pain chronification by analyzing: circuit-specific mGreenLantern expression to define CGIC-to-somatosensory cortex I (SI) projections; behavioral and electrophysiological effects of chemogenetic (DREADD) excitation and inhibition of CGIC; behavioral and immediate-early gene effects of pathway-specific activation and inhibition of CGIC-to-SI projections; and mGreenLantern expression in dendritic arbors of CGIC-to-SI projection neurons to assess CGIC dendritic spine changes following neuropathic pain. These studies demonstrate that signals from CGIC-to-SI are necessary for neuropathic pain. Nerve injury induces plasticity in CGIC dendritic spine morphology, multiweek chemogenetic inhibition of CGIC or CGIC-to-SI projection neurons produces an enduring reversal of neuropathic pain, and DREADD-induced excitation of this pathway in non-neuropathic rats induces allodynia and increases c-Fos expression in CGIC, SI, and pain responsive laminae in spinal cord dorsal horn. Together with recent findings showing that SI modifies incoming nociceptive and touch information, these data demonstrate that input from CGIC-to-SI input shapes SI gating of nociceptive signals and promotes the transition to chronic pain following peripheral nerve injury.

  PublisherOA PDFDOI

• Spinal cord injury in rats disrupts thermoregulation and suppresses stress-induced hyperthermia

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-10

  preprintOpen access

  Abstract Spinal cord injury (SCI) in humans can robustly dysregulate healthy autonomic nervous system function, including thermoregulation. Despite this, the relationship between SCI and autonomic dysfunction remains incompletely understood and is often overlooked in rodent models that emphasize locomotor recovery. One notable autonomic output in rodents is stress-induced hyperthermia, which is a transient core temperature increase caused by an acute stressor. Here, we tested whether SCI in rats dysregulates stress-induced hyperthermia. To assess SCI-induced thermoregulatory dysfunction, we continuously monitored core temperature in male and female rats using implantable telemetry devices before and after a T8 contusion SCI (or sham surgery including laminectomy). Prior to surgery, stress—in response to handling and cage changes— resulted in transient hyperthermia that peaked ∼1°C higher than baseline and lasted 60-90 minutes. Sham-operated rats retained typical stress-induced hyperthermia beginning immediately after surgery. In contrast, SCI transiently abolished stress-induced hyperthermia in both sexes, indicating a profound disruption in autonomic regulation acutely after injury. Within 3-4 weeks after SCI, the stress-induced hyperthermic response gradually returned and reached pre-injury levels by week seven. Therefore, thoracic SCI in rats abolishes stress-induced hyperthermia, which gradually recovers over time post-injury. Overall, this study underscores the impact of incomplete SCI on autonomic function and highlights the need for future research focused on autonomic outcomes. Highlights Handling and care procedures elicit stress-induced hyperthermia in rats Stress-induced hyperthermia was abolished in rats after spinal cord injury Stress-induced hyperthermia gradually returned over the subsequent weeks By 7 weeks, the hyperthermic response had returned to pre-injury levels

  PublisherOA PDFDOI

• Photobiomodulation therapy in neuropathic pain: mechanisms, evidence, and future directions

  Frontiers in Photonics · 2025-12-19 · 2 citations

  articleOpen access

  Neuropathic pain (NP) is a chronic and disabling condition resulting from injury or disease of the somatosensory system. Characterized by sensory disturbances such as allodynia, hyperalgesia, and spontaneous pain, NP remains a major clinical challenge due to the limited efficacy and significant side effects of conventional pharmacological treatments. In recent years, photobiomodulation therapy (PBMT), also referred to as low-level laser therapy (LLLT), has emerged as a promising non-pharmacological strategy for managing NP. PBMT involves the application of red or near-infrared light to biological tissues, triggering a range of photochemical and photophysical responses that enhance mitochondrial function, reduce oxidative stress, modulate inflammation, and support neural repair. This review provides a comprehensive synthesis of the current evidence on PBMT for NP, integrating mechanistic insights with preclinical findings. We discuss the biological underpinnings of PBMT, including mitochondrial activation via cytochrome c oxidase, modulation of cytokines and oxidative stress markers, and upregulation of neurotrophic factors such as BDNF. Preclinical studies in well-established NP models (e.g., chronic constriction injury, spared nerve injury, diabetic neuropathy) demonstrate consistent analgesic effects and neuroprotective outcomes following both local and remote/systemic PBMT applications. We also highlight key limitations and knowledge gaps in the field, including the need for standardized protocols, greater exploration of remote PBMT strategies, and improved consideration of sex-based responses. Finally, we outline future directions, such as integration with multimodal therapies, personalized dosimetry, and the development of wearable and transcranial PBMT technologies. Together, the existing body of evidence supports PBMT as a safe and potentially effective tool for NP management, while underscoring the need for more rigorous and translational research.

  PublisherDOI

• Use of adeno-associated viruses for transgenic modulation of microglia structure and function: A review of technical considerations and challenges

  Brain Behavior and Immunity · 2024-03-11 · 7 citations

  reviewOpen accessSenior author
  PublisherOA PDFDOI

• Chandipura viral glycoprotein (CNV-G) promotes Gectosome generation and enables delivery of intracellular therapeutics

  Molecular Therapy · 2024-05-03 · 3 citations

  articleOpen access
  PublisherOA PDFDOI

• Corrigendum to “Intrathecal non-viral interleukin-10 gene therapy ameliorates neuropathic pain as measured by both classical static allodynia and a novel supra-spinally mediated pain assay, the Two-Arm Rodent Somatosensory (TARS) task” [Brain Behav. Immun. 111 (2023) 177–185]

  Brain Behavior and Immunity · 2024-08-24

  erratumSenior authorCorresponding
  PublisherDOI

• Microglia in neuroimmunopharmacology and drug addiction

  Molecular Psychiatry · 2024-02-02 · 32 citations

  review
  PublisherDOI

Recent grants

• NIH Grant R01DE017782

  NIH · $1.9M · 2012

• NIH Grant R01DA023132

  NIH · $1.9M · 2014

• Targeting neuropathic pain prevention: Modulating the neuroimmunology of peripheral nerve injury

  NIH · $1.7M · 2016–2023

• NIH Grant K05DA024044

  NIH · $247k · 2013

• NIH Grant R03DA017656

  NIH · $149k · 2007

Frequent coauthors

• Steven F. Maier

  University of Colorado Boulder

  451 shared

• Mark R. Hutchinson

  University of Adelaide

  117 shared

• Kenner C. Rice

  National Institute on Alcohol Abuse and Alcoholism

  104 shared

• Peter M. Grace

  The University of Texas MD Anderson Cancer Center

  86 shared

• Erin D. Milligan

  University of New Mexico

  75 shared

• Matthew G. Frank

  University of Colorado Boulder

  67 shared

• Monika Fleshner

  University of Colorado Boulder

  54 shared

• Ruth M. Barrientos

  52 shared

Education

• Ph.D.

  Medical College of Virginia

  1980

Awards & honors

• Distinguished Professor