Queensta Millet

ORCID: 0000-0003-1023-7493
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About
Contact & Profiles
Research Areas
  • Ion channel regulation and function
  • Pain Mechanisms and Treatments
  • Ion Channels and Receptors
  • Erythrocyte Function and Pathophysiology
  • Neuropeptides and Animal Physiology
  • Neurobiology and Insect Physiology Research
  • Botulinum Toxin and Related Neurological Disorders
  • S100 Proteins and Annexins
  • Pain Management and Placebo Effect
  • Thermoregulation and physiological responses
  • Hormonal Regulation and Hypertension
  • Fibromyalgia and Chronic Fatigue Syndrome Research
  • Circadian rhythm and melatonin
  • Neuroendocrine regulation and behavior

University College London
2017-2024

Whitechapel Gallery
2018

University of London
2018

The ability to detect environmental cold serves as an important survival tool. sodium channels NaV1.8 and NaV1.9, well the TRP channel Trpm8, have been shown contribute sensation in mice. Surprisingly, transcriptional profiling shows that NaV1.8/NaV1.9 Trpm8 are expressed nonoverlapping neuronal populations. Here we used vivo GCaMP3 imaging identify cold-sensing populations of sensory neurons live We find ∼80% responsive down 1 °C do not express NaV1.8, genetic deletion does affect relative...

10.1073/pnas.1814545116 article EN cc-by Proceedings of the National Academy of Sciences 2019-02-12

Patients with neuropathic pain often experience innocuous cooling as excruciating pain. The cell and molecular basis of this cold allodynia is little understood. We used in vivo calcium imaging sensory ganglia to investigate how the activity peripheral cold-sensing neurons was altered three mouse models pain: oxaliplatin-induced neuropathy, partial sciatic nerve ligation, ciguatera poisoning. In control mice, were few number small size. animals allodynia, a set normally silent large diameter...

10.1093/brain/awab086 article EN cc-by Brain 2021-03-06

Background: Sensory neurons play an essential role in almost all pain conditions, and have recently been classified into distinct subsets on the basis of their transcriptomes. Here we analysed alterations dorsal root ganglia (DRG) gene expression using microarrays mouse models related to human chronic pain. Methods: Six different were studied male C57BL/6J mice: (1) bone cancer cell injection intramedullary space femur; (2) neuropathic partial sciatic nerve ligation; (3) osteoarthritis...

10.12688/wellcomeopenres.14641.1 preprint EN cc-by Wellcome Open Research 2018-06-25

Background: Functional deletion of the Scn9a (sodium voltage-gated channel alpha subunit 9) gene encoding sodium Nav1.7 makes humans and mice pain-free. Opioid signalling contributes to this analgesic state. We have used pharmacological genetic approaches identify opioid receptors involved in form analgesia. also examined regulation proenkephalin expression by transcription factor Nfat5 that binds upstream Penk gene. Methods: specific µ-, δ- κ-opioid receptor antagonists alone or combination...

10.12688/wellcomeopenres.14687.1 preprint EN cc-by Wellcome Open Research 2018-08-16

Abstract The 2 tetrodotoxin-resistant (TTXr) voltage-gated sodium channel subtypes Na V 1.8 and 1.9 are important for peripheral pain signaling. As determinants of sensory neuron excitability, they essential the initial transduction stimuli, electrogenesis action potential, release neurotransmitters from terminals. 1.9, which encoded by SCN10A SCN11A , respectively, predominantly expressed in pain-sensitive (nociceptive) neurons localized dorsal root ganglia (DRG) along spinal cord...

10.1097/j.pain.0000000000003411 article EN cc-by-nc-nd Pain 2024-10-04

Summary Deletion of SCN9A encoding the voltage-gated sodium channel Na V 1.7 in humans leads to profound pain insensitivity and anosmia. Conditional deletion sensory neurons mice also abolishes suggesting locus analgesia is nociceptor. Here we demonstrate that knockout have essentially normal nociceptor activity using vivo calcium imaging extracellular recording. However, glutamate substance P release from central terminals spinal cord greatly reduced by an opioid-dependent mechanism....

10.1101/2020.06.01.127183 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-06-02

Summary Neuropathic pain patients often experience innocuous cooling as excruciating pain. The cell and molecular basis of this cold allodynia is little understood. We used in vivo calcium imaging sensory ganglia to investigate the activity peripheral cold-sensing neurons three mouse models neuropathic pain: oxaliplatin-induced neuropathy, partial sciatic nerve ligation ciguatera poisoning. In control mice, were few number small size. animals with allodynia, a set normally silent...

10.1101/2020.05.02.073999 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-05-03

Abstract Sensory neuron mechanically-activated slowly adapting currents have been linked to noxious mechanosensation. We identified a Conotoxin, Noxious Mechanosensation Blocker -1, that blocks such selectively and inhibits mechanical pain Using an active biotinylated form of the toxin we 67 binding proteins in sensory neurons neuron-derived cell lines using mass spectrometry. Annexin A6 was most frequently protein. knockout mice showed enhanced sensitivity stimuli. An increase rapidly...

10.1101/155812 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2017-06-26
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