Katharina Zimmermann

ORCID: 0000-0003-2529-0692
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About
Contact & Profiles
Research Areas
  • Ion Channels and Receptors
  • Pain Mechanisms and Treatments
  • Ion channel regulation and function
  • Neurobiology and Insect Physiology Research
  • Neuroscience of respiration and sleep
  • Marine Toxins and Detection Methods
  • Nicotinic Acetylcholine Receptors Study
  • Neuropeptides and Animal Physiology
  • Diabetes and associated disorders
  • Neuroendocrine regulation and behavior
  • Biochemical Analysis and Sensing Techniques
  • Antibiotics Pharmacokinetics and Efficacy
  • Thermoregulation and physiological responses
  • Receptor Mechanisms and Signaling
  • Connective tissue disorders research
  • Bone and Dental Protein Studies
  • Advanced Chemical Sensor Technologies
  • Neuroscience and Neuropharmacology Research
  • Herbal Medicine Research Studies
  • Adipose Tissue and Metabolism
  • Diet and metabolism studies
  • Pituitary Gland Disorders and Treatments
  • Connexins and lens biology
  • Exercise and Physiological Responses
  • Redox biology and oxidative stress

University Hospital Regensburg
2023-2025

Friedrich-Alexander-Universität Erlangen-Nürnberg
2014-2024

Universitätsklinikum Erlangen
2015-2024

Saarland University
2013-2022

University of Cologne
2011-2018

University Hospital Cologne
2012

Harvard University
2008-2011

Boston Children's Hospital
2008

Howard Hughes Medical Institute
2008

Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences
2007

A cardinal feature of inflammation is heightened pain sensitivity at the site inflamed tissue. This results from local release by immune and injured cells nociceptor sensitizers, including prostaglandin E 2 , bradykinin, nerve growth factor, that reduce threshold increase excitability peripheral terminals nociceptors so they now respond to innocuous stimuli: phenomenon sensitization. We show here proinflammatory cytokine interleukin-1β (IL-1β), in addition producing inducing synthesis...

10.1523/jneurosci.3795-08.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-12-24

Detection and adaptation to cold temperature is crucial survival. Cold sensing in the innocuous range of (>10-15 °C) mammalian peripheral nervous system thought rely primarily on transient receptor potential (TRP) ion channels, most notably menthol receptor, TRPM8. Here we report that TRP cation channel, subfamily C member 5 (TRPC5), but not TRPC1/TRPC5 heteromeric are highly sensitive 37-25 °C. We found TRPC5 present mouse human sensory neurons dorsal root ganglia, a substantial number...

10.1073/pnas.1115387108 article EN Proceedings of the National Academy of Sciences 2011-10-24

Cold allodynia, pain in response to cooling, occurs during or within hours of oxaliplatin infusion and is thought arise from a direct effect on peripheral sensory neurons. To characterize the pathophysiological mechanisms underlying acute oxaliplatin-induced cold we established new intraplantar mouse model that rapidly developed long-lasting allodynia mediated entirely through tetrodotoxin-sensitive Nav pathways. Using selective inhibitors knockout animals, found Nav1.6 was key isoform...

10.1016/j.pain.2013.05.032 article EN Pain 2013-05-24

Oxytocin is a hormone with various actions. Oxytocin-containing parvocellular neurons project to the brainstem and spinal cord. release from these suppresses nociception of inflammatory pain, molecular mechanism which remains unclear. Here, we report that noxious stimulus receptor TRPV1 an ionotropic oxytocin receptor. elicits activity in native heterologous expression systems, regardless presence classical In knockout mice, DRG exhibit reduced sensitivity relative controls, injections...

10.1016/j.celrep.2017.10.063 article EN cc-by-nc-nd Cell Reports 2017-11-01

Loss-of-function mutations of NaV1.7 lead to congenital insensitivity pain, a rare condition resulting in individuals who are otherwise normal except for the inability sense making pharmacological inhibition promising therapeutic strategy treatment pain. We characterized novel mouse model NaV1.7-mediated pain based on intraplantar injection scorpion toxin OD1, which is suitable rapid vivo profiling inhibitors. Intraplantar OD1 caused spontaneous behaviors, were reversed by co-injection with...

10.3390/toxins8030078 article EN cc-by Toxins 2016-03-17

We demonstrate a novel dual strategy against inflammation and pain through body-wide desensitization of nociceptors via TRPA1. Attenuation experimental colitis by capsazepine (CPZ) has long been attributed to its antagonistic action on TRPV1 associated inhibition neurogenic inflammation. In contrast, we found that CPZ exerts anti-inflammatory effects profound Micromolar induced calcium influx in isolated dorsal root ganglion (DRG) neurons from wild-type (WT) but not TRPA1-deficient mice....

10.1038/srep28621 article EN cc-by Scientific Reports 2016-06-30

Heat sensitivity shows considerable functional variability in humans and laboratory animals, is fundamental to inflammatory possibly neuropathic pain. In the mouse, at least, much of this genetic because inbred strains differ robustly their behavioral noxious heat. These strain differences are shown here reflect differential responsiveness primary afferent thermal nociceptors heat stimuli. We further present convergent electrophysiological evidence that variable responses due...

10.1073/pnas.0503264102 article EN Proceedings of the National Academy of Sciences 2005-08-23

Abstract Human intoxication with the seafood poison ciguatoxin, a dinoflagellate polyether that activates voltage-gated sodium channels (Na V ), causes ciguatera, disease characterised by gastrointestinal and neurological disturbances. We assessed activity of most potent congener, Pacific ciguatoxin-1 (P-CTX-1), on Na 1.1–1.9 using imaging electrophysiological approaches. Although P-CTX-1 is essentially non-selective toxin shifted voltage-dependence activation to more hyperpolarising...

10.1038/srep42810 article EN cc-by Scientific Reports 2017-02-22

To fulfill its role in protein biogenesis, the endoplasmic reticulum (ER) depends on Hsp70-type molecular chaperone BiP, which requires a constant ATP supply. However, carrier that catalyzes uptake into ER was unknown. Here, we report our screen of gene expression datasets for member(s) family solute carriers are co-expressed with BiP and membrane proteins identifies SLC35B1 as potential candidate. Heterologous E. coli reveals is highly specific ADP acts antiport mode. Moreover, depletion...

10.1038/s41467-018-06003-9 article EN cc-by Nature Communications 2018-08-22
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