K
Katharina Hösl
Researcher at University of Erlangen-Nuremberg
Publications - 6
Citations - 1066
Katharina Hösl is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Neuropathic pain & Nociception. The author has an hindex of 5, co-authored 5 publications receiving 918 citations.
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Journal ArticleDOI
Reversal of pathological pain through specific spinal GABAA receptor subtypes.
Julia Knabl,Robert Witschi,Katharina Hösl,Heiko Reinold,Ulrike B. Zeilhofer,Seifollah Ahmadi,Seifollah Ahmadi,Johannes Brockhaus,Johannes Brockhaus,Marina Sergejeva,Andreas Hess,Kay Brune,Jean-Marc Fritschy,Uwe Rudolph,Uwe Rudolph,Hanns Möhler,Hanns Möhler,Hanns Ulrich Zeilhofer,Hanns Ulrich Zeilhofer,Hanns Ulrich Zeilhofer +19 more
TL;DR: It is shown that their selective activation by the non-sedative (‘α1-sparing’) benzodiazepine-site ligand L-838,417 is highly effective against inflammatory and neuropathic pain yet devoid of unwanted sedation, motor impairment and tolerance development.
Journal ArticleDOI
BOLD fMRI deactivation of limbic and temporal brain structures and mood enhancing effect by transcutaneous vagus nerve stimulation.
TL;DR: This study shows the feasibility and beneficial effects of transcutaneous nerve stimulation in the left auditory canal of healthy subjects and shows brain activation patterns clearly share features with changes observed during invasive vagus nerve stimulation.
Journal ArticleDOI
CNS BOLD fMRI effects of sham-controlled transcutaneous electrical nerve stimulation in the left outer auditory canal - a pilot study.
TL;DR: The results of the study show promise for a specific novel method of cranial nerve stimulation and provide a basis for further developments and applications of non-invasive transcutaneous vagus stimulation in psychiatric patients.
Journal ArticleDOI
Spinal prostaglandin E receptors of the EP2 subtype and the glycine receptor α3 subunit, which mediate central inflammatory hyperalgesia, do not contribute to pain after peripheral nerve injury or formalin injection
Katharina Hösl,Heiko Reinold,Robert J. Harvey,Ulrike Müller,Ulrike Müller,Shuh Narumiya,Hanns Ulrich Zeilhofer,Hanns Ulrich Zeilhofer +7 more
TL;DR: The results indicate that inhibition of glycinergic neurotransmission by EP2 receptor activation does not contribute to pain following peripheral nerve injury or chemical irritation with formalin, providing further evidence that inflammatory hyperalgesia and neuropathic pain involve different mechanisms of central sensitization.
Journal ArticleDOI
Subtype-selective GABAA receptor mimetics—novel antihyperalgesic agents?
TL;DR: Evidence from genetically modified mice now indicates that agents targeting only a subset of benzodiazepine (GABAA) receptors should provide pronounced antihyperalgesic activity against inflammatory and neuropathic pain.