In behavioral experiments, inhibition of nuclear factor-kappaB activation by systemic administration of the IkappaB kinase inhibitor S1627 has been shown to attenuate inflammatory and neuropathic pain. Here, we specifically investigated with electrophysiological recordings in anesthetized rats whether spinal application of S1627 influences hyperexcitability of dorsal horn neurons during an acute knee joint inflammation. Spinal application of S1627 before and early during development of inflammation totally prevented spinal hyperexcitability suggesting an important role of spinal nuclear factor-kappaB in this process. During established inflammation, however, S1627 did not reduce the responses of neurons to mechanical stimulation of the inflamed knee within 2.5 h after spinal administration, thus suggesting that spinal hyperexcitability is not maintained by continuous nuclear factor-kappaB activation.
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http://dx.doi.org/10.1097/01.wnr.0000236867.76347.60 | DOI Listing |
J Neuroinflammation
December 2024
Aix Marseille Univ, CNRS, INT, Inst. Neurosci. Timone, Marseille, France.
Background: Non-invasive photobiomodulation therapy (PBMT), employing specific infrared light wavelengths to stimulate biological tissues, has recently gained attention for its application to treat neurological disorders. Here, we aimed to uncover the cellular targets of PBMT and assess its potential as a therapeutic intervention for multiple sclerosis (MS).
Methods: We applied daily dorsoventral PBMT in an experimental autoimmune encephalomyelitis (EAE) mouse model, which recapitulates key features of MS, and revealed a strong positive impact of PBMT on the sensorimotor deficits.
Nutrients
November 2024
Laboratory of Food and Physiological Sciences, Department of Life and Food Sciences, School of Life and Environmental Sciences, Azabu University, 1-17-71, Fuchinobe, Chuo-ku, Sagamihara 252-5201, Kanagawa, Japan.
The present study examines whether the systemic application of naringenin (NRG) reduces inflammation-induced hyperexcitability in the spinal trigeminal nucleus caudalis (SpVc) related to hyperalgesia, and compares its impact with that of diclofenac (DIC). To provoke inflammation, the whisker pads of rats were injected with complete Freund's adjuvant, and subsequently, mechanical stimuli were administered to the orofacial region to determine the escape threshold. Compared to naïve rats, the inflamed rats showed a significantly lower mechanical threshold, and this reduced threshold returned to normal levels two days post-administration of NRG, DIC, and half-dose DIC plus half-dose NRG (1/2 DIC + 1/2 NRG).
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Institute of Physiology 1/Neurophysiology, Jena University Hospital, Friedrich-Schiller-University, D-07740 Jena, Germany.
Healthcare (Basel)
November 2024
Sensorimotor Function Group, Hospital Nacional de Parapléjicos (SESCAM), 45071 Toledo, Spain.
: Although increased nociceptive excitability and deficient endogenous pain modulation are considered key features of pronociception and central sensitization, their contribution to neuropathic pain (NP) characteristics in SCI is unclear. The aim of this study was to characterize tonic cold perception and endogenous pain modulation in individuals with and without SCI-NP, considering the stage and severity of SCI and, secondarily, NP phenotype. : Temporal summation of pain (TSP) and neuropathic features were assessed using the numerical rating scale (NRS) and Douleur Neuropathique 4 screening questionnaire (DN4) during the tonic cold pressor test (CPT, 12 °C 60 s) applied to the dominant hand and foot.
View Article and Find Full Text PDFInt Rev Neurobiol
November 2024
Danish Pain Research Center, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark; Department of Neurology, Aarhus University Hospital, Aarhus, Denmark.
This chapter aims to review the current pharmacological options for neuropathic pain treatment, their mechanisms of action, and future directions for clinical practice. Achieving pain relief in neuropathic pain conditions remains a challenge in clinical practice. The field of pharmacotherapy for neuropathic pain has encountered significant difficulties in translating substantial advances in our understanding of the underlying pathophysiological mechanisms into clinically effective therapies.
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