Non-steroidal anti-inflammatory drugs (NSAID) only partially inhibit the hyperalgesia in the inflammation induced by carrageenin in the hind rat paw, one of the most frequently used nociceptive tests. We now report that either the guanethidine depletion of peripheral sympathomimetic amines or the treatment with adrenoceptor antagonists (beta-blockers) and a specific dopamine (DA)-1 antagonist (SCH 23390) significantly reduced carrageenin hyperalgesia. These antagonists also abolished the rat paw hyperalgesia induced by several sympathomimetic amines as well as that induced by a selective DA-1 agonist, SKF 38393. Blockade of uptake-1 by cocaine potentiated the hyperalgesia induced by carrageenin and sympathomimetic amines. We conclude that there is a sympathetic component, possibly mediated by a DA-1 type receptor in carrageenin-induced hyperalgesia. This component may predominate in certain types of pain not sensitive to NSAID. If so, selective peripheral DA-1 antagonists could be developed as a novel class of analgesics.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/0014-2999(87)90606-6 | DOI Listing |
Sci Rep
January 2025
Department of Gastroenterological Surgery, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Sympathetic nerves regulate nearly all human organs. Their peripheral nerves are present in tumor tissue. Activation of the sympathetic nervous system promotes malignant transformation in several cancers.
View Article and Find Full Text PDFAddict Sci Clin Pract
January 2025
Department of Medicine, Division of General Internal Medicine, University of Washington/Harborview Medical Center, 325 9Th Avenue, Box 359780, Seattle, WA, 98104, USA.
Background: Initiation of buprenorphine for treatment of opioid use disorder (OUD) in acute care settings improves access and outcomes, however patients who use methamphetamine are less likely to link to ongoing treatment. We describe the intervention and design from a pilot randomized controlled trial of an intervention to increase linkage to and retention in outpatient buprenorphine services for patients with OUD and methamphetamine use who initiate buprenorphine in the hospital.
Methods: The study is a two-arm pilot randomized controlled trial (N = 40) comparing the mHealth Incentivized Adherence Plus Patient Navigation (MIAPP) intervention to treatment as usual.
Psychiatr Clin North Am
March 2025
Department of Neurology, Johns Hopkins University School of Medicine, Kennedy Krieger Institute, Baltimore, MD, USA.
The pathophysiology of tic disorders involves an alteration in the transmission of messages through the cortico-basal ganglia-thalamo-cortical circuit. A major requirement for the passage of a message through this circuit is an intact chemically mediated synaptic neurotransmitter system (ie, neurotransmitters and second messengers). This article reviews the scientific evidence supporting the involvement of a variety of neurotransmitters (ie, dopamine, glutamate, gamma-aminobutyric acid, serotonin, acetylcholine, and the opioid system).
View Article and Find Full Text PDFJ Med Internet Res
January 2025
Centre for Cognitive and Brain Sciences, Institute of Collaborative Innovation, University of Macau, Macau, China.
This study provides preliminary evidence for real-time functional magnetic resonance imaging neurofeedback (rt-fMRI NF) as a potential intervention approach for internet gaming disorder (IGD). In a preregistered, randomized, single-blind trial, young individuals with elevated IGD risk were trained to downregulate gaming addiction-related brain activity. We show that, after 2 sessions of neurofeedback training, participants successfully downregulated their brain responses to gaming cues, suggesting the therapeutic potential of rt-fMRI NF for IGD (Trial Registration: ClinicalTrials.
View Article and Find Full Text PDFElife
January 2025
Department of Cognitive Psychology, University of Hamburg, Hamburg, Germany.
When retrieved, seemingly stable memories can become sensitive to significant events, such as acute stress. The mechanisms underlying these memory dynamics remain poorly understood. Here, we show that noradrenergic stimulation after memory retrieval impairs subsequent remembering, depending on hippocampal and cortical signals emerging during retrieval.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!