Unlabelled: This study investigated if conditioned pain modulation (CPM) varies across the menstrual cycle in healthy, normally menstruating women and investigated correlations between sex hormone levels and CPM across the menstrual cycle. Thirty-six normally menstruating women were tested during 3 phases of the menstrual cycle: early follicular, ovulatory, and midluteal, confirmed by hormone determinations. Mechanical pressure (test stimulus) was applied to the masseter muscle and the induced pain assessed before, during, and after immersion of the hand into ice water (conditioning stimulus) to activate CPM or tepid water (control). Conditioning pain, ie, pain in the hand during CPM/control experiment, and tolerance time were also measured. Test pain intensity was suppressed during CPM in all phases (P < .001), but with more effective suppression during the ovulatry than during the early follicular phase (P < .05). There were no changes in test pain intensity during the control experiment and no significant differences in conditioning pain, or tolerance time between phases. In conclusion, our results showed more effective pain modulation in the ovulatory phase of the menstrual cycle, when estradiol levels are high and progesterone levels are low, than in the early follicular phase when both these hormones are low.
Perspective: Deficient pain modulation is believed to be an important pathogenic factor in many chronic pain conditions that affect women. This article shows that sex hormones modulate conditioned pain modulation, because pain inhibition was more effective in the ovulatory phase of the menstrual cycle than in the early follicular phase.
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http://dx.doi.org/10.1016/j.jpain.2012.04.002 | DOI Listing |
J Cyst Fibros
January 2025
Southern Cross University, Faculty of Health, Coolangatta, Queensland, Australia. Electronic address:
Background: A previous Australia-wide pilot study identified pain as a significant burden in people with CF (pwCF). However, the prevalence, frequency and severity have not been evaluated using validated tools.
Methods: Australian adults, pwCF and healthy controls (HC) were invited to complete an online questionnaire from July 2023 - February 2024, consisting of four validated tools: Brief Pain Inventory, Pain Catastrophising Scale, PAGI-SYM and PAC-SYM.
Arch Biochem Biophys
January 2025
Pharmacological Sciences Research Lab, Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan; Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Electronic address:
Aim: The aim of the current study was to investigate the potential therapeutic effect of kaurenoic acid (KA) against Monosodium Urate Crystals (MSU)- induced acute gout by downregulation of NF-κB signaling pathway, mitigating inflammation and oxidative stress produced by MSU crystals. KA potentially targeted NF-κB pathway activation and provided comprehensive insights through multiple approaches. This was accomplished by advanced analytical techniques.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Zhengzhou University, 100 Science Avenue, Zhengzhou, 450001, China; Institute of Neuroscience, School of Basic Medical Sciences, Zhengzhou University, 100 Science Avenue, Zhengzhou, 450001, China; School of Nursing and Health, Zhengzhou University, 100 Science venue, Zhengzhou, 450001, China. Electronic address:
Chemotherapy-induced neuropathic pain poses significant clinical challenges and severely impacts patient quality of life. Sodium ion channels are crucial in regulating neuronal excitability and pain. Our research indicates that the microRNA-30b (miR-30b) in rat dorsal root ganglia (DRG) contributes to chemotherapy-induced neuropathic pain by regulating the Nav1.
View Article and Find Full Text PDFNeurobiol Dis
January 2025
Department of Pharmacy, Children's Hospital of Nanjing Medical University, Nanjing, China. Electronic address:
A-kinase anchoring protein 79/150 (AKAP79/150) is a crucial scaffolding protein that positions various proteins at specific synaptic sites to modulate excitatory synaptic intensity. As our understanding of AKAP79/150's biology deepens, along with its significant role in the pathophysiology of various human disorders, there is growing evidence that reveals new opportunities for therapeutic interventions. In this review, we examine the fundamental structure and primary functions of AKAP79/150, emphasizing its pathophysiological mechanisms in different nervous system disorders, particularly inflammatory pain, epilepsy, depression, and Alzheimer's disease.
View Article and Find Full Text PDFBehav Brain Res
January 2025
Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin 300052, China; Tianjin Research Institute of Anesthesiology, Tianjin 300052, China. Electronic address:
Neuropathic pain (NP) is a chronic disease state centred on neuroinflammation with a high prevalence and limited effective treatment options. Peroxisome proliferator-activated receptor α (PPARα) has emerged as a promising target for NP management due to its anti-inflammatory properties. Recent evidence highlights the critical role of the gut microbiome and its metabolites in NP pathogenesis.
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