دورية أكاديمية

Oxytocin shortens spreading depolarization-induced periorbital allodynia.

التفاصيل البيبلوغرافية
العنوان: Oxytocin shortens spreading depolarization-induced periorbital allodynia.
المؤلفون: Harriott, Andrea M., Kaya, Melih, Ayata, Cenk
المصدر: Journal of Headache & Pain; 9/17/2024, Vol. 25 Issue 1, p1-10, 10p
مصطلحات موضوعية: HYPOTHALAMUS physiology, OXYTOCIN, IN vitro studies, HETEROCYCLIC compounds, PAIN measurement, RESEARCH funding, EVOKED potentials (Electrophysiology), HYDROCARBONS, NEURONS, DESCRIPTIVE statistics, HYPERALGESIA, MICE, IMMUNOHISTOCHEMISTRY, GENE expression, ANIMAL experimentation, MIGRAINE, ALLODYNIA, CELL receptors
مستخلص: Background: Migraine is among the most prevalent and burdensome neurological disorders in the United States based on disability-adjusted life years. Cortical spreading depolarization (SD) is the most likely electrophysiological cause of migraine aura and may be linked to trigeminal nociception. We previously demonstrated, using a minimally invasive optogenetic approach of SD induction (opto-SD), that opto-SD triggers acute periorbital mechanical allodynia that is reversed by 5HT1B/1D receptor agonists, supporting SD-induced activation of migraine-relevant trigeminal pain pathways in mice. Recent data highlight hypothalamic neural circuits in migraine, and SD may activate hypothalamic neurons. Furthermore, neuroanatomical, electrophysiological, and behavioral data suggest a homeostatic analgesic function of hypothalamic neuropeptide hormone, oxytocin. We, therefore, examined the role of hypothalamic paraventricular nucleus (PVN) and oxytocinergic (OXT) signaling in opto-SD-induced trigeminal pain behavior. Methods: We induced a single opto-SD in adult male and female Thy1-ChR2-YFP transgenic mice and quantified fos immunolabeling in the PVN and supraoptic nucleus (SON) compared with sham controls. Oxytocin expression was also measured in fos-positive neurons in the PVN. Periorbital mechanical allodynia was tested after treatment with selective OXT receptor antagonist L-368,899 (5 to 25 mg/kg i.p.) or vehicle at 1, 2, and 4 h after opto-SD or sham stimulation using von Frey monofilaments. Results: Opto-SD significantly increased the number of fos immunoreactive cells in the PVN and SON as compared to sham stimulation (p < 0.001, p = 0.018, respectively). A subpopulation of fos-positive neurons also stained positive for oxytocin. Opto-SD evoked periorbital mechanical allodynia 1 h after SD (p = 0.001 vs. sham), which recovered quickly within 2 h (p = 0.638). OXT receptor antagonist L-368,899 dose-dependently prolonged SD-induced periorbital allodynia (p < 0.001). L-368,899 did not affect mechanical thresholds in the absence of opto-SD. Conclusions: These data support an SD-induced activation of PVN neurons and a role for endogenous OXT in alleviating acute SD-induced trigeminal allodynia by shortening its duration. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:11292369
DOI:10.1186/s10194-024-01855-7