I am a
Home I AM A Search Login

Papers of the Week


Papers: 20 Jun 2020 - 26 Jun 2020


Animal Studies, Pharmacology/Drug Development

PAIN TYPE:
Migraine/Headache


2020 Jun 20


Neuropharmacology

Capsaicin-sensitive fibers mediate periorbital allodynia and activation of inflammatory cells after traumatic brain injury in rats: Involvement of TRPV1 channels in post-traumatic headache.

Authors

da SilvaFiorin F, do Espírito Santo C C, Santos do Nascimento R, Cassol G, Plácido E, Santos A R S, Brum Marques J L, Brocardo PS, Fighera M R, Royes L F F
Neuropharmacology. 2020 Jun 20:108215.
PMID: 32574651.

Abstract

Post-traumatic headache (PTH) is a condition that frequently affects individuals after traumatic brain injury (TBI). Inflammation is one of the major causes of this disability. However, little is known about the trigger for, and endurance of, this painful process. Thus, the involvement of fibers containing the transient receptor potential vanilloid 1 (TRPV1) channels on the PTH and inflammation after TBI through neonatal treatment with capsaicin are investigated. Fluid percussion injury (FPI) in adult male Wistar rats caused periorbital allodynia in one, three and seven days after injury, and the neonatal treatment reversed the painful sensation in seven days. The lack of TRPV1 channels reduced the activation of macrophages and glial cells induced by TBI in the trigeminal system, which were characterized by glial fibrillary acidic protein (GFAP) and ionized calcium binding adapter molecule-1 (IBA-1) immune content in the ipsilateral trigeminal ganglion, brainstem, and perilesional cortex. Immunofluorescence analyses of the ipsilateral Sp5C nucleus demonstrated a hypertrophic astrocytes profile after TBI which was reduced with treatment. Moreover, effects of succinate sumatriptan (SUMA – 1 mg/kg), TRPV1 selective antagonist capsazepine (CPZ – 2 mg/kg), and TRP non-selective antagonist ruthenium red (RR – 3 mg/kg) were evaluated. Although all mentioned drugs reduced the painful sensation, SUMA and CPZ demonstrated a stronger effect compared to the RR treatment, reinforcing the involvement of TRPV1 channels in periorbital allodynia after TBI. Hence, this report suggests that TRPV1-containing fibers and TRPV1 channels are able to induce inflammation of the trigeminal system and maintain the painful sensation after TBI.