ePoster

Brain activation during inflammatory and non-inflammatory hyperalgesia in a rheumatoid arthritis mouse model

Rita Gálosi, Gábor Kriszta, Éva Borbély, Ádám I Horváth, Valéria Tékus, Nikolett Szentes, Zsuzsanna Helyes
FENS Forum 2024(2024)
Messe Wien Exhibition & Congress Center, Vienna, Austria

Conference

FENS Forum 2024

Messe Wien Exhibition & Congress Center, Vienna, Austria

Resources

Authors & Affiliations

Rita Gálosi, Gábor Kriszta, Éva Borbély, Ádám I Horváth, Valéria Tékus, Nikolett Szentes, Zsuzsanna Helyes

Abstract

The K/BxN serum-induced arthritis mouse model is used as a human rheumatoid arthritis (RA) model. Previous results demonstrated that after the arthritogenic K/BxN serum injections joint edema and inflammation are pronounced for 9 days, then decrease, while hyperalgesia persists. We applied manganese-enhanced magnetic resonance imaging (MEMRI) after arthritogenic K/BxN or non-arthritogenic BxN serum administration on days 9 and 21, to detect pain-related brain activity reflecting the inflammatory and non-inflammatory phases of this model. MRI scans were conducted before and 24 hours after the MnCl2 infusion. T1 maps were calculated and change in T1 relaxation time (dT1) was analyzed. Mechanical hyperalgesia was observed in all mice from day 2 to day 21 after K/BxN serum administration after K/BxN serum administration, with the edema declining after day 9. During the inflammatory phase, dT1 reduction was observed in the cortex, hippocampus, striatum, globus pallidus, nucleus accumbens, septal area, midbrain, and substantia nigra compared to the non-arthritic control group. During the non-inflammatory hyperalgesia phase, dT1 remained reduced in the cortex, while the central gray of midbrain with pons showed full recovery. The reduced dT1 might reflect decreased brain activity, Mn2+ blood-brain barrier transport and/or Ca2+ dyshomeostasis due to neuroinflammatory processes. Reduced cortical activity might explain hyperalgesia, presumably via decreased pain control mechanisms.The work is supported by Hungarian Research Network Chronic Pain Research Group, National Brain Research Program 3.0, National Research, OTKA-K138046, and the EU-funded Project RRF-2.3.1-21-2022-00015

Unique ID: fens-24/brain-activation-during-inflammatory-253f0f62