Sensory and Motor Systems
Author: Mayra Micaela Montes | email: mayramontes1997@gmail.com
Mayra Micaela Montes 1°, Georgina Oriana Mingolo Malnati 1°, Libia Catalina Salinas Castellanos 1°, María Natalia Gobetto 1°, Osvaldo Daniel Uchitel 1°, Carina Weissmann 1°
1° IFIBYNE
Neuropathic pain is one of the key features of ?-galactosidase A (Gla) deficient Fabry Disease (FD). Ion channels play an important role in the pain pathway: the detection of local stimuli, the transmission of electrical impulses to the brain, and their interpretation as pain signals. Acid-sensing ion channels(ASICs) are sensors involved in neural modulation in the central nervous system and pain-associated tissue acidosis in the peripheral system. Upregulation of ASIC1 channels has been documented in many pathological conditions. ASIC1 exists in two variants, ASIC1a and ASIC1b, alternative splice isoforms. Most antibodies detect both isoforms. This work aims at analyzing ASIC1 RNA levels in FD. Previous work by the group in a formalin acute pain mouse model showed an increase in ASIC1 levels at different regions of the pain pathway. In this work, we analyzed the Gla knockout mouse (GlaKO) (Ohshima et al., 1997) model that accumulates Gb3. We detected higher levels of ASIC1 at the anterior cingulate cortex (ACC), spinal cord (SC) and Dorsal Root Ganglia (DRG) in the Glako mice, the same regions that showed an acute increase in the formalin model. However, contrary to the formalin model were RNA levels are not altered, preliminary results showed ASIC1a and ASIC1b RNA levels change in the ACC, SC and DRG of GlaKO mice compared to the wt animals. This work suggests different mechanisms contribute via ASIC1 to pain (and might be modulated in therapies) in acute and chronic models.