Segmental upregulation of ASIC1 channels in the formalin acute pain mouse model

dc.creatorGobetto, María Natalia
dc.creatorSalinas Castellanos, Libia Catalina
dc.creatorContreras, Natalia Estefanía
dc.creatorSodero, Alejandro Omar
dc.creatorCambiagno, Damián Alejandro
dc.creatorMingolo Malnati, Georgina Oriana
dc.creatorMontes, Mayra Micaela
dc.creatorUchitel, Osvaldo Daniel
dc.creatorWeissmann, Carina
dc.date2023-03-23T11:45:51Z
dc.date2023-03-23T11:45:51Z
dc.date2022
dc.date.accessioned2023-08-30T15:38:29Z
dc.date.available2023-08-30T15:38:29Z
dc.identifierGobetto, M. N. Segmental upregulation of ASIC1 channels in the formalin acute pain mouse model [en línea]. Pharmaceuticals. 2022, 15 (12). doi:10.3390/ph15121539. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/16062
dc.identifier1424-8247
dc.identifierhttps://repositorio.uca.edu.ar/handle/123456789/16062
dc.identifier10.3390/ph15121539
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8526229
dc.descriptionAbstract: Background: Hindpaw injection of formalin in rodents is used to assess acute persistent pain. The response to formalin is biphasic. The initial response (first minutes) is thought to be linked to inflammatory, peripheral mechanisms, while the latter (around 30 min after the injection), is linked to central mechanisms. This model is useful to analyze the effect of drugs at one or both phases, and the involvement of ion channels in the response. Acid-sensing ion channels (ASICs) regulate synaptic activities and play important roles in pain conditions. Recently, psalmotoxin-1 (Pctx-1), a toxin that inhibits ASIC1a-constituted channels, and antisense ASIC1a-RNA, intrathecal administered in mice were shown to affect both phases of the test. Methods: The mouse formalin test was performed on C57/BL6 7- to 9-week-old mice. Behavioral tests were conducted and tissue was extracted to detect proteins (ASIC1 and pERK) and ASIC1-mRNA and mir485-5p levels. Results: The injection of formalin was accompanied by an increase in ASIC1 levels. This was detected at the contralateral anterior cingulate cortex (ACC) compared to the ipsilateral side, and both sides of the ACC of vehicle-injected animals. At the spinal cord and dorsal root ganglia, ASIC1 levels followed a gradient stronger at lumbar (L) 3 and decreased towards L5. Gender differences were detected at the ACC; with female mice showing higher ASIC1a levels at the ACC. No significant changes in ASIC1-mRNA levels were detected. Evidence suggests ASIC1 upregulation depends on regulatory microRNAs. Conclusion: This work highlights the important role of ASIC1 in pain and the potential role of pharmacological therapies aimed at this channel.
dc.formatapplication/pdf
dc.languageeng
dc.publisherMultidisciplinary Digital Publishing Institute
dc.rightsAcceso abierto
dc.rightshttp://creativecommons.org/licenses/by-nc-sa/4.0/
dc.sourcePharmaceuticals Vol.15, No.12, 2022
dc.subjectCANALES ASIC1
dc.subjectmiIR485-5p
dc.subjectmiARN
dc.subjectDOLOR
dc.subjectFORMALINA
dc.subjectRATON
dc.titleSegmental upregulation of ASIC1 channels in the formalin acute pain mouse model
dc.typeArtículo


Este ítem pertenece a la siguiente institución