Acid Sensing Channel 1 in Astroglia Is Up‐regulated by Saporin

Abstract

Acid‐sensing ion channels (ASICs) are activated by acidosis and may act as chemosensors in the CNS. RT‐PCR has revealed that ASIC type 1 (ASIC1) is the predominant ASIC transcript in the nucleus tractus solitarii (NTS), but anatomical studies of its expression in the NTS have been lacking. We performed confocal microscopic immunofluorescent histochemistry to examine the distribution of ASIC1 in rat NTS. Previously we showed that saporin causes gliosis in the NTS. Because astrocyte damage may lead to acidosis and result in ASIC1 activation, we tested the hypothesis that saporin treatment increases ASIC1 expression in the NTS. Confocal images showed cells and processes that contained ASIC1‐immunoreactivity (IR) scattered in the NTS, dorsal motor nucleus of vagus (DMV) and area postrema (AP). ASIC1‐IR predominantly colocalized with IR of the astrocyte marker, glial fibrillary acidic protein (GFAP), or the microglial marker, integrin αM (OX42), in the NTS and DMV. The sup‐postremal NTS was the only area where neurons containing IR of a neuronal marker contained ASIC1‐IR. ASIC1‐IR as well as OX42‐IR increased markedly in the NTS 7 days after saporin injection. Saporin caused depletion of GFAP‐IR in the center of the injection, but GFAP‐IR increased in the surrounding area. The increase in ASIC1‐IR was found in cells and processes that contained GFAP‐IR or OX42‐IR. Our results confirm that ASIC1 is increased with saporin‐induced gliosis in the NTS. The increased ASIC1‐IR in microglia may be associated with saporin‐induced inflammation. Potentially increased ASIC1‐IR in astrocytes could play a role in cardiovascular reflex attenuation that occurs after administration of saporin into the NTS. Support: NIH RO1 HL 088090 and a VA Merit Review