Abstract

Catecholaminergic A2 neurons in caudal NTS are activated during stressors such as hypoxia. The aim of this study was to assess the effect of CIH on the mRNA expression levels of AT1a, AT1b and AMPA and NMDA receptor subunits in the A2 neurons. AAV vector mediated delivery of green fluorescent protein (GFP) labeled tyrosine hydroxylase promoter (AAV‐GFP‐TH) was used to label A2 neurons. 7 virus injected rats were exposed to 7 days CIH (alternating 6 min periods of 10% O2 and 4 min of 21% O2 from 8am to 4pm; from 4pm to 8am rats were exposed to 21% O2). Laser capture microdissection was performed to capture A2 neurons from caudal NTS. Total RNA from these neurons was extracted and mRNA levels assessed by quantitative real time reverse transcription PCR and compared between the control and CIH rats using 2‐ÄÄct method. CIH decreased AT1a (p=0.002; control − 1.08 ± 0.13, n=7; CIH − 0.48 ± 0.07, n= 6) and AMPA receptor subunit GluR2 (p=0.03; control − 1.11 ± 0.24, n=7; CIH‐ 0.52 ± 0.12, n= 6) and increased transcription factor FosB (p=0.03; control − 1.14 ± 0.25, n=7; CIH‐ 1.97 ± 0.25, n= 5) mRNA levels in the A2 neurons. CIH did not alter levels of GluR1, NR1, NR2 or delta FosB. These results indicate that exposure to CIH selectively alters receptor subunit mRNAs in A2 neurons which could influence their responses to ligand. Supported by HL88052.

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