Does Acute Heat Stress Differentially‐Modulate RVLM Gene Expression of Ionotropic Neurotransmitter Receptors in Young and Aged F344 Rats?

Abstract

The rostral ventrolateral medulla (RVLM) is involved in the regulation of sympathetic nerve discharge (SND) and arterial blood pressure. Acute hyperthermia produces marked activation of visceral SND in young rats, and the functional integrity of this brainstem region is crucial for sustaining visceral sympathoexcitation to increased internal body temperature (Tc). Visceral SND responses to increased Tc are attenuated in aged compared with young F344 rats, and central mechanisms contributing to age‐associated alterations in SND responses to hyperthermia are not well‐established. The balance between excitatory and inhibitory inputs, mediated primarily by glutamate and GABA neural systems, is important for regulating RVLM neuronal activity. In the present study we hypothesized that, in response to acute hyperthermia, the RVLM gene expression of various excitatory and inhibitory ionotropic neurotransmitter receptors would demonstrate age‐related differences. Tc was increased from 38°C to 41.5°C in young (3–4 months) and aged (23–24 months) anesthetized F344 rats. Total RNA was extracted from RVLM‐containing micropunches and gene expression analysis for ionotropic neurotransmitter receptor subunits was performed using TaqMan real time RT‐PCR. Gene expression levels of glutamate, GABA and glycine neurotransmitter binding receptor subunits were compared between age groups. Gene expression analysis revealed an upregulation in some, but not all, major excitatory NMDA and AMPA neurotransmitter receptor subunits in young compared with aged rats. In addition, major subunits of the inhibitory GABA and glycine receptors demonstrated substantial upregulation in aged compared with young rats. These preliminary data suggest that, in response to acute hyperthermia, aging modulates the functional balance of RVLM excitatory and inhibitory neurotransmitter receptor subunits.Support or Funding InformationNIH AG‐041948.