Abstract
An enhanced glutamate (GLU) function within the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei contributes to neurohumoral activation in heart failure (HF). However, whether altered expression/function of astrocytic GLU transporter 1 (GLT1) plays a role in the imbalanced GLU signalling during HF is still not fully elucidated. Patch clamp recordings from SON/PVN neurons in sham rats showed that blockade of GLT1 (dihydrokainate 300 μM) induced a glutamate‐mediated inward current (~100 pA), which was blunted in HF rats (~65%, P< 0.05). To investigate if a diminished GLT1 expression and/or physical glial retraction contributed to blunted GLT1 function in HF, we performed immunohistochemistry. While no changes in the density of the glial marker GFAP were observed, GLT1 immunoreactivity, as well as its colocalization with GFAP was increased in HF (~70%, P<0.05). Our data suggests that a diminished astrocyte GLT1 function contributes to enhanced GLU function during HF, and effect not due to diminished GLT1 expression and/or neuroglial structural remodeling. Supported by NIH HL‐090948 to JES.
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