Highlights
- •Hypertension is associated with neuroinflammation and RVLM neuron over-activity
- •Neuroinflammation is produced and maintained primarily by microglia
- •Changes in microglial phenotype and morphology can affect neuronal function
- •We found RVLM-specific changes in microglial gene expression and morphology
Abstract
The RVLM of spontaneously hypertensive rats (SHR) contains over-active C1 neurons,
which model the pathology of essential hypertension. Hypertension involves chronic
low-grade neuroinflammation. Inflammation in the brain is produced and maintained
primarily by microglia. We assessed microglial gene expression (P2Y12R and CX3CR1)
and morphology in the RVLM of SHR compared to normotensive Wistar-Kyoto rats (WKY).
The gene expression of the metabotropic purinergic receptor P2Y12 and the fractalkine
receptor CX3CR1 was downregulated in the RVLM of SHR compared to WKY (by 37.3% and
30.9% respectively). P2Y12R and CX3CR1 are required for normal microglial function,
and reduced P2Y12R expression is associated with changes in microglial activity. Histological
analysis showed a 22.9% reduction in microglial cell density, along with 18.7% shorter
microglial processes, a phenotypic indicator of activation, in the RVLM of SHR compared
to WKY. These results indicate a subtle loss of function, or a mild state of inflammation,
in the RVLM microglia of SHR.
Abbreviations:
RVLM (rostral ventrolateral medulla), SHR (spontaneously hypertensive rat), WKY (Wistar-Kyoto rat), CNS (central nervous system), PFA (paraformaldehyde), SBP (systolic blood pressure), LPS (lipopolysaccharide)Keywords
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Article info
Publication history
Published online: December 08, 2018
Accepted:
December 7,
2018
Received in revised form:
November 26,
2018
Received:
August 16,
2018
Identification
Copyright
Crown Copyright © 2018 Published by Elsevier B.V. All rights reserved.