BACKGROUND: Substantia nigra is the main dopaminergic center of the brain. Massive loss of dopaminergic neurons is characteristic for Parkinson’s disease. Arterial hypertension is considered a possible risk factor for Parkinson’s disease development, but to date there is no understanding of the mechanisms that may mediate the effect of high blood pres-sure on the death of dopaminergic neurons and the development of Parkinson’s disease. Since neuroglia is known to make a major contribution to the pathogenesis of neurodegeneration, it is important to evaluate the effect of arterial hypertension on the functional status of glial cells in the Substantia nigra. AIM: The aim of the study was to analyze the features of morphofunctional state of both microglia and astroglia in the Substantia nigra of spontaneously hypertensive rats. MATERIALS AND METHODS: Brain samples from Wistar rats (n = 3) and from spontaneously hypertensive SHR rats aged 9 months (n = 4) were used as a material for the study. Brain sections were immunostained for tyrosine hy-droxylase to identify the Substantia Nigra, for calcium-binding protein Iba-1 to identify microglia, and for glial fibrillary acidic protein to identify astrocytes. RESULTS: Compared to the control, microglial cells in the Substantia nigra of spontaneously hypertensive rats show signs of moderate activation manifested in significant thickening of the processes of microgliocytes. Single microgliocytes exhibit ameboid morphology, indicating their strong activation. A close spatial relationship with the bodies of dopami-nergic neurons was noted for some identified microgliocytes. Astrocytes in Substantia nigra of both Wistar rats and SHR rats show no signs of activation. CONCLUSIONS: Arterial hypertension may be one of the causes of neuroinflammation mediated by microglia in the Substantia nigra. © 2024, Eco-Vector LLC. All rights reserved.
Translated title of the contributionMORPHOLOGICAL CHARACTERIZATION OF GLIAL CELLS IN THE SUBSTANTIA NIGRA OF SPONTANEOUSLY HYPERTENSIVE SHR RATS
Original languageRussian
Pages (from-to)93-99
Number of pages7
JournalMedicinskij Akademiceskij Zurnal
Volume24
Issue number2
DOIs
StatePublished - 2024

ID: 127407356