Microglial Activation Modulates Neuroendocrine Secretion During Experimental Sepsis
Autor: | Maria José Alves da Rocha, Carlos Henrique Rocha Catalão, Luís Henrique Angenendt da Costa, Nilton Nascimento Santos-Junior |
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Rok vydání: | 2021 |
Předmět: |
Male
0301 basic medicine medicine.medical_specialty Vasopressin Vasopressins Central nervous system Neuroscience (miscellaneous) Minocycline Inflammation Oxytocin Systemic inflammation Sepsis 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Internal medicine medicine Animals Rats Wistar Neurons Microglia business.industry Brain medicine.disease Neurosecretory Systems Rats Disease Models Animal 030104 developmental biology Endocrinology medicine.anatomical_structure Neurology Hypothalamus medicine.symptom Corticosterone business 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Molecular Neurobiology. 58:2133-2144 |
ISSN: | 1559-1182 0893-7648 |
DOI: | 10.1007/s12035-020-02241-5 |
Popis: | Sepsis promotes an inflammatory state in the central nervous system (CNS) that may cause autonomic, cognitive, and endocrine changes. Microglia, a resident immune cell of the CNS, is activated in several brain regions during sepsis, suggesting its participation in the central alterations observed in this disease. In this study, we aimed to investigate the role of microglial activation in the neuroendocrine system functions during systemic inflammation. Wistar rats received an intracerebroventricular injection of the microglial activation inhibitor minocycline (100 μg/animal), shortly before sepsis induction by cecal ligation and puncture. At 6 and 24 h after surgery, hormonal parameters, central and peripheral inflammation, and markers of apoptosis and synaptic function in the hypothalamus were analyzed. The administration of minocycline decreased the production of inflammatory mediators and the expression of cell death markers, especially in the late phase of sepsis (24 h). With respect to the endocrine parameters, microglial inhibition caused a decrease in oxytocin and an increase in corticosterone and vasopressin plasma levels in the early phase of sepsis (6 h), while in the late phase, we observed decreased oxytocin and increased ACTH and corticosterone levels compared to septic animals that did not receive minocycline. Prolactin levels were not affected by minocycline administration. The results indicate that microglial activation differentially modulates the secretion of several hormones and that this process is associated with inflammatory mediators produced both centrally and peripherally. |
Databáze: | OpenAIRE |
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