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Chronic Intrahippocampal Interleukin-1β Overexpression in Adolescence Impairs Hippocampal Neurogenesis but Not Neurogenesis-Associated Cognition.

08:00 EDT 8th October 2019 | BioPortfolio

Summary of "Chronic Intrahippocampal Interleukin-1β Overexpression in Adolescence Impairs Hippocampal Neurogenesis but Not Neurogenesis-Associated Cognition."

Both neuroinflammation and adult hippocampal neurogenesis (AHN) are implicated in many neurodegenerative disorders as well as in neuropsychiatric disorders, which often become symptomatic during adolescence. A better knowledge of the impact that chronic neuroinflammation has on the hippocampus during the adolescent period could lead to the discovery of new therapeutics for some of these disorders. The hippocampus is particularly vulnerable to altered concentrations of the pro-inflammatory cytokine interleukin-1β (IL-1β), with elevated levels implicated in the aetiology of neurodegenerative disorders such as Alzheimer's and Parkinson's, and stress-related disorders such as depression. The effect of acutely and chronically elevated concentrations of hippocampal IL-1β have been shown to reduce AHN in rats and mice. However, the effect of exposure to chronic overexpression of hippocampal IL-1β during adolescence, a time of increased vulnerability, hasn't been fully interrogated. Thus, in this study we utilized a lentiviral approach to induce chronic overexpression of IL-1β in the dorsal hippocampus of adolescent male Sprague Dawley rats for 6 weeks, during which time its impact on cognition and hippocampal neurogenesis were examined. A reduction in hippocampal neurogenesis was observed along with a reduced level of neurite branching on hippocampal neurons. However, there was no effect of IL-1β overexpression on cognitive performance. Our study has highlighted that chronic IL-1β overexpression in the hippocampus during the adolescent period exerts a negative impact on neurogenesis and neurite branching.

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Name: Brain, behavior, and immunity
ISSN: 1090-2139
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Medical and Biotech [MESH] Definitions

An interleukin receptor subunit that was originally discovered as a component of the INTERLEUKIN 2 RECEPTOR. It was subsequently found to be a component of several other receptors including the INTERLEUKIN 4 RECEPTOR, the INTERLEUKIN 7 RECEPTOR, the INTERLEUKIN-9 RECEPTOR, the INTERLEUKIN-15 RECEPTOR, and the INTERLEUKIN-21 RECEPTOR. Mutations in the gene for the interleukin common gamma chain have been associated with X-LINKED COMBINED IMMUNODEFICIENCY DISEASES.

Cell surface receptors for INTERLEUKIN-13. Included under this heading are the INTERLEUKIN-13 RECEPTOR ALPHA2 which is a monomeric receptor and the INTERLEUKIN-4 RECEPTOR TYPE II which has specificity for both INTERLEUKIN-4 and INTERLEUKIN-13.

A cytokine subunit that is a component of both interleukin-12 and interleukin-23. It binds to the INTERLEUKIN-12 SUBUNIT P35 via a disulfide bond to form interleukin-12 and to INTERLEUKIN-23 SUBUNIT P19 to form interleukin-23.

An interleukin receptor subunit with specificity for INTERLEUKIN-13. It dimerizes with the INTERLEUKIN-4 RECEPTOR ALPHA SUBUNIT to form the TYPE II INTERLEUKIN-4 RECEPTOR which has specificity for both INTERLEUKIN-4 and INTERLEUKIN-13. Signaling of this receptor subunit occurs through the interaction of its cytoplasmic domain with JANUS KINASES such as the TYK2 KINASE.

An interleukin receptor subtype found on both hematopoietic and non-hematopoietic cells. It is a membrane-bound heterodimer that contains the INTERLEUKIN-4 RECEPTOR ALPHA SUBUNIT and the INTERLEUKIN-13 RECEPTOR ALPHA1 SUBUNIT. Although commonly referred to as the interleukin-4 type-II receptor this receptor has specificity for both INTERLEUKIN-4 and INTERLEUKIN-13

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