Skip to main content
Figure 5 | Journal of Neuroinflammation

Figure 5

From: Calcium dysregulation via L-type voltage-dependent calcium channels and ryanodine receptors underlies memory deficits and synaptic dysfunction during chronic neuroinflammation

Figure 5

Chronic LPS infusion increased activation of microglia but not astrocytes, and treatment with either dantrolene or nimodipine reduced microglia activation. Activated microglia were quantified by counting MHC-II+ cells, and activated astrocytes were quantified by densitometry of GFAP. Hippocampal immunohistochemistry against MHC-II/OX-6 (A) and GFAP was quantified (B, C, D, F, G, H) across specific hippocampal subfields. Although the DG region in LPS-infused rats contains numerous immunoreactive objects, only those OX-6 immunoreactive objects larger than 65 mm2 were included in analysis and are represented in the histograms. GFAP hippocampal gene expression (E) was also quantified. (B) There was no change in the number of MHC-II+ cells in the CA1 subfield of the hippocampus. (C, D) There were significantly more MHC-II positive cells in the CA3 (C) and DG (D) subfield of all LPS-treated groups compared to their aCSF controls. Dantrolene treatment significantly reduced the number of MHC-II+ cells present in the CA3 and DG subfields, and nimodipine treatment significantly reduced the number of MHC-II+ cells present in the CA3. (E) There was a trend toward a drug × group interaction for hippocampal GFAP gene expression, but no statistically significant changes were observed. (F, G, H) There were no significant changes in the amount of GFAP in any of the hippocampal subfields due to either LPS or drug treatment. Data expressed as mean ± SEM. *Indicates a significant difference from treatment-matched aCSF controls, †Indicates a significant difference from LPS + vehicle rats. Significance determined by P < 0.05. LPS lipopolysaccharide, aCSF artificial cerebrospinal fluid, DG dentate gyrus, GFAP glial fibrillary acid protein.

Back to article page