Figure 7.

Neuron-microglia communication through fractalkine receptor is critical in organization of counterregulatory response to insulin-induced hypoglycemia and 2-deoxy glucose-induced neuroglycopenia (A) Blood glucose levels in fed, fasted, fasted + insulin-injected, wild-type and fractalkine receptor deficient (CX₃CR1^−/−) mice (n = 5–20). (B) Comparison of blood glucose responses in fed, wild-type and CX₃CR1^−/− mice to neuroglycopenia induced by i.p. injection of 2-deoxyglucose (2-DG, 200 mg/kg) or vehicle. (C) Blood glucose levels in response to i.p. insulin injection (1IU/ml/kg bw) during insulin tolerance test (n = 12 per groups) (D–F) Mean ± SEM values of plasma corticosterone (D); adrenaline (E) and glucagon (F) levels in fed and fasted + insulin-treated, wild-type and CX₃CR1^−/− mice (n = 3–8). (G) Quantitative analysis of hypoglycemia-responsive Npy and Pomc neurons. Values obtained from fasted + insulin-injected, wild- type and CX₃CR1^−/− mice (n = 6–8) and expressed as percentage of double labeled cells relative to all c-FOS positive neurons in the arcuate nucleus. (H,I) Hypothalamic Agrp and Npy mRNA levels in fed and fasted + insulin-treated, wild-type and CX₃CR1^−/− mice (n = 4–4) as measured by qRT-PCR. Two-way ANOVA followed by Bonferroni’s post-hoc test revealed significant treatment effect indicated by ^#p < 0,05, ^##p < 0,01, ^####p < 0,0001 or genotype effect indicated by *p < 0.05, ****p < 0.0001. Fed: fed, saline-injected group; Fasted: O/N fasted, saline-injected group; Fasted + insulin: O/N fasted, insulin-injected group.