Fig. 3: DSP-4 lesion of noradrenergic neurons attenuates astrocyte Ca²⁺ transients while producing bimodal functional hyperemia.

a Cartoon depicting the experimental scheme for the treatment of mice with DSP-4 (i.p.). b Images of penetrating arteriole and astrocyte Ca²⁺ from an Aldh1l1 Cre-ERT2 x GCaMP6f mouse prior to (0 s), during (1 s), and after (6 s) whisker stimulation in untreated and DSP-4–treated mice. c Immunohistochemistry showing staining of noradrenergic neurons in the LC in untreated and in DSP-4-treated mice and summary of mean intensity. d Time courses of arteriolar cross-section surface area and associated endfoot Ca²⁺ signals in mice with and without DSP-4 treatment. e Summary data of percent peak response of penetrating arteriole in untreated and DSP-4 treated mice. f Summary data showing peak penetrating arteriole cross-sectional surface area and endfoot Ca²⁺ response (%) in untreated and DSP-4–treated mice with (i) attenuated functional hyperemia (n = 9 mice) and (ii) augmented functional hyperemia after DSP-4 treatment (n = 7 mice). g Summary data showing onset time of arteriole cross-sectional surface area and endfoot Ca²⁺ in untreated and DSP4-treated mice in response to a 5-s whisker stimulation. h Summary data showing the duration of changes in arteriole cross-sectional surface area and endfoot Ca²⁺ in untreated and DSP-4-treated mice in response to a 5-s whisker stimulation from. Data are means ± SEM. (*P = 0.01; **P = 0.003; ***P = 0.0001; ****P < 0.0001).