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Fig. 7. Abnormal cardiac sympathetic innervation and autonomic dysfunction in Egr3^-/- mice. Whole-mount lacZ histochemistry was performed on hearts from adult Egr3^+/+:DlZ⁺ and Egr3^-/-:DlZ⁺ mice. In Egr3^+/+:DlZ⁺ mice, sympathetic innervation to the inferior surface of the (A) right atrium and the ventral surfaces of the (B) right and (C) left ventricles could be visualized in detail. (C) Diffuse innervation of the myocardium was visualized in Egr3^+/+:DlZ⁺ hearts (arrowhead). (A'-C') In hearts from Egr3^-/-:DlZ⁺ mice, however, there was a marked decrease in the overall epicardial sympathetic innervation and the small terminal axon branching was markedly diminished (results are representative of three Egr3^+/+:DlZ⁺ and Egr3^-/-:DlZ⁺ hearts analyzed by whole-mount lacZ histochemistry). (D,E) Decreased sympathetic innervation to the heart was accompanied by abnormal physiological response to sympathetic nervous system activation. (D) Heart rate and (E) contractility measurements were similar between untreated (baseline) wild-type and Egr3^-/- mice. Treatment with the central 2-adrenergic antagonist yohimbine (YOH) resulted in a greater than twofold increase in heart rate and myocardial contractility in wild-type mice relative to baseline owing to increased sympathetic activity to the heart. In Egr3^-/- mice treated with YOH, the increase in heart rate and myocardial contractility was significantly diminished compared with wild-type mice (results from five wild-type and seven Egr3^-/- catherized mice; ^*P<0.01, Student's t-test; scale bars: 1 mm in A,B; 0.5 mm in C).

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