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Sympathetic nerve endings are endowed with auto-inhibitory histamine (HA) H3 receptors.Activation of H3 receptors inhibits sympathetic neurotransmission.However little is known about the origin of the endogenous HA that activates presynaptic H3 receptors on sympathetic terminals.The present study provides direct evidence to demonstrate the coexistence of HA and norepinephrine (NE) within sympathetic neurons,and reveals the modulation mechanisms of HA release from sympathetic terminals.The colocalization of HA and NE immunoreactivities was identified within superior cervical ganglia (SCG) neurons,celiac ganglion principal neurons of the mouse,dog and monky as well as in the vas deferens,mesenteric artery axon,and varicosities of the mouse and guinea pig.