Dopaminergic regulation of mate competition aggression and aromatase-Fos colocalization in vasotocin neurons

Recent experiments demonstrate that aggressive competition for potential mates involves different neural mechanisms than does territorial, resident-intruder aggression. However, despite the obvious importance of mate competition aggression, we know little about its regulation. Immediate early gene experiments show that in contrast to territorial aggression, mate competition in finches is accompanied by the activation of neural populations associated with affiliation and motivation, including vasotocin (VT) neurons in the medial bed nucleus of the stria terminalis (BSTm) and midbrain dopamine (DA) neurons that project to the BSTm. Although VT is known to facilitate mate competition aggression, the role of DA has not previously been examined. We now show that in male zebra finches (Taeniopygia guttata), mate competition aggression is inhibited by the D2 agonist quinpirole, though not the D1 agonist SKF-38393 or the D4 agonist PD168077. The D3 agonist 7-OH-DPAT also inhibited aggression, but only following high dose treatment that may affect aggression via nonspecific binding to D2 receptors. Central VT infusion failed to restore D2 agonist-inhibited aggression in a subsequent experiment, demonstrating that D2 does not suppress aggression by inhibiting VT release from BSTm neurons. In a final experiment, we detected D2 agonist-induced increases in immunofluorescent colocalization of the product of the immediate early gene c-fos and the steroid-converting enzyme aromatase (ARO) within VT neurons of the BSTm. Thus, although VT and DA appear to influence mate competition aggression independently, BSTm VT neurons are clearly influenced by the activation of D2 receptors, which may modify future behaviors.