There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
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
D(2) agonist quinpirole, though not the D(1) agonist SKF-38393 or the D(4) agonist
PD168077. The D(3) agonist 7-OH-DPAT also inhibited aggression, but only following
high dose treatment that may affect aggression via nonspecific binding to D(2) receptors.
Central VT infusion failed to restore D(2) agonist-inhibited aggression in a subsequent
experiment, demonstrating that D(2) does not suppress aggression by inhibiting VT
release from BSTm neurons. In a final experiment, we detected D(2) 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 D(2) receptors,
which may modify future behaviors.