Hormones, genes, and behavior

Abstract

With assays of hormone-sensitive behaviors, it is possible to demonstrate both direct and indirect actions of genes on mammalian social behaviors. Direct effects of estrogen receptor gene expression and progesterone receptor gene expression figure prominently in well analyzed neuroendocrine mechanisms for sex behavior, operating through a neural circuit that has been delineated. Indirect effects, notably the consequences of sexual differentiation, display complex dependencies. In a human condition, Kallmann syndrome, the data show a clear, indirect genetic influence on an important human social behavior, in which damage at chromosome Xp-22.3 works through at least six discrete steps to affect libido. Altogether, simplistic extrapolations from lower animals, especially during brief summaries for nonscientists, do not appear justified as we discover and conceptualize genetic influences on mammalian brain and behavior.

Figure 1

Causal relationships of genes to behaviors pose a greater analytic challenge in mammals than in Drosophila because of the multiplicative nature of sensory, motor, and interneuron combinations and because of the greater variety of intermediate behavioral states.

Figure 2

Behaviors of wild-type and ERKO female mice. ERKO females would not show lordosis behavior. Summarized from data in Ogawa et al. (4). ∗, Aggression exhibited by ERKO females mainly offensive attacks typical of intermale aggression.

Figure 3

Administration of antisense DNA directed against PR mRNA directly to the ventromedial hypothalamus significantly reduced lordotic behavior in female rats (A and B). The effect was even larger on courtship (“proceptive”) behaviors, which are known to depend heavily on progesterone. (C). In contrast, rejection behaviors were not affected (D), nor were vocalizations (E). From Ogawa et al. (6).