Individual variation and the endocrine regulation of behaviour and physiology in birds: a cellular/molecular perspective

Abstract

Investigations of the cellular and molecular mechanisms of physiology and behaviour have generally avoided attempts to explain individual differences. The goal has rather been to discover general processes. However, understanding the causes of individual variation in many phenomena of interest to avian eco-physiologists will require a consideration of such mechanisms. For example, in birds, changes in plasma concentrations of steroid hormones are important in the activation of social behaviours related to reproduction and aggression. Attempts to explain individual variation in these behaviours as a function of variation in plasma hormone concentrations have generally failed. Cellular variables related to the effectiveness of steroid hormone have been useful in some cases. Steroid hormone target sensitivity can be affected by variables such as metabolizing enzyme activity, hormone receptor expression as well as receptor cofactor expression. At present, no general theory has emerged that might provide a clear guidance when trying to explain individual variability in birds or in any other group of vertebrates. One strategy is to learn from studies of large units of intraspecific variation such as population or sex differences to provide ideas about variables that might be important in explaining individual variation. This approach along with the use of newly developed molecular genetic tools represents a promising avenue for avian eco-physiologists to pursue.

Figure 1

Relationships between hormone concentrations and activation of hormone-dependent traits. (a) Theoretical models of the relationships between hormone levels and biological responses. At the individual level, the relationship can be represented by various functions such as (i) dose-dependent relationship, (ii) threshold response or (iv) dose-dependent relationship with a LT and a HT corresponding to the maximal level of activation. Both models (ii) and (iv) should result at the population level in similar dose–response relationships (respectively (iii) and (v)). Models (i)–(iii) are adapted from Adkins-Regan (2005) and (iv) and (v) are new interpretations proposed here. We do not consider here the case of inverted U-shape curves also considered by Adkins-Regan. (b) Experimental data illustrating the effects of increasing doses of exogenous testosterone (expressed by the length of the Silastic capsules implanted in castrated males) on the activation of two types of reproductive behaviour, (i) mount attempts and (ii) crowing, and on the growth of (iii) the cloacal gland, an androgen-dependent structure. Both behavioural and morphological responses demonstrate a dose–response relationship with the amounts of testosterone supplied to the subjects. The grey areas indicate the mean±s.e. of corresponding data observed during the same experiment in sexually mature gonadally intact males. Adapted from data in Balthazart et al. (1990).

Figure 2

Schematic of the sequential steps in sex steroid action on cellular responses resulting in the activation of reproductive behaviour. (i) Circulating hormones (H) such as steroids in the plasma are associated in a reversible manner with transport proteins. (ii) When they enter their target cells, sex steroids are potentially metabolized into behaviourally active or inactive metabolites. (iii) Active metabolites will then bind to specific receptors, which will then undergo a number of transformations leading to their association with (iv) specific sites in the DNA. The occupied receptors will at this level serve as transcription factors resulting in a change in transcription of specific genes and their translation into (v) proteins that will ultimately affect behaviour expression. Each of these steps is potentially regulated by a variety of environmental or endocrine factors and could contribute to the modulation of individual differences in behaviour.