Effects of Perinatal and Puberal Steroid Imprinting on Sexual Behavior of Adult Rats
The maturation of hormone receptors runs parallel with the differentiation of the cell ( Hubbert & Miller, 1974). For instance, binding capacity of insulin receptors in rat liver is low during the fetal period and gradually increases as the fetus approaches the time of birth ( Margolis, Tanner, Seminara, & Taylor, 1990). Despite existing variations, receptor maturation is usually completed by the end of the first postnatal month ( Blazquez, Rubalcava, Montesano, Orci, & Unger, 1976).
The maturation process is not spontaneous, as the first encounter of the receptor with the hormone in the perinatal critical period plays a decisive role. Without the presence of the appropriate hormone, the receptor is not able to accomplish its normal maturation and the resultant unmatured receptor is unable to transmit the information and have the cell evoke its normal response ( Csaba & Nagy, 1985). Subsequently, the first encounter with the hormone leads to "hormonal imprinting," after which the binding capacity of receptors -- mainly their density -- increases, and consequently the magnitude of the cell's reaction is enhanced (Csaba, 1980; 1981; 1984; 1986; 1994). This means that hormonal imprinting is a necessity for receptor development, as the cell is waiting for the first encounter with the hormone (see Figure 4. 1). Hormonal imprinting has an evolutionary basis and its importance in the phylogeny of receptors is worth noting ( Csaba, 1985; 1994). In fact, the ontogenetic development of the receptors is a repetition of this evolutionary event, with a metazoan -- physiological significance.