Abstract

Filial imprinting predisposes an animal to form an attachment to animals within a critical period. The critical period for imprinting in chicks (Gallus gallus domesticus) is restricted to the first few days after hatching. As the first topic in my talk, I will introduce our strategy using a combination with molecular methods in analysing the function of microtubule-associated protein 2 (MAP2) as an example in imprinting. We developed an in-vivo RNAi-mediated gene-silencing system and suppressed the up-regulation of MAP2 in vivo accompanying filial imprinting. As a result, filial imprinting in chicks was greatly impaired. The data suggest that the regulation of MAP2 expression is required for imprinting and may modify microtubule stability, thereby leading to cytoskeletal reorganization during imprinting. As the second and main topic, I will show that thyroid hormone signalling is a determinant for the critical period and that imprinting itself primes learning. We found that the concentration of thyroid hormone in brain peaked around hatching, and imprinting caused an additional increase in the concentration through enhanced conversion in brain, enabling imprinting specifically via non-genomic action, i.e., imprinting fuels instantaneous imprinting with thyroid hormone. Four days after hatching, thyroid hormone levels fell to background level. We found, however, that injecting thyroid hormone on day 4 could open a once closed critical period and enable imprinting once again. If thyroid hormone was applied on day 1 without imprinting, chicks became imprintable on day 4．Furthermore, reinforced learning (as well as imprinting) was facilitated by the thyroid hormone fuelling on day 1. Our data indicate that thyroid hormone is a determining factor for the critical period of imprinting and is able to confer memory priming. In other words, imprinting is not a special type of learning that serves a particular function at a particular age. Rather, imprinting appears to play a crucial role in the development of learning in juveniles through the self-fuelling action of thyroid hormone.