In the following study, I tried to link hormonal background conditions to successful olfactory imprinting in sockeye salmon by employing behavioural, endocrinological and electrophysio logical experiments. In the initial experiments, sockeye salmon were exposed to potential imprinting odorants, with or without additional treatment with thyroid hormones, during several juvenile stages between fertilization and beyond the PST. After two years of rearing, these fish were tested for behavioural responses to test odorants in two behavioural arenas. Neither immature nor mature fish reacted behaviourally to the odorants that they had been exposed to previously. Therefore, exposure of juveniles to odorants did not lead to imprinting to those odorants under hatchery rearing conditions. In contrast, juvenile fish that were exposed to test odorants and treated with a combination of T3 and T4 (in all cases) or T3 (in one case) the two most common forms of thyroid hormones, did exhibit an odorant recognition response two years later. However, the response differed between immature and mature fish. Mature fish were attracted to the imprinting odorant, whereas immature fish were repelled by the it. When immature fish were injected with GnRH before testing, their behavioural response was reversed. No behavioural response could be detected in fish that had been challenged with either T3 or T4 alone, in contrast to a combined treatment with both forms. Thus, I found evidence that a combination of T3 and T4 initiated imprinting and that GnRH motivated odorant recognition. To examine the underlying hormonal processes, I first determined plasma thyroid hormone concentrations in sockeye salmon before and after hormonal challenges with thyroid hormones or GnRH. In addition, the activity of the deiodinase enzyme that converts T4 into the other possible forms of thyroid hormones was investigated in sensory and non-sensory tissues. The results suggested that only a combined T3T4 treatment increased the availability of both thyroid hormone forms in blood plasma, while a separate challenge with T4 suppressed T3 availability and vice versa. Moreover, the results provided evidence for deiodinase activity in the olfactory epithelium and the retina and demonstrated that GnRH can modulate the T4 conversion process. This inform ation was helpful for planning and interpretation of the remaining experiments. Results obtained from a classical conditioning paradigm (heart-rate-conditioning), provided support for the hypothesis that GnRH lowers the threshold to an imprinting odorant and that the influence of GnRH was not restricted to an enhancement of motivation. To investigate whether hormonal action could also modulate the sensitivity of the peripheral olfactory system, electrophysiological responses from the olfactory epithelium (electro-olfacto-grams or EOGs) were recorded. The EOG results established that thyroid hormones and GnRH increased the EOG response of adult naïve (never imprinted to an odorant) fish, as did maturity. In the last experiments, I conducted EOG recordings on fish that had been imprinted at a juvenile stage. In summary, EOG recordings revealed that the imprinting process increased sensitivity to the imprinting odorant at maturity, while sensitivity in immature fish was decreased in comparison to non-imprinted fish. In combination with my behavioural results, this could explain why salmon do not enter their natal stream before they reach maturity. At maturity however, I also encountered desensitization to non-imprinting odorants, which might increase the ability to focus the olfactory system to the task of homing.