Behavioral and biochemical mechanisms of olfactory imprinting and homing by coho salmon.

摘要

The final freshwater phase of the Pacific salmon's homing migration is governed primarily by the olfactory discrimination of homestream water. Prior to their seaward migration, juvenile salmon learn site-specific odors associated with their home stream and later use these odor memories for homing. Experimental evidence suggests that olfactory imprinting by salmon occurs during a sensitive period associated with surges in plasma thyroxine levels during smolting. Life-history studies, however, suggest that imprinting may occur prior to smolting. To examine the timing of olfactory imprinting, hatchery-reared coho salmon were exposed to site-specific or artificial odorants at specific developmental stages and their subsequent abilities to respond to these odors as adults were tested behaviorally. These studies indicated that smolting may be a particularly important period for olfactory imprinting but that salmon reared exclusively in a hatchery may have impaired imprinting ability. Further studies indicated that rapidly rising plasma thyroxine is not required for imprinting but that migration may play an important role. The behavioral responses of precociously mature salmon to a putative pheromone was also examined.; The biochemical mechanisms underlying olfactory recognition of amino acids and imprinted odorants was also examined. Adenylyl and guanylate cyclase in imprinted coho salmon olfactory cilia were characterized and their roles in olfactory signalling were examined. The properties of adenylyl and guanylate cyclase were consistent with a role in olfactory transduction. Adenylyl but not guanylate cyclase was stimulated by high concentrations of amino acid odorants. Both enzymes were slightly stimulated by the imprinted odorant phenylethyl alcohol but a difference in enzyme sensitivity between imprinted and unimprinted fish was only observed with guanylate cyclase activity in maturing fish. In higher vertebrates, olfactory transduction is mediated by the type III adenylyl cyclase enriched in olfactory cilia. The regulation of this enzyme and other adenylyl cyclase isoforms by the m4 muscarinic receptor was also examined. Activation of m4 muscarinic receptor is thought to inhibit adenylyl cyclase activity but co-transfection studies indicated that crossover from inhibitory to stimulatory G protein coupling can occur.