Abstract
Pacific herring (Clupea pallasi) are estuarine fish that spawn in reduced salinity water. The spermatozoa are virtually motionless upon spawning into water of varying salinities and only initiate motility upon contact with a chorion-bound glycoprotein. Sperm can remain in the water column for up to 24 hrs, yet are still capable of fertilizing eggs. Immotility in the environment is maintained as a result of herring sperm utilizing reverse sodium (Na)-calcium (Ca) exchange (Ca2+ in, Na+ out) as a mechanism for increasing intracellular calcium at motility initiation. The primary initiator of motility, Sperm Motility Initiation Factor (SMIF) requires protein kinase C activation that in turn appears to increase the reverse Na-Ca exchanger. A nondiffusible chemoattractant, Micropylar Sperm Attractant (MSA) is also present on the chorion immediately surrounding the micropyle opening in herring (as well as other fish and insects) that induces a rapid increase in intracellular Ca2+ when sperm come in contact with it and this causes sperm to make sudden turns toward the canal opening. As such, herring sperm appear to undergo at least two increases in intracellular Ca2+: one at motility initiation by SMIF, and a further increase as they contact MSA at the micropylar opening.
Keywords: Circular motility, Flagellar bending, Herring, Micropylar Sperm Attractant, Micropyle, Motility initiation, PKC, Sodium-calcium exchange, Sperm Motility Initiation Factor.