Ticks are important pests of animals and humans and are capable of transmitting pathogens that cause serious diseases. In the tick, salivary glands act as organs of fluid secretion. Ixodid ticks, including the lone star tick, feed for relatively long periods on host animals. Throughout feeding, the tick encounters several defense mechanisms initiated by the host, which include: inflammatory/immune responses, clotting and blood vessel constriction. Salivary gland secretions counter the host defense system by secreting a cocktail of bioactive molecules along with excess the fluid. This cocktail includes prostaglandins. Prostaglandins regulate a variety of physiological processes that are involved in the host parasite interaction. In order for prostaglandins to be synthesized, the salivary glands must regulate the release of its precursor, arachidonic acid (AA). Previous work has shown that dopamine released from nerves, initiates an influx of Ca2+into the glands, activating an intracellular phospholipase-A2, leading to the release of arachidonic acid. Arachidonic acid is then converted to prostaglandins via the cyclooxygenase pathway. The exact mechanism of how arachidonic acid is released after gland stimulations by dopamine is still unclear. My results show that stimulation of glands with PPHT-HCl, a dopamine D2 agonist, potentiates the release of arachidonic acid. The possibility of a D2-like dopamine receptor was supported by results showing that SCH 23390, a dopamine D1receptor antagonist, potentiates the release of AA. Other results show that “second messenger” molecules such as cAMP and protein kinase C are involved in regulation after initial stimulation by dopamine.
Species 1: Acari Ixodidae Amblyomma americanum (lone star tick)
Keywords: arachidonic acid
The ESA 2001 Annual Meeting - 2001: An Entomological Odyssey of ESA