Actions of some transmitters and their antagonists on salivary secretion in a tick

Abstract

Cholinomimetics (pilocarpine, carbachol, physostigmine, acetylcholine, acetyl-beta-methylcholine) and sympathomimetics (dopamine, epinephrine), when injected into the hemolymph, provoked salivary fluid secretion in the female ixodid tick Amblyomma hebraeum Koch. Atropine, but not tubocurarine or toxiferine, abolished pilocarpine-induced secretion without reducing the response to dopamine. Reserpine and guanethidine likewise selectively attenuated pilocarpine-induced secretion. Following extirpation of the synganglion, pilocarpine no longer provoked a secretory response whereas dopamine did. Thus, the salivary gland appears to be innervated directly by catecholaminergic rather than cholinergic secretory nerves. It is suggested that pilocarpine elicits salivation by interacting with muscarinic-type cholinergic receptors situated either on the cell bodies of the secretory nerves, or alternatively in the integrative or sensory pathway.

Ancestral reconstruction of tick lineages

“…In ixodid salivary glands, MIP and SIFamide probably regulate dopamine secretion from the basal acinar cells of acini II and III into the acinar lumen, where dopamine then binds to the dopamine D1 receptor to stimulate secretion of secretory granules (Šimo et al 2014, 2012, 2011, 2009b). In this regard, injection of argasids and ixodids with cholinergic stimulants, such as pilocarpine and carbachol induces salivation (Howell, 1966;Kaufman, 1978;Tatchell, 1967a). Cholinergic stimulants do not act on isolated salivary glands of hard or soft ticks (Kaufman, 1978;Mans, 2002;Maritz-Olivier, 2005), suggesting that they act on the central nervous system, whereas stimulation of isolated argasid and ixodid salivary glands with dopamine induces secretion (Kaufman, 1977;Mans, 2002;Maritz-Olivier, 2005).…”

“…In this regard, injection of argasids and ixodids with cholinergic stimulants, such as pilocarpine and carbachol induces salivation (Howell, 1966;Kaufman, 1978;Tatchell, 1967a). Cholinergic stimulants do not act on isolated salivary glands of hard or soft ticks (Kaufman, 1978;Mans, 2002;Maritz-Olivier, 2005), suggesting that they act on the central nervous system, whereas stimulation of isolated argasid and ixodid salivary glands with dopamine induces secretion (Kaufman, 1977;Mans, 2002;Maritz-Olivier, 2005). Sequence homologs for the receptor for SIFamide (sifa-r) have been detected in salivary gland transcriptomes of ixodid and argasid ticks, suggesting that the SIFamide-dopamine system may be conserved in all ticks (Egekwu et al 2016;Šimo et al 2013; B.J.…”

Studies on possible role of catecholamines in regulation of sex pheromone gland activity in American dog tick,Dermacentor veriabilis (Say)

“…Five microliters of a 10 -3 M solution of dopamine, 6-hydroxydopamine (6-OHdopamine) (as the hydrochloride), cyclic AMP, acetylcholine, pilocarpine, serotonin, reserpine (Sigma Chemical Co., St. Louis, Missouri) or DL-c~-methyl-m-tyrosine methyl ester hydrochloride (98 % pure, MTME, a gift from E Papavasiliou, Veterans Hospital, Hampton, Virginia) was administered to D. variabilis females. Ticks apparently tolerate these dosages, which exceed typical physiological concentrations, as demonstrated by Kaufman (1978).…”

Stimulation of amylase and sialic acid releases from dog submandibular gland slices by pilocarpine or high K+ medium: A possible role of calmodulin for their releases.

“…Although there have been many investigations on the effects of adrenergic and cholinergic agonists on the release of amylase and K+ from the salivary glands of several species (VREUGDENHIL and ROUKEMA, 1975;BOGART and PICARELLI, 1978;KAUFMAN, 1978;KAUFMAN and WONG, 1983), the reports in which the release of sialic acid from the salivary gland is studied are few. DOUGLAS and PoISNER (1964) and SAMLI and GESCHWIND (1968) reported that high K} concentrations in the medium provoked the release of vasopressin and luteinizing hormone from pituitary gland.…”