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ARS Home » Southeast Area » Booneville, Arkansas » Dale Bumpers Small Farms Research Center » Research » Publications at this Location » Publication #232376
Title: Signaling Pathways Used by Ergot Alkaloids to Inhibit Bovine Sperm Motility

Author
item WANG, HEHAI - UNIV OF AR
item Looper, Michael
item JOHNSON, ZELPHA - UNIV OF AR
item RORIE, RICK - UNVI OF AR
item ROSENKRANS, CHARLES - UNIV OF AR

Submitted to: In Vitro Cellular and Developmental Biology - Animal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/12/2009
Publication Date: 5/19/2009
Citation: Wang, H., Looper, M.L., Johnson, Z.B., Rorie, R.W., Rosenkrans, C.F. 2009. Signaling pathways used by ergot alkaloids to inhibit bovine sperm motility. In Vitro Cellular and Developmental Biology - Animals. 45(8):483-489.

Interpretive Summary: Decreased performance of one bull will affect the pregnancy rate of 20 to 25 cows. Minimal research exists on the negative effects of toxic tall fescue on bull reproductive performance. Less is known of how alkaloids found in toxic fescue have their effects on sperm cells. Scientists from the University of Arkansas and ARS in Booneville, AR, investigated the signaling pathways involved in the inhibitory effects of the ergot alkaloids ergotamine (ET) and dihydroergotamine (DEHT) on bovine sperm motility using specific inhibitors. Results suggest that ET and DHET decrease bovine sperm motility via alpha adrenergic receptors and independent of G-protein signaling pathways. Most of these alkaloids are fat soluble, suggesting that they may easily move across sperm membranes to directly interact with intracellular signaling molecules. Beef producers should minimize the use of toxic fescue during the breeding season to optimize pregnancy rates of the cowherd. Use of nontoxic forage diets or grain supplementation during the breeding season will alleviate the detrimental effects of toxic fescue on sperm motility. This information is important to livestock producers and extension personnel.

Technical Abstract: Ergot alkaloids exert their toxic or pharmaceutical effects through membrane receptor-mediated activities. This study investigated the signaling pathways involved in the in vitro inhibitory effects of both ergotamine (ET) and dihydroergotamine (DEHT) on bovine sperm motility using specific inhibitors. Motile bovine spermatozoa were prepared using a Percoll gradient and incubated with ergot alkaloids with and without receptor inhibitors. Co-incubation of ET or DHET with 100 microM prazosin (alpha 1-adrenergic receptor inhibitor) decreased (P less than 0.05) sperm motility when compared with controls. In addition, pre-incubation of spermatozoa with 10 or 20 microM prazosin and DHET also reduced (P less than 0.05) sperm motility. Sperm motility was increased (P less than 0.05) when co-incubations included ET and yohimbine (alpha 2-adrenergic receptor inhibitor); conversely, co-incubation of yohimbine (100 microM) and DHET decreased (P less than 0.05) sperm motility when compared with controls. Pertussis toxin and cholera toxins (effectors of stimulatory and inhibitory G-proteins, respectively) altered (P less than 0.05) sperm motility in a concentration dependent manner; however, co-incubation of pertussis or cholera toxins with ergot alkaloids had no interactive (P greater than 0.83) effects on sperm motility. Co-incubation of Rp-cAMP with 50 microM DHET had no effect (P greater than 0.05) on sperm motility; whereas, the co-incubation of 22.4 microM Rp-cAMP with 50 microM ET increased (P less than 0.05) sperm motility when compared with 0 or 224 microM Rp-cAMP (49, 65, 59, and 54%; respectively for (0, 22.4, 45.8 and 224 microM of Rp-cAMP). An interaction between BAPTA-AM (a chelator of intracellular calcium) and alkaloids also impacted (P less than 0.05) sperm motility. Generally, co-incubating spermatozoa with BAPTA-AM and ET increased sperm motility; however, co-incubation with DHET decreased sperm motility except with 41 microM BAPTA-AM. Collectively, these observations suggest that ET and DHET decrease bovine sperm motility via alpha adrenergic receptors and independent of G-protein signaling pathways.