Plasma Luteinizing Hormone Levels in Response to Gonadotropin-Releasing Hormone Agonist and Clonidine in Trypanosoma congolense-Infected Female Goats

• Published in: Brain research bulletin 1997, Vol.44 (5), p.591-595
• Main Authors: Ng’Wena, A.G.M, Patel, N.B, Wango, E.O
• Format: Article
• Language: English
• Subjects: Activity Cycles; Animals; Clonidine - pharmacology; Female; Goats; Gonadotropin-Releasing Hormone - analogs & derivatives; Gonadotropin-Releasing Hormone - pharmacology; Humans; Hypothalamus; Luteinizing Hormone - blood; Luteinizing Hormone - metabolism; Reproduction; Trypanosoma congolense; Trypanosomiasis; Trypanosomiasis, African - blood
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/S0361-9230(97)00305-5

Trypanosomiasis, a parasitic disease of humans and animals, occurs over a wide area of Africa and imposes a large socioeconomic burden on the people. In the present study, we investigated whether trypanosomiasis-induced reproductive disorders were due to pituitary or hypothalamic dysfunction by determining plasma luteinizing hormone (LH) response to gonadotropin-releasing hormone (GnRH) agonist or clonidine in Trypanosoma congolense -infected female goats. With GnRH agonist administration, the total amount of LH secreted over a 140-min sampling period on day 23 and day 60 postinfection was consistently higher (71 and 21%, respectively) in infected goats compared to controls. In contrast, clonidine administration to infected goats on day 28 and day 69 postinfection failed to significantly alter the LH pulse frequency or the mean LH pulse amplitude over a 80-min sampling period. The results, especially the lack of response to clonidine, indicate that trypanosomiasis impairs GnRH release from the hypothalamus.