LH and testosterone responses to five doses of a GnRH analogue (buserelin acetate) in 12-month-old Thoroughbred colts.

This research investigates how the reproductive hormones of young male Thoroughbred horses respond to various doses of a gonadotropin-releasing hormone analogue, buserelin. The study found that increasing doses prompted release of luteinising hormone (LH), but responses varied among individuals and did not consistently trigger increases in testosterone.

Methodology

• The researchers used 13 male Thoroughbred yearlings, with each treatment group containing between 3 and 8 colts.
• The horses were given doses of buserelin, a synthetic hormone used to stimulate reproductive hormone production, at varying levels: 0.5, 1, 5, 10, and 40 micrograms.
• Jugular venous blood samples were taken at various intervals before and after buserelin administration: -10, 0, 10, 20, 30, 40, 60, 120, and 180 minutes.

Findings

• There were marked increases in LH concentrations in colts that received 5, 10, or 40 micrograms of buserelin, but not for those who were given 0.5 or 1 microgram.
• The highest peak LH concentrations and average areas under the curve were found in the colts that received the highest buserelin dose (40 micrograms), compared to those who received the lower doses of 0.5 or 1 microgram.
• Testosterone concentrations rose in some, but not all, colts given doses of 1, 5, 10, or 40 micrograms of buserelin.

Conclusions and Implications

• There was a dose-dependent response – the percentage of horses that responded to buserelin, in terms of increased LH and testosterone production, grew with each increasing dose. The highest buserelin dose led to hormone responses in all colts.
• However, each colt responded in an “all or nothing” manner – either they had a significant increase in LH or they did not.
• Further, not all the colts that had a significant LH increase showed a subsequent increase in plasma testosterone concentrations, suggesting that different mechanisms may determine the LH and testosterone responses. This could be due to insufficient LH response in these individuals to stimulate the Leydig cells, which are responsible for testosterone production.