novel approaches to expression and detection of oestrus in dairy cows

novel approaches to expression and detection of oestrus in dairy cows novel approaches to expression and detection of oestrus in dairy cows

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1.2.1.1 Follicular Phase There are a fixed number of primordial follicles established during foetal development (Webb et al., 2004), which deplete thereafter as many follicles become atretic because follicle growth occurs continuously throughout the cow’s reproductive life (Fortune, 1993). Cattle are monovular therefore as primordial follicles are recruited most become atretic and do not progress through to selection of the single dominant follicle, and few follicles (4mm in diameter, until follicles reach 6-8mm diameter, when one follicle is selected for continued growth and becomes dominant and will either ovulate or undergo atresia (Webb et al., 2003). Follicular development is governed by a period of gonadotrophin independence followed by a period of dependence (Webb et al., 2004). During recruitment, each wave is preceded by increases of FSH secretion lasting 1-2 days, stimulating growth of smaller follicles,

ecomes the main inhibitor of FSH and dependency switches to LH (Ginther et al., 1997). Growth of the dominant follicle continues, and the increase in oestradiol causes increased GnRH pulse frequencies, promoting LH secretion. This in turn stimulates oestradiol production by the granulosa cells (Fortune, 1994). This has a local effect on follicle development, but also a systemic effect, acting upon the hypothalamic-pituitary axis to increase LH production further, by positive feedback (Aerts and Bols, 2010). This ultimately results in oestrus, controlled by oestradiol, and the LH surge resulting in ovulation. 1.2.1.2 Oestrus & Ovulation It is this rise in oestradiol; enhanced by LH, stimulating production of androgen in the theca cells (Garverick et al., 2002) and the subsequent androgens being converted into oestradiol by aromatase enzyme from granulosa cells, which causes oestrus (Fortune, 1994). The positive feedback mechanism between oestradiol and LH, causes LH pulse frequency to increase to about 1 pulse per hour (Roche, 2006). The increase in LH concentration causes a cascade of events that induce the release of the oocyte into the oviduct, by an inflammatory response; involving prostaglandins, particularly prostaglandin E (PGE), produced by the follicle (Aerts and Bols, 2010). Prostaglandins stimulate the proliferation of cells and production of proteolytic enzymes to disrupt the follicle wall, releasing the oocyte (Espey, 1980). This process is ultimately under the control of the follicle itself, timing when it is appropriate to trigger the LH surge for ovulation by production of oestradiol (Roelofs et al., 2010), usually about 10-14 hours after oestrus (Forde et al., 2011). 1.2.1.3 Luteal Phase LH is the key hormone stimulating luteinisation of the theca and granulosa cells post ovulation, forming the CL from the cells of the ruptured cavity (Alila and Hansel, 1984). The CL consists of small and large luteal cells, which have steroidogenic properties (Smith et al., 1994), which secrete progesterone, along with a range of other cell types. The function of the CL is to produce progesterone, in order to maintain pregnancy if a conceptus is present (Forde et al., 2011). Sustained production of progesterone suppresses GnRH pulse frequency and hence LH secretion to prevent ovulation, but does allow enough LH for the continuation of follicular waves and dominant follicle growth (Savio et al., 1990). 7

ecomes the ma<strong>in</strong> <strong>in</strong>hibi<strong>to</strong>r <strong>of</strong> FSH <strong>and</strong> dependency switches <strong>to</strong> LH (G<strong>in</strong>ther<br />

et al., 1997). Growth <strong>of</strong> the dom<strong>in</strong>ant follicle cont<strong>in</strong>ues, <strong>and</strong> the <strong>in</strong>crease <strong>in</strong><br />

oestradiol causes <strong>in</strong>creased GnRH pulse frequencies, promot<strong>in</strong>g LH<br />

secretion. This <strong>in</strong> turn stimulates oestradiol production by the granulosa<br />

cells (Fortune, 1994). This has a local effect on follicle development, but<br />

also a systemic effect, act<strong>in</strong>g upon the hypothalamic-pituitary axis <strong>to</strong><br />

<strong>in</strong>crease LH production further, by positive feedback (Aerts <strong>and</strong> Bols,<br />

2010). This ultimately results <strong>in</strong> <strong>oestrus</strong>, controlled by oestradiol, <strong>and</strong> the<br />

LH surge result<strong>in</strong>g <strong>in</strong> ovulation.<br />

1.2.1.2 Oestrus & Ovulation<br />

It is this rise <strong>in</strong> oestradiol; enhanced by LH, stimulat<strong>in</strong>g production <strong>of</strong><br />

<strong>and</strong>rogen <strong>in</strong> the theca cells (Garverick et al., 2002) <strong>and</strong> the subsequent<br />

<strong>and</strong>rogens be<strong>in</strong>g converted <strong>in</strong><strong>to</strong> oestradiol by aromatase enzyme from<br />

granulosa cells, which causes <strong>oestrus</strong> (Fortune, 1994). The positive<br />

feedback mechanism between oestradiol <strong>and</strong> LH, causes LH pulse<br />

frequency <strong>to</strong> <strong>in</strong>crease <strong>to</strong> about 1 pulse per hour (Roche, 2006). The<br />

<strong>in</strong>crease <strong>in</strong> LH concentration causes a cascade <strong>of</strong> events that <strong>in</strong>duce the<br />

release <strong>of</strong> the oocyte <strong>in</strong><strong>to</strong> the oviduct, by an <strong>in</strong>flamma<strong>to</strong>ry response;<br />

<strong>in</strong>volv<strong>in</strong>g prostagl<strong>and</strong><strong>in</strong>s, particularly prostagl<strong>and</strong><strong>in</strong> E (PGE), produced by<br />

the follicle (Aerts <strong>and</strong> Bols, 2010). Prostagl<strong>and</strong><strong>in</strong>s stimulate the<br />

proliferation <strong>of</strong> cells <strong>and</strong> production <strong>of</strong> proteolytic enzymes <strong>to</strong> disrupt the<br />

follicle wall, releas<strong>in</strong>g the oocyte (Espey, 1980). This process is ultimately<br />

under the control <strong>of</strong> the follicle itself, tim<strong>in</strong>g when it is appropriate <strong>to</strong><br />

trigger the LH surge for ovulation by production <strong>of</strong> oestradiol (Roel<strong>of</strong>s et<br />

al., 2010), usually about 10-14 hours after <strong>oestrus</strong> (Forde et al., 2011).<br />

1.2.1.3 Luteal Phase<br />

LH is the key hormone stimulat<strong>in</strong>g lute<strong>in</strong>isation <strong>of</strong> the theca <strong>and</strong> granulosa<br />

cells post ovulation, form<strong>in</strong>g the CL from the cells <strong>of</strong> the ruptured cavity<br />

(Alila <strong>and</strong> Hansel, 1984). The CL consists <strong>of</strong> small <strong>and</strong> large luteal cells,<br />

which have steroidogenic properties (Smith et al., 1994), which secrete<br />

progesterone, along with a range <strong>of</strong> other cell types. The function <strong>of</strong> the CL<br />

is <strong>to</strong> produce progesterone, <strong>in</strong> order <strong>to</strong> ma<strong>in</strong>ta<strong>in</strong> pregnancy if a conceptus<br />

is present (Forde et al., 2011). Susta<strong>in</strong>ed production <strong>of</strong> progesterone<br />

suppresses GnRH pulse frequency <strong>and</strong> hence LH secretion <strong>to</strong> prevent<br />

ovulation, but does allow enough LH for the cont<strong>in</strong>uation <strong>of</strong> follicular waves<br />

<strong>and</strong> dom<strong>in</strong>ant follicle growth (Savio et al., 1990).<br />

7

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