The completion of meiosis in the secondary oocyte during fertilization results in the extrusion of the second polar body. The haploid ovum is formed as a result. The meiotic arrest and maturation of the oocyte involve events such as the activation of mitogen-activated protein kinase (MAPK). The outer-lying thecal layers of the ovary are responsible for this process. The mural granulosa cells, which are highly steroidogenic, differentiate into the corpus luteum and remain in the ovary after ovulation. On the other hand, the cumulus cells, also known as cumulus oophorus and corona radiata, surround the oocyte. The innermost layer of cumulus cells forms gap and adhesion junctions with the oocyte. During ovulation, the cumulus cells are released along with the oocyte, forming the cumulus-oocyte complex. These cumulus cells play a crucial role in the movement of the oocyte through the fimbriated end of the oviduct via a ciliary transport mechanism, ultimately leading to fertilization. 
The growth of early antral follicles relies on pituitary follicle-stimulating hormone (FSH). As antral follicles grow larger, they become more dependent on FSH for their growth and viability. The recruitment of 2 to 5-mm follicles for rapid growth occurs due to a transient increase in FSH towards the end of the previous menstrual cycle. 
The oocyte undergoes rapid growth in the early stages of antral follicles, which then slows down in larger follicles. During the antral stage, the oocyte synthesizes the necessary components for the cell cycle, enabling it to complete meiosis I at the time of ovulation. However, after ovulation, the human egg arrests at metaphase II until it is fertilized by sperm. In early primary and secondary follicles, the oocyte fails to complete meiosis I due to the lack of specific meiosis-associated proteins. However, larger antral follicles acquire meiotic competence but still remain arrested until the LH surge in the middle of the menstrual cycle. This meiotic arrest is maintained by elevated levels of cyclic adenosine monophosphate (cAMP) in the mature oocyte. 
A model explaining the resumption of meiosis after the LH surge involves various factors such as the GPR3 protein-coupled receptor, cGMP, cAMP, PKA, and PDE3A. The GPR3 receptor, which is constitutively active, maintains high cAMP levels. The oocyte-specific phosphodiesterase PDE3A degrades cAMP to inactive AMP. Before the LH surge, cGMP inhibits PDE3A, and cGMP is produced in cumulus and granulosa cells and enters the oocyte through gap junctions.
The secondary oocyte completes meiosis at fertilization and extrudes second polar body. Haploid ovum •Fig. 44.18 Eventsinvolvedinmeioticarrestandmaturationoftheoocyte.MAPK,mitogen-activatedproteinkinase.(ModifiedfromWhiteBA,PorterfieldSP.Endocrine Physiology. 4thed.Philadelphia:Mosby;2013.) the outer-lying thecal layers. Mural granulosa cells become highly steroidogenic and remain in the ovary after ovulation to differentiate into the corpus luteum.
Cumulus cells are the inner cells that surround the oocyte (they are also referred to as the cumulus oophorus and corona radiata). The innermost layer of cumulus cells maintains gap and adhesion junctions with the oocyte. Cumulus cells are released with the oocyte (collectively referred to as the cumulus-oocyte complex) during the process of ovulation. Cumulus cells are crucial for the ability of the fimbriated end of the oviduct to “capture” and move the oocyte by a ciliary transport mechanism along the length of the oviduct to the site of fertilization (see
Early antral follicles are dependent on pituitary FSH for normal growth. Large antral follicles become highly dependent on pituitary FSH for their growth and sustained viability. As discussed later, 2to 5-mm follicles are recruited to enter a rapid growth phase via the transient increase in FSH that occurs toward the end of the previous menstrual cycle.
The Gamete
The oocyte grows rapidly in the early stages of antral follicles; growth then slows in larger follicles. During the antral stage the oocyte synthesizes sufficient amounts of cell cycle components so it becomes competent to complete meiosis I at ovulation. (Note that the human egg arrests after ovulation at a second point, metaphase II, until it is fertilized by sperm.) Thus in early primary and secondary follicles, the oocyte fails to complete meiosis I because of a dearth of specific meiosis-associated proteins. However, larger antral follicles gain meiotic competence but still maintain meiotic arrest until the midcycle LH surge. Meiotic arrest is achieved by maintenance of elevated cyclic adenosine monophosphate (cAMP) levels in the mature oocyte (
Figs.
•Fig. 44.19 ModelofhowLHsurgeleadstoresumptionofmeiosis.PDE,phosphodiesterase.Granulosa & cumulus cells ZP GPR3 AMP cAMP PKA PDE 3A MEIOTIC ARREST (–) (–) LH SURGE LHSURGEcGMPcAMPMEIOTICRESUMPTIONGsACPDE3AcGMP cGMP cGMP 44.18 44.19 ). The constitutively active (i.e., not requiring a ligand) Gs protein-coupled receptor GPR3 maintains high cAMP. The oocyte-specific phosphodiesterase PDE3A degrades cAMP to inactive AMP. Before the LH surge, PDE3A is inhibited by cGMP, which is produced within cumulus and granulosa cells and enters the oocyte via gap junctions.