718 Chapter 20
Figure 20.18 A human spermatozoon. ( a ) A diagrammatic
representation and ( b ) a scanning electron micrograph in which a
spermatozoon is seen in contact with an ovum.
HeadMidpieceEnd pieceAcrosomePrincipal piece(a)Acrosome Head Midpiece Principal piece(b)into an upper midpiece that contains a fibrous sheath and mito-
chondria around the axoneme; a principal piece with only the
fibrous sheath around the axoneme; and an end piece consist-
ing only of the axoneme. Sperm in the seminiferous tubules are
nonmotile; they become capable of flagellar movement and thus
motility outside of the testis in the epididymis.
Hormonal Control of Spermatogenesis
The formation of primary spermatocytes and entry into early pro-
phase I begins during embryonic development, but spermatogene-
sis is arrested at this point until puberty, when testosterone secretion
rises. Testosterone is required for completion of meiotic division
and for the early stages of spermatid maturation. This effect is
probably not produced by testosterone directly, but rather by some
of the molecules derived from testosterone (the 5 a -reduced andro-
gens and estrogens, described earlier) in the tubules. The testes
also produce a wide variety of paracrine regulators—transforming
growth factor, insulin-like growth factor-1, inhibin, and others—
that may help to regulate spermatogenesis.
Testosterone, secreted by the Leydig cells under LH stimu-
lation, acts as a paracrine regulator by stimulating spermato-
genesis in the seminiferous tubules. Testosterone can initiate
spermatogenesis at puberty and can maintain spermatogen-
esis in the adult human testis. As mentioned previously, estro-
gen produced in the testes (from testosterone) may also be
required for spermatogenesis, although its role is not currently
understood.
Surprisingly, FSH is not absolutely required for spermato-
genesis, as demonstrated by men who have mutated and non-
functional FSH receptors. LH-stimulated testosterone secretion
promotes spermatogenesis, whereas FSH only enhances this
effect. The FSH receptors are located in the Sertoli cells, as pre-
viously described, and FSH stimulates Sertoli cells to produce
androgen-binding protein and inhibin. A newborn male has only
about 10% of his adult number of Sertoli cells, and this increases
to the adult number as a boy enters puberty. It appears that FSH,
acting together with testosterone, promotes this proliferation of
Sertoli cells. Without FSH, spermatogenesis would still occur but
would commence later in puberty.
Likewise, maintenance of spermatogenesis in the adult
testis requires only testosterone. However, FSH is required for
maximal sperm production, and so it may be required for opti-
mal fertility. Therefore, hypothetical male contraceptive drugs
that blocked FSH might reduce, but probably would not abol-
ish, fertility. The enhancement of testosterone-supported sper-
matogenesis by FSH is believed to be due to paracrine regulators
secreted by the Sertoli cells.Male Accessory Sex Organs
The seminiferous tubules are connected at both ends to a tubu-
lar network called the rete testis (see fig. 20.11 ). Spermatozoa
and tubular secretions are moved to this area of the testis and are
drained via the efferent ductules into the epididymis (the plural is
epididymides ). The epididymis is a tightly coiled structure, about
5 meters (16 feet) long if stretched out, that receives the tubular
products. Spermatozoa enter at the “head” of the epididymis and
are drained from its “tail” by a single tube, the ductus, or vas,
deferens.
Spermatozoa that enter the head of the epididymis are
nonmotile. This is partially due to the low pH of the fluid in
the epididymis and ductus deferens, produced by the reabsorp-
tion of bicarbonate and the secretion of H^1 by active transport
ATPase pumps. During their passage through the epididymis,
the sperm undergo maturational changes that make them more
resistant to changes in pH and temperature. The pH is neutral-
ized by the alkaline prostatic fluid during ejaculation, so that