“Indifferent” ducts of embryo Y chromosome present Y chromosome absent Male Female uterus ovary vagina penis testis

Biology of gender Sex chromosomes determine gonadal sex (testis-determining factor) Phenotypic sex is depends on development of external genitalia w/hormone

Differentiation of genitalia depends on whether testosterone is present At 7 weeks Undifferentiated genitalia

Intersex individuals experience opposite sex hormones during early development or are insensitive to normal hormones. Some examples: Androgen insensitivity Lack of enzyme for testosterone production Congenital adrenal hyperplasia (enzyme missing to produce cortisol, aldosterone. Steroids converted to androgens instead.)

Male reproductive anatomy

Descent of the testes During fetal development, testes move from abdomen into scrotum Inguinal area is a common spot for hernias (intestine pokes through abdominal wall) The scrotum provides a cool area optimal for spermatogenesis

Sperm production Epididymis The cells of Leydig in testes secrete testosterone (T) T secreted at puberty produces 2o sex characteristics, spermatogenesis, & maintain tracts Ductus deferens Seminiferous tubules

Sperm production Spermatogenesis: spermatogonia (2N) spermatozoa (N) Epididymis Spermatogenesis: spermatogonia (2N) spermatozoa (N) Ductus deferens Seminiferous tubules

Meiosis Mitosis Sertoli cell Sertoli cell Lumen of seminifeous tubule Spermatids Secondary spermatocyte Meiosis Sertoli cell Primary spermatocyte Sertoli cell Spermatogonium Mitosis

Controlling sperm production Unlike females, males produce sperm from puberty onward Spermatogenesis controlled by LH and FSH

LH & FSH in males LH acts on Leydig cells for T prod’n FSH acts on Sertoli cells for sperm prod’n (inhibin provides negative feedback)

Causes of infertility? Sperm production, viability influenced by: Smoking, marijuana use Alcohol abuse Anabolic steroids, overly intense exercise, stress Tight underwear, pants Environmental pollutants (pesticides, lead, paint, radiation, heavy metals)

Sperm storage Spermatids become motile and are stored in epididymis and ductus deferens

Making something to swim in Seminal vesicles supply fructose, prostaglandins for muscle contraction, & fibrinogen Prostate gland secretes alkaline fluid and clotting enzymes Bulbourethral glands add mucus for lubrication Urinary bladder Seminal vesicle Prostate gland Bulbourethral gland Ductus deferens Testis

Signals for erection and ejaculation Arousal Pudenal nerves carry signals from penis to lower spinal cord & brain Spinal reflex and brain send PNS signals to penile arterioles Arousal causes muscle contractions that incr. physical stimulation – positive feedback Ejaculation Dramatic shift to SNS – contractions move semen to urethra and out

Female reproductive anatomy Ovaries produce estrogen, progesterone, and are site of oogenesis Estrogen: maintenance of the female tracts, 2o sex characteristics, ova maturation and release

Oogenesis overview Oogonia divide mitotically Meiosis I produces a primary oocyte (diploid), surrounded by follicle cells These oocytes develop into secondary oocytes on a cyclical basis

Ovarian cycle Follicular phase - first half of cycle when follicles mature and are ovulated Luteal phase - second half of cycle when uterus is prepared for implantation Follicular Luteal

Looking within the ovary…follicular phase Primary follicle Follicle cells oocyte FSH and LH levels are increasing

Looking within the ovary…follicular phase Follicle cells secrete estrogen Dividing follicular cells Primary oocyte Thecal cells

Looking within the ovary…follicular phase antrum Antrum collects fluid with estrogen Estrogen inhibits FSH and LH, so FSH

Low to moderate levels of estrogen

Late follicular phase Follicle (thecal) cells Antrum High estrogen levels promote LH secretion w/ positive feedback loop primary oocyte Follicle (granulosa) cells

High levels of estrogen

Late follicular phase Mature follicle Oocyte finishes meiosis I it now is a 2o oocyte Antrum

Pop! Ovulation! secondary oocyte Egg is flushed out Follicle remains

Luteal phase Corpus luteum secretes progesterone and estrogen corpus

Estrogen and progesterone Estrogen initiates preparation of endo- and myometrium, ‘prime’ uterus for progesterone (follicular phase) Progesterone endometrium vascularization, glycogen, decrease contractions (luteal phase) Progesterone inhibits LH and FSH (this is how birth control pills work)

Birth control pills, patches, rings BCP contain estrogen and progestin (or just progestin if nursing or estrogen-sensitive) They vary in type of progestin and amount of estrogen. Inhibit LH and FSH, so no ovulation Thicken cervical mucus Thicken uterine lining, inhibiting implantation ‘Morning after’ pills contain a much higher dosage

Changes in endometrium If the corpus luteum degenerates, progesterone drops and menstruation occurs Degenerating corpus luteum

But if there are sperm around… Fertilization normally occurs within a day of ovulation Contractions of the myometrium help some sperm reach the oviduct acrosome in action

Embryo forms before reaching the uterus Cleavage Blastocyst Embryo Fertilization Trophoblast Implants the embryo Ovulation Implantation

Settling into the uterus… Blastocyst secretes chorionic gonadotropin Endometrium has glycogen, and becomes more vascularized from progesterone 40% of blastocysts never implant

Settling into the uterus… Trophoblast enzymes digest proteins of the endometrium. This carves a hole for implantation. Endometrium Endometrium Trophoblast Embryo Embryo

Embryo Eventually forms chorion

Placenta development Placenta = chorion from embryo and uterine lining from mother. These tissues interlock like ‘fingers’ Projections of chorion have capillaries to form placental villi. They extend into the mother’s blood.

Placenta development Gasses, wastes, nutrients diffuse bw capillaries of mother and fetus Drugs, pollutants, chemicals also diffuse mother’s blood Amniotic sac Placental villus Chorion

Fertilization Delivery Human chorionic gonadotropin (hCG) Estrogen Progesterone Fertilization Delivery

Question: What are some insufficiencies of the feto-placental unit? The placenta cannot make estrogen or progesterone on its own A placenta can be ‘insufficient’ to support fetal growth due to blood flow problems Hypertension, diabetes, anemia, blood thinners, clotting disorders, smoking. Placental abruption (placenta breaks away)

Question: How does the body change during pregnancy? movie

Getting ready for birth.... ACTH and cortisol from the fetus promote prostaglandins, initial contractions occur High levels of estrogen make the uterus more sensitive to oxytocin and initiate gap junctions in myometrium Uterus has mild contractions. Baby’s head is down in pelvis

Positive feedback with oxytocin Stretching the cervix causes more oxytocin to be released Oxytocin induces stronger contractions

Lactation