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Gonads
- produce hormones and gametes
- includes
- testes
- ovaries
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Internal sex organs
connect gonads to outside
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external sex organs
external genatalia
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development of gonads
- undifferentiated through 6th week
- SRY gene on Y chromosome develops testes
- No Y chromosome or no SRY gene results in a default to female ovaries
- gonads produce sex-specific hormones that direct sexual development
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development of internal sex organs (male)
- embryos contain female and male precursors- wolffian ducts (males), mullerian ducts (female)
- Testicular hormones stimulate the wolffian ducts to create male internal sex organs
- Must secrete two hormones:
- AntiMulalarian- defeminize and get rid of mullarian ducts
- Androgens- masculinize
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Male internal sex organs
- Epidydimis
- vas deferens
- seminal vesicles
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development of internal sex organs (female)
if no hormone is secreted, the mullarian ducts will develop into female reproductive organs
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female internal sex organs
- fimbriae
- fallopian tubes
- uterus
- upper 2/3 of vagina
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Development of external sex organs
- Presence of androgen results in male genetalia- penis, scrotum
- Absence of androgen results in female genetalia- labia, clitoris and lower 1/3 of vagina
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organizational effects
early hormones that set up the brain for sexual activity but are not online yet
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activational effects
causes sexual maturity and capability
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androgen insensitivity (syndrome)
- lack of androgen receptors in XY individuals
- results in testes, no internal organs, typical female external genetalia but shallow vagina
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persistant mullerian syndrome
- failure to produce anti-mullerian hormone as an XY individual
- results in testes, internal male organs and mullerian ducts or even female internals in addition, and external male (cancer)
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turner syndrome
- only one X chromosome present (XO)
- develop along female track
- no gonads, no puberty and usually small in stature
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Hormones
- responsible for secondary sex characteristics
- include
- estradiol
- androgens
- androgen (adrenal gland)
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Estradiol
breasts, uterus and vagina maturation, body fat storage, hip widening
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Androgen
facial hair, larynx growth, pubic hair, muscle, gentalia
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Androgen (adrenal gland)
body hair (major source for females
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puberty begins with
- CASCADE
- gonadotropin-releasing hormone (GnRH)
- stimulates anterior pituitary gland to release gonadotropic hormones
- these hormones stimulate gonads to release estradiol, progesterone, androgen
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Masculinization/defeminization
- androgen exposure during neural development is required for both in behavioral patterns
- absence of androgens results in female sexual behavior
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Congenital adrenal hyperplasia
- adrenal glands of genetic females secrete abnormally high amounts of androgens, starting during gestation
- masculinizing effect in brain and external genetalia
- higher than average homo/bisexual
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Pheromone effects in animals
- •Animals - pheromones affect reproductive physiology in
- several ways
–Lee-Boot effect – - attenuated estrous cycles
–Whitten effect – the - odor of a male will begin the estrous cycle
–Vandenbergh effect – accelerated - onset of puberty
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Pheromone effects in humans
–Synchronized - menstrual cycles
–Shorter - cycles when exposed to men
–Androstadienone (androgenic - chemical) increases positive mood in females, decreases mood in males
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Sexual Orientation
- Prenatal hormone exposure appears to influence sexual orientation
- EXPL Congenital adrenal hyperplasia, androgen insensitivity
- Also genetically influenced
- 52% concordance rate with identical male identical twins and 48% in female
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Hormonal control in males
- In lower animals in testosterone and a receptive female are present, sexual activity will occur
- For humans testosterone must also be present
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Sexual behavior in lower animal males
–Rats - and other lower animals – in the presence of testosterone, a male rat will
- mount a receptive female repeatedly
•Intromission - – entry of the penis into the vagina
•Pelvic - thrusting – rhythmic movement to produce genital friction
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Sexual behavior in lower female animals
- •Lower mammals (rats)
- – female sexual behavior
- depends on the presence of estradiol and progesterone
–Secretion - of these hormones results in:
•Receptivity - – willing/able to copulate
–Lordosis reflex occurs in the - presence of a male rat
•Proceptivity – eagerness to - copulate
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Coolidge effect
(lower animals) once a male has achieved intromission, pelvic thrusting, and ejaculation and is the refractory period, if another receptive female comes by it can begin the process again
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hormonal control females
- primate and humans- have the ability to copulate at all times, not dependent on hormones
- hormones however do influence sexual interest
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Neural control of sexual behavior males
- •Medial Amygdala
- –Sexually dimorphic (~85% larger in males)
–Lesions disrupt sexual behavior
–Receives: - •Chemosensory input
•Hormonal input - •Somatosensory input from the genitals
–Projects to the MPA - •Medial Preoptic Area (MPA)
–Contains - Sexually Dimorphic Nucleus (3-7x larger in males than females)
- –Lesions of this area abolish sexual behavior
–Projects to the PAG and PGi
- •Nucleus paragigantocellularis (PGi)
- –Located in the medulla, inhibits spinal cord sexual reflexes
–Input from the MPA to the PGi suppresses this inhibition - •Periaqueductal grey (PAG)
–Region of the midbrain, stimulates the spinal cord sexual reflexes
–Input from the MPA to the PAG activates these connections - •Spinal motor neurons
–Innervate the pelvic organs and muscles involved in copulation
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Neural control of sexual behavior females
•Medial amygdala
–Projects to the VMH & MPA - •Ventromedal nucleus of the hypothalamus (VMH)
- –Lesions of the VMH abolish lordosis
–Activated by mAmyg input and estradiol and progesterone
–Projects to the PAG
- •Medial Preoptic Area projects to:
- –PGi - suppressing inhibition to spinal neurons
–PAG - - projects directly to spinal motor neurons involved in clitoral arousal
- •Periaqueductal grey region (PAG)
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Regulatory mechanisms
- system variable- what you are measuring
- Set point- optimal amount of system variable
- detector- what tells you if the set point is not achieved
- correctional mechanism- something that fixes it back to set point (sweating, eating, using restroom)
- Negative feedback, satiety signal- that you have achieved set point, or (neg) you need to get back to set point
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Ingestive behaviors
- eating and drinking are correctional mechanisms
- Satiety signals determine ingestive behaviors
- works faster than negative feedback, by monitoring correctional behavior
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Fluid compartments
- Intercellular- fluid in cell
- Extracellular
- Intravascular- blood(level)
- Interstitial- surrounding fluids
- Cerebrospinal- CNS
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Isotonic
intracellular and interstitial fluid are in balance
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Hypertonic
too much salt outside, not enough water inside
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hypotonic
too little salt outside, too much water inside
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Osmotic thirst
loss of water from the intercellular compartment
- •A salty meal raises sodium in the blood plasma
- > draws water out of the interstitial fluid
- > interstitial fluid becomes hypertonic
- >draws water out of the cells
- >cells lose volume
- > osmotic thirst
- Monitored by osmoticreceptors located in hypothalmnus and OVLT
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Volumetric thirst
- •Results when
- intravascular fluid volume is decreased
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Volumetric thirst receptors
–Atrial baroreceptors in the heart and large veins monitor blood volume - •If blood volume decreases, baroreceptors detect the decrease in stretch and stimulate thirst
- •Receptors in the kidneys also detect decreased blood volume
- –Secrete the enzyme renin
–Renin catalyzes angiotensin II
–Angiotensin II
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Neural regulation of thirst
- •Region surrounding the anteroventral 3rd ventricle (AV3V) - integrates thirst signals
- –Osmoreceptors in AV3V (anterior hypothalamus & OVLT)
•Project to the median preoptic nucleus in AV3V - –Nucleus of the solitary tract (medulla)
•Receives sensory input from atrial baroreceptors
•Projects to the median preoptic nucleus - –Subfornical organ
•Angiotensin II in the blood acts on receptors in the SFO - •Projects to the median preoptic nucleus
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Absorption phase
- •Absorptive phase – food is in the digestive system
- –Carbohydrates are broken down into glucose
•Rise in blood glucose - > parasympathetic nervous system activity
- •Insulin (hormone) released from the pancreas
–Allows all of the body’s cells to use glucose - –Prompts the conversion of glucose into glycogen
•Remaining glucoseconverted into fat, stored in adipose cells for long-term needs
–Proteins are broken down into amino acids
•Building blocks for protein synthesis
•Others converted to fat and stored in adipose cells
–Fats remain fats
•Stored directly in adipose tissue
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