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76 Cards in this Set

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  • Back
Homeostatic Mechanisms
Negative feedback. Detector of setpoint (osmoreceptors of osmolarity changes). Correctional mechanisms receive signals -> neg feedback -> detector can then turn correc mech. off.
Body Fluid Compartments
Intracellular fluid (67%)
Extracellular fluid [Interstitual/btwn cells 26%; Intravascular fluid/plasma/H20/etc 7%; Cerebrospinal fluid <1%]
Osmotic Pressure and Movement of Water
Isotonic: normal; intra/extracellular compartments are equal. No osmotic pressure of H20 (or ions' pressure). (Always influx)
Osmotic Pressure and Movement of Water
Hypertonic (1) Hypotonic (2)
1) More ions/solute outside. Pulls water out of cell. Occurs w/ all cells not just neurons. 2) More water outside osm pressure draws water into cell.
Water Balance
[Neg Free water balance: More water leaving your body than is being put in; Pos Free water balance: more water inside than out of body – hypotonic. (Hence, less solutes in body...)]
Intake: electrolyte-free water; Isotonic solution [Na+ + K+] --> Body Fluids [Na + K] Excretion: Electroyte free; Water isotonic solution. //Positive free water balance = hypotonic. Free water balance: water w/oout ions. Hypo/hypertonic: in or out of cell.
Osmometric Thirst
[Osmolality = concen of solutes in body fluids; not just rec. but actual neurons. Base of brain (tip); stimulate thirst, takes a while to be ingested.]
Tendency to seek and ingest water due to an intracellular vs. extracellular (interstitial) fluid imbalance.
Does NOT require intravascular plasma loss.
Induced by ingestion (e.g. salt) and sweating.
Osmometric Thirst
Stimulated by “osmoreceptors”
Neurons sensitive to osmolality that likely surround the portion of the anterior hypothalamus that borders the anteroventral third ventricle (AV3P).
Cellular Dehydration & Thirst
Increased Solute concentration of interstitial fluid causes osmoreceptors to lose water and shrink in size
What does alcohol have to do with thirst?
Distribution and total amount of body water profoundly affect the volume of alcohol in body.
Interesting Facts:
Less than 10% of alcohol consumed is excreted (breath, sweat, urine), 90-95% must be metabolized by the liver. Alcohol inhibits the release of vasopressin by the posterior pituitary, which results in excess urination when drinking alcoholic beverages. Vasopressin induces H20 rel. from kidneys; retain salt->feel dehydrated.
Volumetric Thirst
Tendency to drink due to a loss of blood plasma (intravascular) volume.
Loss of blood plasma = Hypovolemia. Causes:
Sweating (both Osmo and Volu), bleeding, nausea and/or vomiting. Two detectors: Cation (Na+ + K+) and Volume Detectors
Must be sensitive to changes in both osmolality and overall volume of plasma.
The Nephron
Nephrons in kidneys (both in circul sys, surrounding nephron) Nephron: functional unit of kidney (over a million per kidney) Microscopic; complex; extract waste products to bladder. Put H20 and salt back into intravas fluid & into cells. (B/c they detect changes two ways) Regulate water & cation/solute content. Juxtaglomerular appparatus (JGO) These cells line bv in nephron; detectors of the kidney (fluid vol and osmolality of blood in kidney)
Hypovolemia & Thirst
Reduced blood flow in general (also in kidneys) -> JGO (detect change)->cells rel. Renin enzyme -> catalyzes events -> Angiostensin 2(responsible for drinking beh changes)
Hypovolemia & Thirst cont.
1) Adrenal gland on kidney release -> Aldosterone (makes kidney retain Na+ and crave salt) 2) Also effects brain: Pituitary Gland (rel of vasopressin. Back to kidney. Hormone induces kidney to retain H20 (inhibited by alchohol-> opp effect of vasopressin) 3) Vasoconstriction (inc in blood pressure. Constriction of bv; smaller)
Baroreceptors induce volumetric thirst
In circular sys but not in kidney; main heart and veins. Diag of brainstem-> BR (b. rec) in heart & bc -> send info to Nuc of Sol tract (NTS). Directly to brain.
Neural Mechanisms of Thirst
Midsag. rat brain. Subfornical organ, Median Preoptic Nucl, Av3V (above hypothal; where osmorec are); NTS (furthest back)
Neural Mechanisms
[see fig 11-8]
Osmorec in AV3V and subforn detect changes in Angiotensin in blood. Send axons to Med Preop Nuc which induces thirst. *Integrator of osmometric & volum. thirst* Osmorec/neurons in AV3V are a send axons to med preop. Unknown how from med pre op nuc to desire from thirst.
Hypodipsia: Deficient Water Intake
Despite similar rises in plasma sodium concentrations, healthy elderly men become less thirsty and drink less than healthy young men.
Osmoreceptor neuron and/or Angiotensin II?

Some psychiatric patients, such as those with schizophrenia, display a failure to drink and hypernatremia (high plasma Na+ levels).
Satiety does Not Equal Restored Nutrients
State or perception of being full.
Lack of hunger. Not cells having all nec nutrients. Hours but feel full after minutes.
Metabolic Phases
Body uses energy continuously, but consumption is intermittent. Therefore, it must store energy.
Fasting Phase
Short-term reservoir: Glucose (simple sugar)-> via insulin -> Glycogen (stored by liver, complex carb)
Long-term reservoir:
fat to Glucose (triglycerides) (via glucagon, secreted by pancrease as is insulin)
Metabolic Phases
Absorptive Phase
Occurs when food is being digested (absorbed) and glucose levels begin to rise. Rise in glucose -> Increased insulin production Nutrients not used as energy are stored: (as glycogen or fat).
Metabolic Phases
See diag. Most glucose goes to brain and is stored as Glycogen or fat (fat almost always stored as fat). Protein: muscles for energy or as fat.
--Glucose transport into neurons/glia does not require insulin. Therefore, they can use glucose even when insulin is absent. Necessary because brain does not have fatty acid transporters, can only use glucose for energy.
Hunger Initiation Signals
Environmental & Social Factors
Time of day, olfactory/visual/auditory stimulation, psychological factors (e.g. anxiety & depression). Physiological Factors: Hypoglycemia = Fall in glucose levels.
Hunger Initiation Signals
Receptors for Hunger?
(see diag)
Liver: Glucose + Fatty Acid
Brain: Glucose Detectors
Satiety Signals: Short-term
Gastric (stomach) Factors: Stomach can detect presence of food and nutrient quality.
Intestinal Factors: CCK and PPY
Satiety Signals: Short-term
Intestinal Factors: cont.
Cholecystokinin (CCK) - Controls the rate of food movement from stomach to intestine.
Involved in short-term satiety. Peptide YY (PYY)
Secreted by intestine, receptors in hypothalamus.
Reduces food intake.
Satiety Signals: Long-term
Fat (adipose) cells
1 gram of fat > 2X energy compared to glycogen
Leptin (Secreted by fat cells
Decreases food intake, increases metabolism.)
OB Mice
Lack OB gene producing leptin
Neuronal Mechanisms: Brainstem role in Hunger & Satiety
Disconnects the brainstem from rest of the brain. Forebrain has no control over beh anymore that are controlled by motor neurons caudal to transection; brainstem controls mechanisms to stay alive. Pleasurable effects of eating controlled partly by brainstem. Hindbrain also has control of muscles involved in ingestive beh.
Decerebrate rats
Still display some hunger and satiety behaviors.
Neuronal Mechanisms: Lateral Hypothalamus and Hunger
Melanin-concentrating hormone (MCH) and Orexin secreting neurons: Stimulate hunger and reduce metabolic rate. Axons of these cells travel to cortex, brainstem nuclei, thalamus and spinal cord.
Neuronal Mechanisms: Lateral Hypothalamus and Hunger
Neuropeptide Y (NPY) secreting neurons
- Located in the arcuate nucleus of hypothalamus
- Stimulate MCH and Orexin neurons in lateral hypothal to produce hunger.
Ghrelin: Released by stomach, stimulate NPY neurons
Neuronal Mechanisms: Hypothalamus and Hunger
Brainstem =
Motivation &
Stimulation of the
Lateral Hypothalamus increases food intake
Neural Mechanisms of Satiety
- Secreted by fat (adipose) cells. - Inhibits NPY cells and stimulate CART-releasing cells in the arcuate nucleus. - Suppresses feeding and increases metabolism.
Neural Mechanisms of Satiety
CART-releasing cells
- Prevent release of MCH and orexin.
- CART peptide is released following cocaine administration.
PYY = inhibit NPY cells to reduce hunger. Leptin = inhibits NPY cells but has an excitatory effect on CART cells (amplifies signal). Ghrelin produced most by empty stomach.
Eating Disorders: Anorexia Nervosa
Four Features of Anorexia:
(Showed higher insulin levels than normal subjects for a chance to inc energy; patients are interested in food)
Intense fear of becoming fat: often accompanied by food restriction, vomiting, diuretics, and/or strenuous exercise. Weight Loss: < 85% of “average body weight” (ABW) or 17.5 “body mass index” 3. Distorted Body Image: significant misperception of the shape and/or size of one’s body, denial of the seriousness of the current low body weight, or basing one’s self-evaluation heavily on body weight or shape.
4. Lack of Menstruation (Amenorrhea): Loss of normal hormonal production/regulation (likely due to NPY suppression of ovulation).
Features of Bulimia Nervosa
1. Binge eating: consuming large amounts of food in a short time period (within 2 hours); feeling of not being able to stop. 2. Compensation: trying to prevent weight gain through self-induced vomiting, laxatives, diuretics, enemas or other medications; fasting, or excessive exercise. 3. Frequency: at least 2 binge eating episodes a week for 3 months.
4. Low Self Worth: largely based on eating habits and weight.
Sexual Development and Sexual Behavior
The most important category of social behavior—essential for species survival
Reproductive behaviors are sexually dimorphic—they are different in males and females
Parental behavior
Sexual Development
23 Pairs of chromosomes = human
One set from each parent
22 of the 23 pairs of chromosomes govern physical development independent of sex
The 23rd pair—the Sex Chromosomes—determine whether the individual is male or female
Sex is determined at fertilization
All ova (eggs) contain an X chromosome
Each spermatazoa (sperm) contains either an X or a Y chromosome
Sex is determined by makeup of the pair:
XX - Female XY - Male
(First 8 - 10 wks, same path; states 21-22 see differentiation, about 60 days vs stages 16-17 with set neural development) Begin with same exernal genitalia before 8 wks. Phallus, urethral fold, u. slit, genital swelling, tail. Completion of process by 12th week. Same tissues developed into different structures.
What’s Y got to do with it?
Embryos are bisexual
Mullerian internal sex organ for females evolve into inner 2/3 of vagina. Wolffian (male) system. One set of gonads: testes later or ovaries later.
A single gene on the Y chromosome (Sry) produces testis-determining factor
causes gonads to become testes
Testes release Anti-Müllerian Hormone and Androgens.
M whithers away in males and w whithers away in females.
Evidence for Embryonic Bipotentiality: Androgen Insensitivity Syndrome (XY)
No functioning androgen receptors
Gonads develop into Testes (Sry)
Defeminization (Anti-Müllerian hormone)
Masculinization fails; internal sex organs do not develop, external genitalia are female
Incidence for complete AIS is about 1:15,000 births
Male genotype, female phenotype
[Sec sex char via hormone therapy, raised as women but xy; appear as babies to be females. Testes remain in body but no scrotum. Wolffian sys does not fully develop; outer 1/3 of vagina developes, no uterus]
Evidence for Embryonic Bipotentiality
Persistent Müllerian Duct Syndrome (XY)
Mutation of AMH receptors
Masculinization succeeds; external genitalia are male
Defeminization fails; BOTH sets of internal sex organs develop
[Usu male behavior. Testes are functional; neither sex organ is functional; no outer opening of vagina]
Turner Syndrome
1:2500 female births
X genotype; no defeminization or masculinization
No gonad development; “Female is nature’s default”
Usu female behavior. Ovaries do not fully develop either; somewhat female external genitalia; problems arise at puberty -> no sec sex char. Problems with nonverbal communic?
Sexual Maturity: Puberty
Occurs when cells in the hypothalamus secrete gonadotropin-releasing hormone (GnRH)
GnRH stimulates the anterior pituitary gland to secrete two gonadotropic hormones:
Leutinizing Hormone
Follicle-Stimulating Hormone
Present in both sexes but named for effects in females!
In response, ovaries produce estradiol and testes produce testosterone
Results in development of secondary sex characteristics
Hormonal Control of Sexual Behavior: Males
Mostly studied in rats and hamsters
Behavior has five parts
Pelvic Thrusting
Refractory Period: A period of time after copulation during which the male will not engage in sexual behavior
Coolidge Effect: Diminished refractory period in the presence of a new female
Behavior (in rats) has been poorly studied
“Receptivity” is related to gonadal hormones
Estradiol and then progesterone peak just before peak receptivity. Estradiol peak in middle; progest at end of month.
Hormonal Control of Sexual Behavior
In Gonadectomized Male Rats
(Early T and Later T, no female sexual beh; Male sexual beh: evidence of masu)
E & P have an activational effect in an non-adronized animal. (Early Testos, later E & P: no female sexual beh; no male sexual beh. Evidence of defeminization: E & P fails to facilitate female sexual beh.)
Sexual Orientation
Is sexuality a biological trait or a behavior?
Money (1972) suggested that individuals have the potential to become male or female within the first two years of life
Bell et al. (1981): study of several hundred male and female homosexuals
Found no predictive childhood environmental factors; suggests biological basis for sexuality
The case of Bruce/Brenda (“John/Joan”)
David Reimer
Born as an identical twin to his brother
Penis was destroyed during circumcision
his brother’s circumcision was then cancelled
Parents enlisted the help of John Money
At 22 months, sexual reassignment surgery was performed, and “Bruce” became “Brenda”
Raised as a female
Prenatal Hormone Exposure and Sexuality
Congenital Adrenal Hyperplasia
Excessive amounts of androgens released from the adrenal glands
Boys develop normally
Girls undergo masculinization
Enlarged clitoris, labia
Increased incidence of “masculinity” (Fig 9.11)
Incidence of homosexuality in these females is significantly higher than in the general population (nearly 50%?)
Prenatal Hormone Exposure and Sexuality
((see last diag!!))
Androgen Insensitivity Syndrome
Genetic XY, raised as girls
Display no difference in sex drive, activity and satisfaction compared to general population
No increased incidence of homosexuality
Together with findings from individuals with CAH, these observations suggest that:
Prenatal androgen exposure is a significant factor in determining sexuality
Sexual attraction to men is the “default”
Disturbances of prenatal androgen exposure may lead to both female and male homosexuality
Evidence of defeminization:
E & P added to a full grown male rat will not facilitate female sexual beh, and not male sexual behavior either (despite T added at birth b/c no T added later which would cause masculinization)
Male Rat Brain
- Olfactory bulb is very important (as in female rats). Projects to Medial Amgydala - to Medial Preoptic Area. [OB-MA-MPA w/ sexually dimorphic nucleus)
Male Rat Brain: Medial Preoptic Area
- Destruc abolishes sexual beh. - Prenatal stress reduces size of sexually dimorphic nuc and dec sexual beh. - Mating causes production of Fos protein. - Injec of testosterone enhances sexual beh of castrated rates.
Female Rats
[PAG: destruc abolsihes sexual beh; estradiol treatment/stimulation of VMH inc neural activity; neurons contain estrogen and progest rec]
Olf bulb - Medial Amgydala - VMH (what MPA is to males) No sexually dimorphic nuc. Destruc abolishes sexual beh - PAG - Reticular fromation.
Sexual Behavior: Summary
Hormones play two roles in sexual development and behavior
Organizational: Prenatal exposure to androgens masculinize sex organs AND brain structures
Activational: Exposure to sex hormones (estradiol, progesterone, testosterone) in adulthood leads to the expression of sexual behavior
Gender and Sexuality depends on brain organization
Prenatal Hormone Exposure and Sexuality: Congenital Adrenal Hyperplasia
Excessive amounts of androgens released from the adrenal glands (Masc in/ext sexual organs)
Boys develop normally
Girls undergo masculinization
Enlarged clitoris, labia
Increased incidence of “masculinity” (50% homosexual?)
Androgen Insensitivity Syndrome
Genetic XY, raised as girls
Display no difference in sex drive, activity and satisfaction compared to general population
No increased incidence of homosexuality.
Together with findings from individuals with CAH, these observations suggest that:
Prenatal androgen exposure is a significant factor in determining sexuality
Sexual attraction to men is the “default”
Levels of prenatal androgen exposure play a role in both female and male homosexuality
- No difference in current androgen levels; 20,000 with AIS (No internal sex organs) Stress raises androgen levels in mothers - no clear findings.
Sexuality and Genetics
Related to a homosexual man/woman: for the monozy twin about 1/2 het, 1/2 hom; for the dizgy twin: 78-84% het, 22-14% hom; adopted brother/general population 10:1 ratio (females 94% het).
1) Satiety mechanisms:
2) Detectors responisible for initiating volumetric thirst are located in the:
1) Monitor the activity of correctional mech (Do not replenish depleted nutrients) 2) kidneys, heart, and large blood vessels
1) Most/all of the signals for osmometric and volu thirst appear to be integrated in the: 2) The short-term fuel reservoir is located in the:
1) Region around the anterior third ventricle. 2) cells of the liver and muscles and is filled w/ glycogen.
1) During the absorptive phase of metabolism: 2) During the fasting phase:
1) the blood level of glucose rises. 2) Most cells live on fatty acids.
1) Cutting the vagus nerve prevents: 2) Detectors that monitor the availability of nutrients outside the bbb are located in the:
1) Hunger signals originating in the liver from reaching the brain. 2) Liver
1) Injections of CCK: 2) Legions of the VMH produce overeating and lesions of the Lat hypothal
1) Surpress eating. 2) abolish eating.
1) Injec of MCH in the lat ventricles of the brain in rats: 2) Neuropeptide Y, which is secreted by neurons whose cell bodies are located in the: 3) CART
1) induce eating. 2) arcuate nucleus, stimulates ravenous eating. 3) neurons do not contain leptin receptors.
1) Appetite can be suppressed by the activation of rec for: 2) The uncoupling protein may be one of the factors in determining:
1) leptin, serotonin, CART. 2) metabolic efficiency
1) High-fat meals: 2) The cerebrospinal fluid of anorexics contain elevated levels of:
1) Produce less of an inc in plasma leptin levels than low-fat meals. 2) NPY
1) A peptide nt found in the lat hyp neurons that stimulate appetite and reduce met rate. 2) Peptide hormone that produces thirst and salt appetite:
1) MCH 2) Angiostensin.
1) CCK: 2) Osmometric thirst:
1) Hormone secreted by duodenum; may provide satiety signal. 2) Occurs when tonicity of interstitual fluid inc.
1) Peptide produced after meals in amounts proportional to its size. 2) An example of the activational effects of sex hormones:
1) PYY. 2) Production of sperm.
1) Event first marking the beginning of puberty: 2) The LH surge causes: 3) The accelerated onset of puberty in a female rodent caused by the odor of a male is the:
1) Secretion of GnR hormones by hypothal. 2) ovulation. 3) Vandenbergh effect.
1) The size of the sexually dimorphic nucleus... 2) The MPA receives ss info from the genitals through connections with:
1) Of the preoptic area is controlled by the amount of androgens present during fetal devel. 2) Central tegmental field of the midbrain; the medial amygdala
1) A female rat w/ bilateral lesions of the ventromedial nuclei will: 2) E & P exert their effects on female sexual beh by activating neurons in the:
1) not display lordosis 2) ventromedial nuc of the hypothal.
1) Elec stimulation of the periaqueductal gray matter facilitates: 2) Just before parturition, the level of estradiol:
1) lordosis. 2) Rises, the level of progesterone begins to fall, and the level of prolactin rises.
1) Sensory organ that mediates effects of some pheromones: 2) Hormone that causes dev of ovarian follicle and maturation of ovum. 3) Nuc in brain; plays an essential role in male sexual beh and parental beh.
1) vomernasal. 2) FSH 3) MPA