Psych 50 Hormone And Behavior

Front 1

What were Berthold's conclusions with rooster experiment?

Back 1

1: Testes can be transplanted
2: They can function and produce sperm
3:No specific nerves direct testicular function
4: testes make a secretory blood-borne product

Front 2

Main guy for organizational/activational hypothesis. What was the experiment?

Back 2

-William Young
-exposed pups prenatally to androgen and compared activational effects of maculinized female
- (follow up studies)castrasted males early and compared activational effects with normal males (castrated later).

Front 3

3 criteria for behavior assessment

Back 3

1: objective? can it actually be observed?
2: reliable?
3: valid?

Front 4

4 methods of hormone level manipulation

Back 4

1:Administering it
2: eliminating hormone-secreting cells
3: antagonist
4: genetic manipulation (knockout).

Front 5

What is activated after protein hormone bind to receptor?

Back 5

G protein

Front 6

After G protein activation, increase/decrease in cAMP leads to what?

Back 6

decrease: inhibit enzyme activity
increase: opp

Front 7

What happens when there's too much hormone

Back 7

receptor downregulation

Front 8

what are tropic hormones?

Back 8

hormones released by anterior pituitary

Front 9

melatonin has receptors where?

Back 9

retina, hypothalamus, and anterior pituitary

Front 10

Which nuclei is important for circadian rhythms?

Back 10

SCN

Front 11

Which nuclei is important for production of oxytocin?

Back 11

PVN

Front 12

Which nuclei is important for synthesis of vasopressin?

Back 12

SON

Front 13

4 RH

Back 13

GnRH
CRH
TRH
GRH

Front 14

6 tropic hormones

Back 14

LH
FSH
TSH
Prolactin
GH
ACTH

Front 15

Describe relationship between hypo and ant pit

Back 15

1) RH from “neurosecretory” cells in hypo enters primary plexus of portal system
2) RH are carried down the pituitary stalk by the portal system
3)RH increase or decrease the release of ANT pit hormones into the general circulation

Front 16

Describe relationship between hypo and post pit.

Back 16

1: OT & VP are synthesized in the PVN and SON of the hypo
2: OT & VP are carried by axonal transport down the pituitary stalk
3: OT & VP are released into general circulation from neural endings in the POST pit

Front 17

functions of thyroid gland

Back 17

metabolism (including body temp regulation), reproduction, growth, differentiation

Front 18

function of parathyroid hormone

Back 18

calcium regulation

Front 19

name 3 adrenal cortex zones, starting with outer one.

Back 19

Zona glomerulosa
zona fasciculata
Zona reticularis

Front 20

androgens, glucorticoids, mineralcorticoids release from...

Back 20

adrenal cortex

Front 21

NA, AD, dopamine, enkephalins release from...

Back 21

adrenal medulla

Front 22

name effects from adrenal gland hormones (8)

Back 22

1.Sodium retention in kidney
2.Increases carbohydrate 3.metabolism
4.Anti-stress hormone
5.Weak androgenic activity
6.Increases blood pressure
7.Replenish energy stores after stress
8.Analgesic effects (pian relief)

Front 23

what hormones do the pancreas release? Which type of cell produces each?

Back 23

insulin (beta), somatostatin (gamma), glocagon (alpha)

Front 24

what is the overall function of the pancreas

Back 24

blood glucose homeostasis

Front 25

4 layers of of follicle cells

Back 25

theca externa, theca interna, granulosa cells, liquor folliculi

Front 26

mature follicle secretes ____ and mature corpus luteum secretes ____

Back 26

estrogens, progestins

Front 27

Lh causes theca interna to release ____ and FSH causes granulosa cells to ____ and secrete ___

Back 27

androgens, convert androgesn to estrogens, progesterone

Front 28

gametes in the testes come from:

Back 28

sertoli cells

Front 29

androgens in testes come form

Back 29

leydig cells

Front 30

What does LH do in the testes? What does FSH do in the testes?
What feedsback these processes?

Back 30

-release of T which feeds back to brain
- same thing and spermatogenesis. Inhibin feeds back to brain.

Front 31

what is ANP? What organ secretes it? What does it do?

Back 31

-Atrial Natriuretic Peptide
-heart
-Causes kidney to excrete sodium, controls blood volume and blood pressure

Front 32

gastrin: What organ secretes it? What does it do?

Back 32

-stomach
-secretes HCL

Front 33

What 4 hormones does the gut (small intestine) secrete and what do they do?

Back 33

-CCK (bladder contract, moves bile into small intestine)
-Motilin (moves food along "")
-Secretin (neutralizes stomach acid)
-GIP(stimulates secretion of insulin)

Front 34

Erythropoietin
Cacitriol
What organ secretes them? What do they do?

Back 34

-kidneys
-1st stimulates prod of red blood cells 2nd up uptake of calcium from SI

Front 35

What group of hormones are derivative of tyrosine?

Back 35

The protein hormones: catecholamines and thyroid hormones

Front 36

The process by which an organism is originally set up to become either male or female.

Back 36

sexual determination

Front 37

The process during development through which an individual becomes either male or female.

Back 37

sexual differentiation

Front 38

What is the protein product in the SRY gene?

Back 38

TESTES DETERMINATION FACTOR

Front 39

undifferentiated gonad called?

Back 39

germinal ridge

Front 40

What role does testes play in development of internal genitalia? ovaries?

hint: ducts

Back 40

-testes: secretes mullerian inhibitory hormone and T needed for Wolffian development.
-ovaries = nothing

Front 41

In the sexually indifferent stage: what does the genital tubercle develop into? urethral folds? Labioscrotul swelling?

Back 41

-clit/penis head
-labia minora/shaft
-labia majora/scrotum

Front 42

What is needed for development of male external genitalia?

Back 42

DHT

Front 43

what is α-fetoprotein

Back 43

what binds to estrogen in developing females so it won't masculinize her.

Front 44

What were the 4 conclusions of the WNT-4 (signaling molecule) exp?

Back 44

-w/out Mullerian duct does not develop
-instead wolffian duct develops
-w/out it ovaries release T
-

Front 45

Name 4 sex differentiation diseases. What happens in each?

Back 45

-Turner's syndrome (fail to make steroids)
-CAH (high pre-natal androgen exposure)
-AIS (defective receotors)
-5 alpha reductase deficiency (cannot convert T into DHT

Front 46

normal external genitalia at birth, sexed as females, malformed ovaries, no secondary sex characteristics, slow growth, sterile

Back 46

Turner's syndrome

Front 47

from mother (on X chromosome), regular development of testes, regular secretion of T, sterile, raised and look like females.

Back 47

AIS

Front 48

androgen produces high levels of androgens instead of cortisol, enlarged adrenal cortex, treated with life-long cortisol treatment

Back 48

CHA

Front 49

Gonadal steroids interact with (or activate) fully developed brain structures to shape behavior. The brain is NOT changed here, but the way it controls behavior is.

Back 49

activational effects

Front 50

CNS development is influenced by gonadal steroids. This hormonal influence has a lasting effect on male and female brain organization and, hence, behavior.

Back 50

organizational effects

Front 51

Name 3 charactersitics of 2m females.

Back 51

Interfemale aggression
Less attractive to males
Longer ovarian cycles

Front 52

A chemical that when absorbed into the body either mimics or blocks hormones and disrupts the body's normal functions.

Back 52

endocrine disruptor

Front 53

-failure to prevent miscarriages
-health problems for many of these women's children.
1971, doctors report high rates of unusual vaginal cancers in teenage girls, traced to mothers' use of DES.
-The girls also suffered birth defects of the uterus and ovaries, and immune system suppression.
what caused all did?

Back 53

DES-synthetic estrogen given to mothers to prevent miscarriages in the 50's and 60's.

Front 54

alligators:
Penis = 25% smaller
Testosterone = 70% less (but not coorelated to penis size)

Population decline

Strange structures seminiferous tubules

What is going on????

Back 54

Teeny weenies! Possibly linked to synthetic estrogens (Florida).

Front 55

what's happened to men over the years?

Back 55

% of men with normal sperm decrease, testicular mass decrease, seminiferous tubule mass decrease

Front 56

95% of Americans sampled have this neuroendocrine disruptor in their bodies. Rats exposed to it were more susceptible to cancer-causing chemicals as adults.

Back 56

Bisphenol A

Front 57

what two pathways are important in the zebra finch for song?

Back 57

efferent motor pathway
auditory trasnmission pathway (learning)

Front 58

what are the three Sexually dimorphic regions in bird species that sing?

Back 58

Area X, RA, HVc

Front 59

Female zebra finch will only sing like male if...as opposed to early exposure to...___ and combination of ___ late exposure

Back 59

-early exposure to estrogen and later activation with T/DHT
-DHT
-no exposure

Front 60

3 Ways Hormones Influence Sexual Differentiation of Brain

Back 60

Prevent cell death in specific brain regions (SDN-POA), Promote outgrowth of dendrites and axons of specific neurons (AVPV), Target-derived neurotrophic function (SNB).

Front 61

What was soc ontroversial about LeVay's experiment?

Back 61

Claimed nature effect for homosexuality: gays had smaller volumes of INAH3 nuclei

Front 62

Sexually dimorphic regions in brain (4)

Back 62

-SDN-POA (men bigger)
-AVPV (denser in dentrinic branches and more dopamine neurons)
-arcuate nucleus (projected heavier from AVPV and more synapses in females)
-spinal nuclues...(SNB)/Onuf nuclues in humans (not in females: T keeps it alive through stimulation).

Front 63

Play behavior among rhesus monkeys: organizational/activational effect?

Back 63

organizational and environment important

Front 64

_____ has more androgen activity. T improves memory in men.

Back 64

hippo

Front 65

differences between brain halfs' weight in men and women

Back 65

different between left and right more pronounced in men.

Front 66

Epididymis? where?

Back 66

long tube, storage duct for sperm (6 wks)
-on top of testes

Front 67

Vas deferens? where?

Back 67

tube, transports sperm
(travels from testes up yto where the bladder is

Front 68

Prostate gland? where?

Back 68

milky fluid, major portion of semen (below bladder...big round thing)

Front 69

Seminal vesicle? where?

Back 69

contents contribute to ejaculate (jalapeno thing next to bladder

Front 70

What is needed for erections and what is dependent on? what does it do?

Back 70

NO, DHT (at 40 DHT levels start to decline),vasodilator & increases mitochondrial respiration

Front 71

NO part of the production of what which leads to the relaxation needed for erection? How does viagra help this process?

Back 71

cGMP, prevents cGMP from converting into PDE5

Front 72

6-ways to quantify male sexual behavior.

Back 72

-amount of time the male spends sniffing female’s odors (chemoinvestigation)
-mount latency
-number of mounts
-number of intromissions
-ejaculation latency
-Post-ejaculatory interval

Front 73

What conclusions can be drawn about the role of E and T in male sexual performance? motivation?

Back 73

Testosterone is important both for sexual motivation (i.e., wanting to mate) and performance (i.e., being able to mate). Estrogen (converted from testosterone) is crucial for maintaining/restoring mating ability (performance), but only if combined with testosterone.

Front 74

what accounts for different sex drives in rats?

Back 74

estrogen receptors

Front 75

4 main areas activated by sexual activity

Back 75

accessory olfactory bulb, MPOA, nucleus accumbens, medial nucleus of the amygdala

Front 76

Evidence for a Key Role of the MPOA in Male Sexual Behavior (4)

Back 76

lesioning, implant studies, electrical stimulation, gene expression studies (shows activation of fod genes strongly after mating)

Front 77

MPOA involved with what aspect of male sexual behavior? if you lesion it what restored it?

Back 77

consumatory, dopamine

Front 78

what happen to dopamine levels in nucleus accumbens during consumatory behavior

Back 78

rises

Front 79

what aspect is is amygadal involved with in male sexual behavior?

Back 79

appetitive

Front 80

what's the conclusion between dopamine, amygdala, MPOA?

Back 80

the amygdala increases dopamine release in the mPOA during appetitive and consummatory components of sexual behavior

Front 81

_____ receptor agonists restore sexual behavior in amygdalar-lesioned rats

Back 81

dopamine

Front 82

where is serotonin released?

Back 82

Raphe nuclei in the brain stem

Front 83

serotonin released in the ___ of the hypo typically ___ sexual behavior.

Back 83

LHA, inhibits (esp released during post ejaculatory stage)

Front 84

Dopamine levels in the ____ (reward circuit) are altered with _____ infusion into the LHA

Back 84

nucleus accumbens, serotonin

Front 85

Three potential roles for nitric oxide in regulating male sexual behavior

Back 85

facilitates dopamine release, activates HPG axis, negative feedback (inhibits aromatase release...estrogens release domapine remember).

Front 86

Evidence for stimulatory effects of opioids

Back 86

1. naloxone blocks re-initiation of sex after sexual exhaustion
2. Opioids activate DA neurons in midbrain
3. enhances orientation of male towards female rat.

Front 87

Evidence for inhibitory effects of opioids

Back 87

1. Endorphin activity in POA inhibitd consummatory aspects of male sex including erection
2. Naloxone in POA enhances ejaculatory performance
3. Long-term opiate use suppresses LH secretion, reduction in testosterone

Front 88

3 components of female sexual behavior

Back 88

Attractivity
Proceptivity
Receptivity

Front 89

A Measure of Attractivity (actal method/exp)

Back 89

The Three-Chamber Preference Test

Front 90

a measure of proceptivity (actual method/exp)

Back 90

can be measured using a choice-arena

Front 91

what is lordosis quotient

Back 91

# lordosis/ #mounts* 100

Front 92

what restores complete normal sexual beahavior in rats

Back 92

E+P

Front 93

Sex Differences in PreferredInter-Intromission Intervals...what do they each care about?

Back 93

male: shorter intervals, ejaculation
female:longer intervals, sperm transport, progestational state.

Front 94

how exactly does pacing ensure better results.enought stimulation:

Back 94

prolactin released from ant pit, then maintains corpus luteum which secretes P which helps egg implant.

Front 95

TERMINATION OF RECEPTIVITY
w/out sex
w/sex
w/paced sex

Back 95

-18-20 hrs
-terminates sooner
-terminates fastest.

Front 96

endometrium

Back 96

lining of the uterus

Front 97

Overview of Circuitry Involved in Lordosis

Back 97

POA (inhibits).
VMN-->midbrain central grey--> medullary reticular formation(lower brain stem)-->spine neurons

Front 98

role of hypo, midbrain central grey, mudullaru reticular formation, and spine in lordosis

Back 98

1. Responds to hormones, peptides, receptors & hormones are produced
2. Transforms and relays hypothalamic signaling to reticular formation
3. Integrates postural information, vestibular and proprioception
4. Receives sensory stimulation, then generates motor response

Front 99

how is lordosis allowed to occur when hypo normally inhibits VMN?

Back 99

entrogen causes disinhibition

Front 100

Evidence for a crucial role of the VMN in female sexual behavior (3)

Back 100

- Lesions of the VMN reduce lordosis
-In ovariectomized female rats, estrogen implants into the VMN reinstate female sexual receptivity (weak)
-Estrogen AND progesterone into VMN of OVX rats = normal sexual behavior

Front 101

Estrogen implant in VMN= lordosis? proceptivity?
Progesterone implant in VMN of estrogen primed rats: proceptivity?
VNAB (ventral noradrenergic bundle) lesions= lordosis? proceptivity?

Back 101

-yes , no
-yes
-no, yes

Front 102

Lordosis does not occur in
---- receptor knockout mice

Back 102

P

Front 103

-LH facilitates CL
-CL produces prog (too)
-Prog inhibits sex behav.
what phase is this? follicle?

Back 103

estrus, none...primary corpus luteum

Front 104

-begin follicular phase estrogen levels rise
-LH and FSH stimulate follicular development
What phase is this? follicle?

Back 104

Diestrus, primary and seocndary follicle

Front 105

follicle secretes high levels of estrogen and progesterone
-causes GnRH pulse
-GnRH causes LH surge
= behavioral estrous
What phase is this?

Back 105

proestrus, graafian follicle

Front 106

describe 5 stages of the human menstrual cycle.

Back 106

-1.Primary follicle formation = primary oocyte + follicle cells-Follicle cells enlarge (FSH stimulates follicle growth)
-2.Secondary fol. Fluid-filled cavity
-3. Tertiary (Graffian follicle),central chamber (antrum) appears
-4.Primary oocyte matures to 2ndary oocyte, ovulation (LH surge).
5. Formation of the CL follicle cells collapse form CL

Front 107

Criteria for an adiposity (satiety) signal (5)...which two fill the criteria?

Back 107

1.Circulates at levels proportional to fat stores
2. Enter brain in proportion to the [plasma]
3. Receptors in “energy related” brain areas
4. Admin. directly into brain = stop eating
5. Loss = overeating (KO, lesion, antagonist)
-leptin and insulin.

Front 108

leptin secreted by...
brain receotors in...

Back 108

fat cells
hypo: arcuate nucleus

Front 109

Metabolic interactions and the well-fed state (6)

Back 109

1. food broken down into glucose, free fatty acids, and amino acids in gut
2. insulin released
3. glucose stored
4. glucose powers brain
5. powers muscle and some stored there.
6. excess glucose stored in adipose tissue, leptin released.

Front 110

Functions of insulin

Back 110

aa -> ketone bodies
Prevents glycogenolysis
glycogen from glucose

Front 111

Metabolic interactions and the fasting state (5)

Back 111

1. glucagon released
2. glycogen, amino acids, glycerol converted into glucose.
3. glucose and ketones power brain
4. ketone and free fattyc acid fuel muscles
5. lypolysis in adipose tissue, leptin secretion inhibited

Front 112

GET GLUCOSE TO THE BRAIN: (4)

Back 112

1.Glycogenolysis
Glycogen -> glucose
2.Lipolysis
Fats -> FA & glycerol
3.Activation of SYM NS = lipolysis
4.Gluconeogenesis
aa -> glucose

Front 113

under extreme deprivation what 3 hormones produced/neuros.

Back 113

NE, Cort, GH

Front 114

CNY signals that increase food intake

Back 114

NYP
MCH
AgRP

Front 115

proof that NYP increased food intake (2) and problem (1)

Back 115

1. NPY into the hypo potently increases food intake
2.disruption of NPY genes reduces hyperphagia in obese mice
problem: NPY KO completely normal

Front 116

AgRP...where is it secreted?its effects?

Back 116

1.proof that NYP increased food intake
2.Obesity = when agouti protein is overexpressed in the brain
3.Neurons that secrete NPY also secrete AgRP

Front 117

4 things about FSH (proof of how it works, what it does, where it's secreted, asociated with what other parts of the brain?)

Back 117

1.Increases food intake and reduces metabolic rate
2. MCH directly into the brain evokes feeding
3. MCH cell bodies = LHA
4. Form synapses with several structures involved in motivational processes...axons from NYP.AgRP neurons reach here.

Front 118

Signals that DECREASE food intake in CNS and Peripheral

Back 118

-melanacortins, CRH, TRH, CART
-insulin, CCK, Leptin

Front 119

alpha-MSH has two receptors...
which one's absence causes obesite in mice and humans
where is alpha-MSH secreted

Back 119

MC3, MC4
MC4
arcuate nucleus

Front 120

Key hypothalamic areas implicated in adiposity signaling and regulation of food intake

Back 120

Arcuate nucleus = first order (target) neurons, PVN & PFA = second order (effector) neurons

Front 121

Candidates for the second order neurons in the hypothalamic response to adiposity signaling

Back 121

TRH, CRH, Oxytocin supporess eating...Orexin and MCH stimulate eating

Front 122

Evidence for importance of endogenous factors: (3)

Back 122

1.Animals in spacecraft maintain biological rhythms
2.Animals held in adjacent cages, without exposure to any exogenous factors, differ in their biological rhythms
3.Biological rhythm of one animal can be transferred to another animal through tissue transplants.

Front 123

How Can Endogenous Rhythms be Demonstrated?

Back 123

1.measure behavior(wheel running)
2.Generate a timeline of the behavior
3.Generate an actogram
4.Tinker with the light cycle and observe effects on circadian rhythms

Front 124

Photoperiodism

Back 124

the use of daylength to time annual cycles

Front 125

Evidence for a Crucial Role of the SCN in Biological Rhythms (3)

Back 125

1. SCN lesion disrupts all rhythms
2. Severing SCN connections to other brain structures leaves an “island” of SCN activity, but abolishes rhythms in disconnected structures
3. SCN removal  transplantation studies show that SCN reinstates rhythmicity OF DONOR.

Front 126

Behaviors/Brain regions that are influenced by SCN (4)

Back 126

Feeding
Reproduction
EnDay length/ seasonality
ergy availability

Front 127

How does the SCN control ovarian cycle (what does it to and how)?

Back 127

--responsible for precise timing of LH surge. Lesion there = no ovarian cycle.
--Direct connection between SCN and GnHR cell bodies in preoptic area

Front 128

Long day breeders
Short-day breeders

Back 128

1.Mate in spring rear in summer
2.Mate in autumn Gestate in winter. Rear in summer

Front 129

Hans Selye

Back 129

founder of modern stress research

Front 130

General adaptation syndrome (GAS)-Hans Selye

Back 130

alarm, resistance, exhaustion

Front 131

3 main points of resistance phase:

Back 131

1. mobilization of remianing energy reserves and conservation of glucose released (GH, Cort)
2.Elevation of blood glucose concentration (cort, and glucagon)
3. conservation of salts and waters, loss of k+ and H+ (mineralcorticoids).

Front 132

Systems Inhibited By Stress
(4)

Back 132

1. Parasympathetic nervous system
2.hypothalamic-pituitary-gonadal axis
3.insulin secretion
4.Growth hormone release

Front 133

Key organs of the immune response (4)

Back 133

Lymph nodes
Thymus
Spleen
Bone marrow

Front 134

Participates in negative
Feedback for stress response
Inhibits HPA axis.

Back 134

hippo

Front 135

prood of stress impairing hippo (3)

Back 135

1. Patients with PTSD have hippo atrophy and deficits in recall tasks.
2.Administration of cortisol to humans impairs verbal declarative memory
3.People dignosed with depression and hypercortisolaemia show hippo-dependent memory impairments

Front 136

How is memory studied in the lab? (2)

Back 136

The Morris Water Maze, The 8-arm Radial Maze
...can see impaired spatial memory and object recognition deficits.

Front 137

Stress ______ memory and dendritic morphology in the _______

Back 137

inhibits, hippo

Front 138

stress increases ___ release in hippo which results in excitotoxicity via ____ levels

Back 138

glutomate, glucocorticoid

Front 139

Factors Influencing Responses to Stress

Back 139

control, predictability, social support, genetic make-up/personality

Front 140

Moyer: classification of aggression (7-3T)

Back 140

Maternal, Predatory, learned- and irrtiable, fear-induced, territorila, inter-male, sex- and rank related.

Front 141

Some methods used to evaluate aggression (7)

Back 141

muricide (mouse-killing)
shock-elicited fighting
isolation-induced aggression
resident-intruder aggression
maternal aggression
brain-stimulation
dominance-related behaviours in primates

Front 142

Evidence that androgens mediate aggressive behavior (4)

Back 142

1. puberty
2. seasons changes
3. males more than females
4. no more with castration

Front 143

Steroid hormones effect social status in male red-deer in 2 ways

Back 143

direct in brain and antlers

Front 144

The Challenge Hypothesis John Wingfield...talk about bird experiments

Back 144

Plasma T levels and aggressive behavior are positively correlated during periods of social instability or challenge...when no then no...birds had increased T after behavior..so T did not cause behavior

Front 145

Brain circuits for affective attack in Syrian Hamsters (activity high where?)(4)

Back 145

Medial Amygdala
Stria terminalis
Hypothalamus
PAG- midbrain

Front 146

ER alpha knockouts did what to aggression? soy diet

Back 146

hardly any, increased it

Front 147

Evidence that serotonin is involved in the regulation of aggressive behavior - mice (3)

Back 147

1.After prolonged isolation, mice become aggressive and serotonin levels decrease

2. The lower the serotonin concentration the higher the defensive aggressive response to foot shock.

3. Mice lacking serotonin receptors attacked an intruder more quickly and intensely than normal mice

Front 148

Blocking ___ receptors inhibits aggression in hamsters

Back 148

AVP

Front 149

Four different levels of analysis

Back 149

immediate causation, development, evolution, and adaptive function.