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UA / Psychology / PY 413 / What is the function of mullerian ducts?

What is the function of mullerian ducts?

What is the function of mullerian ducts?

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Physiological Psych Final Exam


What is the function of mullerian ducts?



REPRODUCTIVE BEHAVIORS  

Sexual Development**

• Males and females have undifferentiated gonads in early stage of prenatal development • Wolffian ducts: precursors to male reproductive organs

o develops into vas deferens & seminal vesicles

• Mullerian ducts: precursors to female reproductive organs

o develops into ovaries, uterus, & upper vaginal area

• SRY gene: sex-determining region on the Y chromosome-causes gonads to develop into  testes-the sperm producing organs

• Testes: produce androgens to inc growth, produce Mullerian-inhibiting hormone (MIH) to  inhibit development of Mullerian ducts


Where is steroid derived from?



Steroid Hormones 

• Androgens (male) & Estrogens (female)

• Derived from cholesterol If you want to learn more check out What are the two substructures of peripheral nervous system?

• 3 ways of influencing cells

1. bind to membrane receptors-ex. neurotransmitters

2. enters cell-affects protein synthesis

3. chromosome binding-activate or inactivate certain genes

• Androgens: testosterone (10x higher in men than women)

• Estrogens:

o Estradiol-higher in women than men, menstrual cycle

o Progesterone-activates uterus & maintains pregnancy, 40x higher in pregnant women Organizing Effects of Sex Hormones 

• Organizing effects: long-lasting structural effects


How are hormones and human behavor related to each other?



o Puberty: men-facial hair, penis growth, change in voice; women-breast development o Influence activity in brain areas

▪ sexually dimorphic areas of the brain differ between males and females; larger  in males and contributes to sexual behavior

▪ anterior hypothalamus: men-sexual behavior, women-menstrual cycle

• Sex hormones determine whether the body develops male or female genitals during the  sensitive period of the of the first trimester-sexual differentiation We also discuss several other topics like What do textbooks illustrate?

o testosterone: high level converted to dihydrotestosterone leads to male external  genitalia, low level leads to female external genitalia

o estradiol: effects internal organs, less influence than testosterone

Brain Development & Sex Hormones 

• Alpha-fetoprotein: binds with estradiol and prevents it from entering developing cells; does  not bind to testosterone

• Testosterone is converted to estradiol once it enters the cell to have influencing effects • Excess estradiol in the blood leads to development of more masculine features • Childhood behavior If you want to learn more check out What influences the economy?

o toy preference: boys-cars, balls, light up things; girls-dolls, tea sets

▪ preference at age 3 consistent throughout childhood to age 13

• Sex differences: pain tolerance, stress, psychological disorders

Activating Effects of Sex Hormones 

• Activating effects: temporary, continuing only while a hormone is present or shortly beyond • Testosterone & estradiol inc release of dopamine & other receptors to inc sexual arousal  o stimulation of D1 & D5 receptors facilitates penis erection

o stimulation of D2 receptors leads to orgasm  

• Oxytocin responsible for relaxation & lack of anxiety after orgasm

• Seratonin inhibits sexual activity by blocking dopamine release

• Hormones & human behavior

o inc testosterone levels leads to higher sexual arousal, partner seeking even in a  relationship, & greater enjoyment of sex

o dec testosterone levels leads to dec interest in sex & dec male sexual activity  o testosterone releases nitric oxide which inc & sustains erection (ex. Viagra prolongs  effects of nitric oxide)

o testosterone reduction (unrelated to impotence) has been tried as a means of  controlling sex offenders; side effects of diabetes, weight gain, and depression Menstrual Cycle Don't forget about the age old question of What are the purpose of political parties?

• Approximately 28 days We also discuss several other topics like What is the ingathering of the exiles?

• Produced by hypothalamus and pituitary gland interaction with the ovaries • At the end of menstruation:

o anterior pituitary releases follicle-stimulating hormone (FSH)-promotes the growth of a  follicle in the ovary

o follicle nurtures ovum in the ovary

• Middle of menstruation:

o inc amounts of estradiol produced by follicle

o anterior pituitary inc release of FSH and luteinizing hormone (LH)-causes follicle to  release ovum

o remnant of follicle (corpus luteum) releases progesterone which prepares uterus for  implantation of ovum

o –periovulatory period: when ovulation occurs, maximum time of fertility, highest level  of estrogen in the body & inc sexual responsiveness

• Ovum is not fertilized: uterine lining cast off, hormone levels decline If you want to learn more check out What are the five foundations of economics?

• Ovum is fertilized: inc estradiol & progesterone (40x normal)

Birth-Contol Pills 

• Interfere with feedback between ovaries & pituitary

• Combination pill: most common, contains estrogen & progesterone which prevents surge of  FSH & LH that would otherwise release an ovum

Sex Hormones & Maternal Behavior 

• Inc sensitivity to estradiol in pregnancy in areas responsible for maternal behaviors • After birth:

o inc levels of estradiol & prolactin-causes inc attn to the infant after birth & milk  production

o affects in medial preoptic area & anterior hypothalamus

• Vasopressin-synthesized by the hypothalamus & secreted by posterior pituitary, strongly  associated with forming long term bonds and relationships; helps facilitate olfactory  recognition, influence caretaker & protective behaviors of young

• Male’s prolactin levels inc and testosterone levels dec after birth, especially if he interacts with  the child

• Hormones vs. experience- hormones do not control, just facilitate

Mate Selection 

• Gender differences due to different reproductive pressures

• Symmetry is “universally” viewed as attractive

• Female preferences: monogamy to inc chance of lifelong mate, a provider • Male preferences: advantageous to be promiscuous to inc chance of spreading genes to  offspring

Gender Identity-what we consider ourselves to be

• Biological differences-“sex differences”

• Feelings about oneself-“gender differences”

Intersexes 

• Anatomies intermediate between male or female

• Underdeveloped or ambiguous genitalia

o Can be caused by migration of the SRY gene, exposes women to higher androgen  levels

• Congenital adrenal hyperplasia (CAH): overdevelopment of the adrenal glands from birth  causing excess testosterone production; genetic female exposed to excess testosterone can  be partly masculinized

• Androgen insensitivity: XY chromosome pattern with female genitalia; caused by lack of  androgen receptors to activate genes

Sexual Orientation 

• Genetic disposition

o Higher incidence of homosexuality on the maternal relatives of homosexual men • Birth order- higher probability of homosexual men with older brothers-link in X chromosome • Prenatal hormones & in males, reactions to mother’s immune system  

 

EMOTIONAL BEHAVIORS  

Emotion is defined in components-physical, subjective, valence, and motivation.  Emotion has components of cognitions, feelings, and actions.  

Emotions & Nervous System 

• sympathetic- fight or flight

• parasympathetic- rest & digest

o to a point, as arousal inc, performance inc

• Role of feedback from the body:

o James-Lange theory: autonomic arousal and skeletal actions preceed the feeling  aspect of emotion (ex. feel afraid because you run away)

o Schacter & Singer’s cognitive theory: physical response of emotion is related to  intensity/appraisal of the situation

Body Actions Influence Emotion 

• Manipulating expressions: facial-zygomaticus major (smile)-research shows people who hold a  pen in their teeth forcing a smile feel more amusement than those holding a pen in their lips  forcing a frown

o duchenne smile-genuine smile, zygomaticus major + orbicularis oculi (crows feet) • Mobius syndrome: facial paralysis- people with this condition feel emotion but cannot express  • Benefits of BOTOX: Ach antagonist; injections show dec emotional processing, dec emotional  reactions, less negative emotions

• Controlling facial expression-cranial nerves

o facial nerve (cranial nerve VII) controls outer muscles of facial expression

o trigeminal nerve (cranial nerve V) controls deeper muscles for jaw, chewing, etc. • Muscle control in face is combined ipso/contralateral control

o upper 1/3 combined, lower 2/3 only contralateral

Communication 

• universal emotions of anger, sadness, happiness, fear, disgust, surprise, contempt, and  embarrassment

• cultural and individual differences

• tone of voice carries emotional information

• eyeball whites: more white=fear, less white=happy

The Limbic System 

• forebreain areas surrounding the thalamus-critical for emotion

• hypothalamus-regulates sympathetic/parasympathetic nervous system

• amygdala-fear based learning, critical for all emotions

Brain Activation of Disgust(“bad taste”)

• Insular cortex-smell & taste- to avoid contamination disgust is learned to avoid harm • Moral disgust- (ex. sex offenders) disgusted by things against our moral backgrounds Brain Areas of Emotion 

• Ventromedial prefrontal cortex (vmPC)-decision making

o allows you to make judgements and deliberate consequences

o difficulty learning moral & social cues if damaged

• Anterior Cingulate Cortex (ACC)

o important for understanding errors in conscious body

o larger ACC related to greater harm avoidance

o works with orbital frontal cortex to make decisions

o inhibits aggression

Brain Hemispheres **

• left hemisphere

o behavioral activation system(BAS): activity left hemisphere marked by low to moderate  autonomic arousal and a tendency to approach

▪ high extroversion related to greater left hemisphere activity

• right hemisphere

o behavioral inhibition system (BIS): activity in right hemisphere which inc attn and  arousal, inhibits, action, and stimulates emotions such as fear and disgust, avoidance

▪ introversion, more negative emotions, and depression related to greater right  hemisphere activity

Amygdala 

• regulates anxiety levels

• controls autonomic responses

o startle reflex-extremely fast (200ms)-stimulates pons 3-8ms after noise, pons tenses the  muscles especially the muscles of the neck to protect from injury

• bed nucleus of the stria terminalis- stria terminalis is a set of axons that connects this nucleus  to the amygdala; responsible for long-term, generalized emotional arousal

• damage to the amygdala interferes with inhibited learning of fear & inhibited relation of fear  with emotional consequences

o toxoplasma gondii: parasite produced by cats that can infect other mammals, causes  damage to amygdala-rat fearlessly approaches cat and is eaten

o Kluver-Bucy syndrome in monkeys-monkeys with this are tame and placid-impaired at  learning what to fear and die as a consequence

o Urbach-Wiethe disease in humans: case of SM

▪ calcium builds up in amygdala and causes deterioration over time

▪ impaired at processing emotional information and learning what to fear

▪ SM robbed/assaulted multiple times-no fear response, could recognize  

cognitive aspects of emotion but not feelings

Anxiety & Fear 

• Indirect pathway of fear (conscious fear)

o senses????thalamus????cortex????amygdala

• Direct pathway of fear (unconscious fear)

o senses????thalamus????amygdala????cortex

• Anxiety-fear spreading

• GABA-key neurotransmitter in reducing fear

o high GABA=low fear, low GABA=high fear

Anxiety Disorders 

• panic disorder: frequent periods of anxiety and occasional attacks of rapid breathing, inc  heart rate, sweating, and trembling-extreme arousal of the sympathetic nervous system  • relief from anxiety

o anti-anxiety drugs-benzodiazepines (ex. diazepam-valium, alprazolam-xanax)-binds to  GABA receptors to enhance effects of GABA

o alcohols effects on GABA receptors is responsible for the anti-anxiety effects o systematic desensitization-gradual exposure to feared stimulus in hopes of extinction Concepts of Stress 

• any kind of nonspecific bodily response to some type of demand

• general adaption syndrome:  

o alarm stage-adrenal glands release epinephrine stimulating the sympathetic nervous  system; cortisol released to inc blood glucose providing energy; aldosterone released  to maintain blood salt & blood volume

o resistance stage-sympathetic response declines, adrenal glands continue secreting  hormones that enable body to maintain alertness

o exhaustion stage-tired, inactive, and vulnerable due to prolonged stress-nervous  system and immune system lack the energy to sustain their responses

Stress & Hypothalamus-Pituitary-Adrenal Cortex Axis (HPA axis)**

• Stress activates 2 systems in the body: (1) sympathetic nervous system (2) HPA axis • HPA axis for prolonged stressors

• hypothalamus releases corticotrophin releasing hormone (CTH)????pituitary gland releases  adrenocorticotropic hormone(ACTH)????stimulates adrenal cortex to secrete cortisol which  enhances metabolic activity, elevates blood levels of sugar, and increases alertness Immune System 

• Cells that protect the body against viruses, bacteria, and other intruders

• Leukocytes (white blood cells)-kill invaders

o B cells: secrete antibodies which are Y shaped proteins that attach to cell surface  proteins called antigens, attack unfamiliar antigens, mature in the bone marrow o T cells: attack intruders directly, mature in the thymus gland

o Natural killer cells: attack tumor cells and cells infected with viruses

o cytokines: combat infections and stimulate prostaglandins to produce  

fever/sleepiness/lack of energy so body can fight off invaders

• Psychoneuroimmunology: deals with the ways experiences alter the immune system and how  the immune system in turn influences the CNS

o stressful experiences cause CNS to activate immune system

o brief stressors strengthen immune system (ex. exercise)

o prolonged stress can damage hippocampus due to cortisol release causing inc  metabolic activity which causes hippocampus to become vulnerable  

BIOLOGY OF LEARNING AND MEMORY  

Types of Memory 

• Short-term memory: aka working memory, working memory is limited & fades quickly, pre frontal cortex important for working memory, dec as we age

• Long-term memory: unlimited & perpetual, hippocampus important for long-term memory • Consolidation: something stored in short-term memory for a sufficient period of time  transitioning to long-term memory

o emotionally significant memories form quickly because of secretion of epinephrine and  cortisol

• Reconsolidated: when we remember something, we remember the last time we remembered  it, not the original memory

• Implicit memory processing: unconscious memory processing, an influence of experience on  behavior, even if you do not recognize that influence

• Explicit memory processing: known memory, deliberate recall of information • Declarative memory: typically explicit, “I declare _____ happened”

• Procedural memory: memory about knowing how to do something, implicit memory dealing  with development of motor skills and habits

The Hippocampus 

• Important for declarative memory, spatial memory, and memory for context • Patient HM suffered from severe epilepsy, had surgery to remove hippocampus  o had difficulty forming new long-term memories-anterograde amnesia

o poor episodic memory (memories of single personal events) & declarative memory o procedural memory remained intact

o better implicit than explicit memory

o intact short-term memory

• hippocampus important for rapid storage of an event/episodic memory whereas basal ganglia  learn gradually which is important for developing habits and seeing complex patterns Basal Ganglia 

• implicit learning

• procedural memory

• Parkinson’s disease patients have trouble forming implicit memory but not declarative Types of Amnesia(memory loss)

• anterograde amnesia: inability to form memories for events that happened after brain  damage

• retrograde amnesia: loss of memory for events that occurred before brain damage • Korsakoff’s Syndrome: brain damage caused by prolonged thiamine (vitamin B) deficiency o common in chronic alcoholics-alcohol lacks vitamins

o symptoms of apathy, confusion, and memory loss

• confabulation-making up memories to fill in gaps

• Alzheimer’s disease: age related degenerative condition

o affects 50% of people over the age of 85, 99% of cases are late onset

o mild memory impairment gradually progresses to other cognitive deficits

o genes controlling early-onset Alzheimer’s:

▪ accumulation of protein amyloid-B inside and outside neurons damages  

dendritic spines, decreases synaptic output, and decreases plasticity; damaged  structures cluster into plaques and cause atrophy in the braon

▪ tau protein is the intracellular support structure of axons, altered tau protein  builds up in tangles

Improving Memory 

• arousal enhances memory

• caffeine/Ritalin

• mnemonics-chunking  

• relating/rephrasing

• imagery-method of loci

Learning 

• Hebbian synapse: synapse that inc in effectiveness because of simultaneous activity in the  presynaptic and postsynaptic neurons

• Habituation: a dec in response to a stimulus that is presented repeatedly and accompanied  by no change in other stimuli

• Sensitization: an increase in response to mild stimuli as a result of exposure to more intense  stimuli

Long-Term Potentiation**

• LTP: one or more axons connected to a dendrite bombard it with a rapid series of stimuli; the  rapid burst of intense stimulation leaves some of the synapses potentiated

• 3 properties of LTP for its cellular basis of learning & memory:

o specificity-only active synapses strengthened

o cooperativity-simultaneous stimulation by 2+ axons produces LTP much more strongly  than does repeated stimulation by just one axon

o associativity-pairing a weak input with a strong input enhances later response to the  weak input

• LTP in hippocampal neurons: AMPA receptor excited by glutamate????depolarization removes  magnesium???? NMDA receptors excited

o ionotropic receptors-when stimulated they open a channel to let ions enter the  postsynaptic cell

• long-term depression (LTD): a prolonged decrease in response at a synapse, occurs for axons  that have been less active than others

 

COGNITIVE FUNCTIONS  

Asymmetry of Function 

• contralateral connections

• left visual field projects onto right half of each retina sending axons to right hemisphere while  right visual field projects onto left half of retina sending axons to left hemisphere • right hemisphere: perceiving emotions, global/big pictures

o those with damage have trouble interpreting humor, sarcasm, inflection of voice • left hemisphere: language processing, local/small details

o left hemisphere damage have better ability to understand emotion

Development of Lateralization & Handedness 

• planum temporale: section of the temporal cortex, larger in the left hemisphere for 65% of  people

• 95% of right handers have language processing in left hemisphere & lefties resemble righties • hemisphere dominance should not be overemphasized

Corpus Callosum 

• largest connection between the left and right hemisphere

• set of myelinated axons-white matter

• cutting of the corpus callosum:

o early treatment for epilepsy

o creates split-brain individual

• anterior & hippocampal commissure used for exchange of information between hemispheres;  some info can be transferred even after severance of corpus callosum

Language Acquisition 

• social interaction

• sensitive period-early childhood

• children better at pronunciation and learning grammatical constructs

• second language learning-individuals who learn a second language before age 6 show  bilateral processing

Brain Damage & Language**

• aphasia: severe language impairment

• Broca’s area: one of the first areas localized to cognitive function

o Broca’s aphasia (nonfluent aphasia)-impaired language production

o damage results in language disability & inability to understand grammar,  comprehension deficits in speech, and emission of many filler words

• Wernicke’s area-near auditory cortex

o Wernicke’s aphasia (fluent aphasia)-impaired language comprehension

▪ damage causes impaired ability to name objects

▪ anomia-difficulty recalling the names of objects

PSYCHOLOGICAL DISORDERS  

Drug Mechanisms 

• antagonist-drug that blocks a neurotransmitter

• agonist-drug that mimics or increases the effects of a neurotransmitter

• affinity-drug has an affinity for a receptor if it binds to it

• efficacy- drug’s tendency to activate the receptor

• nucleus accumbens-central to reinforcing experiences of all types; axons releasing  norepinephrine and dopamine work here

Major Depressive Disorder(MDD)

• feeling sad/helpless everyday for weeks at a time; episodic

• DSM characteristics: low energy, low pleasure, feelings of worthlessness

o global-affects all aspects of life

o perpetual-never ending

• absence of happiness better descriptive than inc sadness

Biological Influence on MDD 

• viral infections-borna disease (1/3 of individuals with MDD carry this)

• hormonal: women-post partum depression affects 20% of women (drop in estradiol &  progesterone); men-low testosterone levels

• right hemisphere dominance-individuals with MDD show greater right hemisphere  dominance, most people with depression have inc activity in the right prefrontal cortex • genetic link: moderate aassociation in immediate family but no depressive gene; gene x  environment interaction most predictive

Seratonin Transfer Protein & MDD 

• facilitates serotonin reabsorption

• short form vs. long form gene

o individuals with 2 short forms show greater chance of developing depression especially  following major stressful events

ANTIDEPRESSANT DRUGS**  

Tricyclics

• operate by blocking the transporter proteins that reabsorb serotonin, dopamine, and  norepinephrine into the presynaptic neuron after their release; block histamine receptors, Ach  receptors, & sodium channels

• effect is to prolong the presence of neurotransmitters in the synaptic cleft where they  continue stimulating the post-synaptic cell

• profound side effects: drowsiness, dry mouth, difficulty urinating

Selective Seratonin Reuptake Inhibitors(SSRIs)

• block reuptake of serotonin

• operate similar to tricyclics but fewer side effects

• SNRIs-block reuptake of serotonin combined with norepinephrine  

Monoamine Oxidase Inhibitors(MAOIs)

• blocks monoamine oxidase, a presynaptic enzyme that metabolizes catecholamines and  seratinin into inactive forms; blockage of this metabolizes catecholamines and serotonin  slowing breakdown in synaptic cleft

Atypical Antidepressants 

• wellbutrin-prevents reuptake of norepinephrine, not serotonin

• 2+ weeks before behavior change seen

Effectiveness 

• not simply serotonin based-seratonin levels not linked to depressive symptoms in control  groups

• individuals with depression have low brain-derived neurotrophic factor (BDNF) • BDNF important for synaptic plasticity, learning, and proliferation of new neurons in the  hippocampus

o because of low BDNF, individuals with depression show a smaller hippocampus and  impaired learning ability

Nonpharmalogical Treatments 

• combination of drugs & psychotherapy-cognitive behavioral therapy; shows inc in metabolism  of certain brain areas

• electroconvulsive therapy (ECT)-electrically induce a seizure-most immediate relief when no  relief from antidepressant drugs; not long-lasting

• altered sleep patterns

• deep brain stimulation

• exercise!!!!! inc blood flow to brain and inc levels of serotonin and BDNF

BIPOLAR DISORDER aka manic depressive disorder  

Characteristics 

• Bipolar I- full blown manic cycle alternated with depressive cycle-rapid cycling • Bipolar II-mild mania, mainly depression

• Mania/manic symptoms- very productive, feel on top of the world, feel they can accomplish  anything resulting in risky behaviors

• glucose-brain uses more in manic phase & dec in depressive phase

• high heritability

Treatment 

• lithium salts-stabilize mood & prevent relapse-work by dec glutamate activity

• drugs effective that block synthesis of arachidonic acid which is produced during brain  inflammation

SCHIZOPHRENIA  

• characteristics: deterioration of functioning in everyday life

o positive symptoms (additive behavior)- hallucinations (normally auditory), delusions,  scattered speech/thinking

o negative symptoms (absence of behaviors)-lack of emotions, loss of speech abilities,  decreased socialization, isolation

Causes 

• genetic component: predictive genes linked to schiz, genetic contribution from relative with  schiz

• neurodevelopmental: abnormalities in development of nervous system pre-/neo-natally, poor  nutrition of mother, premature birth, low birth weight, more common in low SES groups • brain abnormalities: enlarged ventricles, disorganized/smaller hippocampus, hypofrontality less frontal activity

Brain Activity 

• during auditory hallucinations: inc activity of broca’s area, ernicke’s area, middle temporal  gyrus; reduced functional frontotemporal connectivity  

• during delusions: dec activity of cortical midline structures like medial prefrontal cortex,  anterior cingulate cortex, insula, and ventral striatum

Treatments 

• antipsychotic/neuroleptic drugs (ex. chlorprozamine-thorazine & haloperidol-haldol)  o these drugs relieve positive symptoms but not negative symptoms, block dopamine  synapses

o tardive dyskinesia-tremors caused by prolonged use of antipsychotics

• *dopamine hypothesis of schizophrenia: schiz results from excess activity at dopamine  synapses

o substance induced psychotic disorder-results from abuse of cocaine and meth because  these drugs prolong the activity at dopamine synapses, produces positive symptoms of  schiz (hallucinations & delusions)

o individuals with schiz have twice as many D2 dopamine receptors

• *glutamate hypothesis of schizophrenia: schiz results from deficient activity at glutamate  synapses in the prefrontal cortex

o in many brain areas dopamine inhibits glutamate release, or glutamate stimulates  neurons that inhibit dopamine release---therefore inc dopamine would produce the  same effects as dec glutamate

o individuals with schiz have fewer glutamate receptors & low release of glutamate • frontal lobotomy-severing of prefrontal cortex from the rest of the brain-disrupts personality  and memory

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