neuro final

• exocrine: sweat glands, release chemicals into ducts, which carry them to targets
• endocrine: ductless, release chemicals (HORMONES) into circulatory system, to targets

• 1) amino acid derivatives
• 2) peptides and proteins
• 3) steroids

epinephrine, which is released from the adrenal medulla and synthesized from tyrosine

short, long

chlesterol, a type of fat molecule

steroids. other hormones produce effects by binding to receptors in cell membranes. steroid molecules are small and fat soluble so they can penetrate cells, affecting them in a second way by binding to receptors within the cytoplasm or nucleus. they can DIRECTLY influence gene expression

steroid hormones

male testes an female ovaries, which produce sperm and ova

create sperm and egg cells, produce and release steroid hormones

androgens and estrogens and progestins

testosterone

estradiol

progesterone, prepares the uterus and breasts for pregnancy

regulates glucose and salt levels in the blood, also releases small amounts of all the sex steroids that are released by the gonads

tropic- most pituitary hormones are tropic

gonadotropin

anterior pituitary

28 day cycle of fluctuations in gonadal and gonadotropic hormones in women

visual input to the nervous system was controlling the release of tropic hormones from the anterior pituitary

hypothalamus

VASOPRESIN and OXYTOCIN- peptide hormones that are synthesized in the cell bodies of neurons in the paraventricular nuclei and supraptic nuclei of the hypothalamus.

neurosecretory cells

• oxytocin stimulates contractions of the uterus during labor and the ejection of milk during suckling
• vasopressin is an antidiuretic hormone, facilitates the reabsoprtion of water by the kidneys

hypothalamopituitary portal system

portal veins (veins that connect one capillary network with another)

releasing

release-inhibiting factors

the release of thyrotropin from the anterior pituitary, which stimulates the release of hormones from the thyroid.

that hypothalamic reeleasing hormones control the release of hormones from the anterior pituitary ,

BOTH the anterior pituitarys gonadotropins

• FSH: follicle stimulating hormone
• LH: luteinizing hormone

1) signals from the nervous system 2) signals from hormones 3) signals from nonhormonal chemicals in the blood

glucose, calcium, sodium

pulsatile

6

ovary, testis

gene of Y chromosome which triggers the synthesis of Sry protein, which causes the medulla of each primordial gonad to grow and develop into a testis. there is NO FEMALE COUNTERPART to teh sry protein

Sry protein

capacity to develop into the male reproductive ducts (seminal vesicles/vas deferens)

capacity to develop into the female ducts (uterus, vagina, fallopian tubes)

mullerian-inhbiting substance; mullerian system degenerates and testes descend into the scrotum

• removal of the ovaries
• removal of the testes
• removal of gonads

develop from the same precursor, called a bipotential precursor

glans (becomes head of penis/clitoris), urethral folds, lateral bodies, labioscrotal swellings. the development of these are controlled by the presence of absence of testosterone

the female cyclic pattern of gonadotropin release develops unless the preprogrammed female cycclicity is overriden by testosterone

aromatase

perinatal testosterone does not directly masculinize the brain, brain is masculinized by estradiol that has been aromatized from perinatal testosterone

1) findings demonstrating the masculinizing efects on the brain of early estradiol injections 2) findings showing that masculinization of the brain does not occur in response to testosterone that is administered with agents that block aromatization

alpha fetoprtein. deactivates circulating estradiol by binding to it. testosterone is immune to alpha feto protein, so it can travel from the testes to the brain where it is converted to estradiol. the estradiol is not broken down in the brain because alpha fetoprotein does not penetrate the blood brain barrier

aromatization

placental barrier.

masculinzes and defeminizes

feminizes and demasculinizes

solicitation behaviors

features other than reproductive organs that distinguish sexually mature men and women

the only anterior pituitary hormone that does not have a gland as its primary target. increases during puberty, directly acts on bone and muscle tissue to produce a growth spurt

adrenocorticotropic

released by adrenal cortex and is normally responsile for the growth of pubic and underarm hair in females; androgens cannot be the male hormones when they also influence females

Sry protein

ovaries

mullerian-inhibiting

androgens

labia major

gonadotropin

androstenedione

androstenedione

before

mamawawa

a mutation to the androgen receptor gen rendered her androgen receptors unresponsive; external genitals, brain, and behavior were female, but internal female reproductive ducts did not develop

caused by congenital adrenal hyperplasia- a deficiency in the release of cortisol from the adrenal cortex, which results in compensatory adrenal hyperactivity and the excessive release of androgens. this does not really effect males but females are usually born with an enlarged clioris and fused labia; which can be corrected

not correlated

a period of 12-18 hours during which the emale is fertile, receptive, proceptive, and sexually attractive

estrous cycle

true fact

androgens

growth promoting effects;

• negative feedback--- reduceds gonadotropin and reduces testicular activity and sterility, breast growth
• in women- amenorrhea, sterility, hirsuitism, growth of clitoris, blandess, deepening of voice, etc.

estradiol (reduces inflammation, encourage axonal regeneration, promote synaptogenesis, increase adult neurogenesis)

estradiol

androgenic insensitivity syndrome

adrenogenital syndrome

ablatio penis

orchidectomized

ovariectomized

impotent

gynecomastia

amenorrhea

hirsuitism

cerebral hypoxia

• 1) researchers have focused on relatively simple, controllable copulatory behaviors of animals, which are controlled by hypothalamus
• 2) hypothalamus controls gonadotropin release, obvious place to look for sexually dimorphic structures and circuits
• 3) early studies confirmed that hypothalmus does play a major role in sexual behavior

medial preoptic area

sexually dimorphic nucleus

estradiol

medial preoptic area

lateral tegmental field

ventromedial nucleus

progestorne

by an increase in the number of progesterone receptors that occurs in the VMN and surrounding area following an estradiol injection

periaqueductal gray

twin studies: 52 % of MZ twin brothers and 22 % of DZ twin brothers were homosexual

YUP

finding that the probability of a man's being homosexual increases as a function of the number of older brothers he has; large effect; probability increases by 33 % for every older brother he has- 15% of gay men can attribute homosexuality to this

explains fraternal birth order effect mothers become more immune to some masculinizing hormone in male fetuses, which deactivates masculinizing hormone in younger brothers

rats humans etc will administer brief bursts of elecrical stimulation to site in the brain, pleasure centers

dopaminergic neurons projecting from mesencephalon into various regions of telencephalon. neurons composing this system have cell bodies in two midbrain nuclei- substantia nigra and ventraltegmental area

nucleus of ventral striatum

• 1) many of brian sits at which self stimulation occurs are part of the mesotelencephalic dopamine system, or project irectly to the mesotencephalic dopamine system
• 2) cerebral dialysis studies show that ISS is associated with an increase in dopamine release in the mesocorticolimbic pathway
• 3) dopamine agonists tend to increase intracranial s.s., and antagonists tend to decrease it
• 4) legions of the mesocorticolimbic pathway disrupt intracranial self stimulation

rats press a level to inject drugs into themselves, learn to self administer,

rats receive a drug in one compartment of a two compartment box, then rats usually prefer the drug compartment

• 1) lab animals self administer microinjections of addictive drugs directly into nucleus accumbens
• 2) microinjections of addictive drugs into NA produced a conditioned place preference for the compartment in which they were administered
• 3) lesions to NA or ventral tegmental area blocked the self administration of drugs
• 4) self administered of addictive drugs were associated with elevated dopamine

• molecules in the presynaptic memrane of dopainergic neurons that attract dopamine molecules int he synaptic cleft and deposit them back inside the neuron.
• brain imaging studies show that dopamine function is diminshed in human addicts. when addicts are exposed to their drug or to stimuli associated with their drug, NA and other parts of the dopamine pathway become hyperactive

• neutral stimuli can trigger dopamine relase in NA
• stimuli that signal rewards can develop rewarding properties of their own
• dopaminergic neurons with cell bodies in ventral tegmental area fire at a rate related to the value of the reward. expected reward delivered= no change in firing. greater than expected reward=increased firing. less than expected=firing decreased
• dopamine levels reflect reward value, but not in a straightforward level

• nucleus accumbens
• mesocorticolimbic pathway
• prefrontal lobes: decision to take a drug
• hippocampus: information about previous relevant experiences
• amygdala: coordinate positive or negative emotional reactiosn

• change in how striatum reacts to drugs and drug associated cues
• spreads from nucleus accumbens to dorsal striatum
• prefrontal corte x

• priming doses of the drug
• drug associated cues
• stress

• prefrontal cortex: primin ginduced relapse
• amygdala: conditional cue-induced relapse
• hypothalamus: stress induced relaspe

• 1 percent
• 1) delusions
• 2) inappropriate affect
• 3) hallucinations
• 4) incoherent thought
• 5) odd behavior

antischizophrenic drug.

active ingredient of snakeroot plant, antischizophrenic

• -effect manifests only after two or three weeks
• onset is associated with motor effects similar to parkinsons disease
• acting through same parkinsons pathway

• schizophrenia is caused by too much dopamine, and anti drugs exert effecs by decreasing dopamine levels
• reserpine depletes dopamine by breaking down synapses
• drugs like amphetamine and cocaine can trigger schizophrenic episods, increase the levels of dopamine and monamines in the brain
• chlopromazine and reserpine antagonize transmission at dopamine synapses but in different ways: chlorpromazine binds to dopamine receptors at dopamine synapses, reserpine: depletes the brain of dopamine

rather than high dopamine levels, the main factor in schizophrenia i shigh levels of activity at dopamine receptors

high

potent antizschizophrenic drugs with a relatively low affinity for dpamine receptors--- puzzle solved because dopamine binds to more than one receptor subtype.

• phenothiazines: bind effectiely to D1 and D2 receptors
• butyrophenones: bnd effectiely to D2 receptors bur not D1

selective bindings of butyrophenones == schizophrenia is caused by hyperactivity specifically at D2 receptors rather than all dopamine receptors

antischizophrenic drugs

• first atypical neuroleptic which has an affinity for d1 and d4 but not d2
• recen tresearch implicates other neurotransmitters like glutamate and serotonin
• clozapine is effectie in treating schizos who have not responded to typical neuroleptics and does not produce parkinsonian side effects
• produces a severe blood disorder in some patients who use it
• led to qualification of the d2 theory of schizophrenia because atypicals bind weakly to d2, and

time lag indicates that the blockage of d2 receptors is not the specific mechanism of the neuroleptics therapeutic effect; triggers some slo w developing compensatory change in the brain

• enlarged ventricles
• reduced volume in 50 brain areas
• reductions in the number of neurons in many areas,
• 1) little evidence of specific structural damage to dopaminergic circuits
• 2) dopamine theory provides no rationale for the diffuse pattern of brain damage

do brains of schizophrenics develop abnormally, or do they develop normally and then suffer some damage

• 1) substantial damage already exists in first episode schizophrenics
• 2) devleopment of damge to diff areas of the brain does not follow the same time course in all patients

• positive: respond better to neuroleptics
• incoherence, hallucinations, delusions
• caused by increased neural activity
• negative: lack of affect, cognitive deficits, proverty of speech
• caused by brain damage

• reactive: in response to a negative experience
• endogenous: no apparent cause

bipolar/unipolar depression

• 1) monoamine oxidase inhibtors
• 2)tricyclic antidepressants
• 3) lithium
• 4) selective monoamine reputake inhibitors

• first antidepressant drug, originally developed for TB
• monoamine agonist
• increases levels of norepinephrine and serotinin by inhibiting the activity of monamine oxidase, which breaks down monoamine neurotransmiters in the cytoplasm

• monoamine oxidase inhibitors for affective disorders
• side effects: cheese effect
• foods which contain tyramine run the reisk of strokes caused by surges in blood pressure

side effect of MAO inhibitorss; when people who take MAO i's and consume tyramine rich food run the risk of strokes caused by surges in bloodpressure

• three rings of atoms
• imipramine
• block reuptake of serotonin and norepinephrine, increasing their levels in the brain

first tricyclic antidepressant

• blocks mania
• mood stabilizer, blocks rapid transition between depression and mania

• SSRIS, exert agonistic effects by blocking reuptake of serotonin from synapses
• prozac
• few side effects
• effective against a wide range of psychological disorders

50% improved

• only 25% actually helped by antidepressent
• when depression is a component of bipoalr, it is more resistant to antidepressants

depression is associated with underactivity at serotonergic and noradreneric synapses, based on the fact that drugs are all agonists of serotonin, norepinephrine , or both

• when an insufficient amount of a NT is released at a synapse, compensatory increases in the number of receptors for that neurotransmitter
• weak support

depressed people release more stress hormones

• more than 50% of depressed patients display dramatic improvements after one night of sleep depression
• excercise increases adult neurogenesis in hippocampus

• most prevalent of any disorder- 17%
• 1) generalized anxiety disorders
• 2) phobic a
• 3) panic disorders
• 4) OCD
• 5) posttraumatic stress disorder
• agoraphobia

• 1) benzodiazepines
• -chlordiazepoxide/diazepam
• -most widely prescribed
• -side effects
• -highly addictive
• 2) serotonin agonists
• 3) antidepressants
• -comorbitdity

anti anxiety drugs, often effective against depression

• -elevated plus maze test
• -defensive burying test
• -risk assessment test

-possible role in anxiety disorders of deficits in both GABAergic and serotonergic transmission

• disoder of tics
• begins in early life
• genetic component

• amino acid derivatives
• peptide/proteins

steroids

produce sperm cells and ova

• follicle stimulating hormone
• luteinizing hormone

• peptides
• released by gonadotropinreleasing hormone

estradiol

estradiol, progresterone

more fashionable, concerned w/appearance, sexy

lordosis (intromission faciliatating arched back posture signaling female rodent receptivity)

GABA

monoamines

• 1) activating
• 2) organizing

• -milk ejection, uterine contractions
• -maternal behavior
• -stimulated by nursing
• -facilitative, but not necessary for, maternal behavior

derived from androgen and estrogen

medial preoptic area

• largest in males interested in females
• moderate in gay males
• smallest in females

• drug tolerance that results from changes that reduce the reactivity of the sites of action to the drug
• tolerance to psychoactive drugs

• -reduce number of receptors
• -decrease efficiency with which drug binds to existing receptors
• -diminish impact of receptor binding on the activity of the cell

tolerance to a drug's certain efect requires that it actually exerts that effect

• premise: alcohol decreases convulsions. rats can develop tolerance to anticonvulsant effect
• hypothesis: alcohol given before, not after, convulsions iwll create an anticonvulsion effect tolerance

essential for learning

greater cocaine use

exposure to alcohol smell and taste=activation of nucleus accumbens, ACC< VTA, insula

• 1) hypofrontality
• 2) genes v. environment
• 3)adolescent drug use
• 4) stressful experiences

• immediate: CA enters, facilitates NT release
• increases GABA in lateral hypothalamus
• desensitation of receptors over repeated exposure

• highly addictive (70%)
• high relapse (20% can quit)

ventral tegmental area

smokers are more stressed between doses

• 25% pregnant women smoke
• readily crosses placenta
• nicotinic Acch receptors present by prenatal week 8
• long term effects on brain function
• underactivity in dopamine and norepinephrine neurons

• GABA agonist
• NMDA antagonist
• memory disruption
• endogenous opioid agonist
• painilling effect
• stimulates VTA--NA pathway

• .3% of live births
• brain damage, retardation, poor coordination, physical deformity
• no time or amount that is safe

• half 8th graders, 3/4 high schoolers use alcohol
• reward and prefrontal inhibiton pathways still developing

emotion inducing sensory stimuli are received and interpreted by the cortex, which triggers changes in the visceral organs via the autonomic nervou ssystem and in the skeletal muscles via the somatic nervous system. autonomic activity and behavior triggered by the emotional event produce the feelings of emotions, not vice versa

emotional stimuli have two independent excitatory effects: exicte feelings of emotion in the brain and the expression of emotionin the autonomic and somatic nervous system. views emotional experience and emotional expression as parallel processes that have no direct causal link

different predictions about the role of feedback from autonomic and somatic ns activity

• JL: emotional experience depends entirely on feedback fr
• CB: emotional experience is independent of such feedback

• pattern of behavior in monkeys whose anterior temporal lobes were removed
• -consumption of almost anything
• -inappropriate sexual behavior
• -tendency to repeatedly inestigate familiar objects
• -lack of fear
• -tendency to investigate objects w/ mouth
• -damage to the amygdala
• -

• method of interrogation employing autonomic nervou ssytem indexes of emotion to infer the truth of the subjects responses
• control question technique
• success rate in mock crime studies is 80%
• detects EMOTIONS not lies

• universality of facial expressions
• primary facial expressions: suprise, anger, sadness, disgust, fear, happiness
• facial feedback hypothesis:
• voluntary control of facial expression: microexpressions

unprovoked aggressive behavior that is directed at a conspecific for the purpose of establishing, altering, or maintaining a social hierarchy. in mammals, primarily among males.

• testosterone increases social aggression in the males of many species; aggression is largely abolished by castration
• in some species, castration has no effect on social aggression. in others, it reduces aggression during breeding season but not other times
• relation between aggression and testosterone levels is difficult because aggression can itself increase testosterone

• 1) direct one
• 2) indirect one that projects via the auditory cortex

• both mediate fear conditioning to simple sounds
• only cortical route is capable of medaiting fear conditioning to complex sounds

hippocampus

nuclsi.

lateral nucleus of the amygdala

prefrontal lobe

hippocampus

james-lange theory

sham rage

hippocampus

orbicularis oculi

social aggression

face of the attacking rat

social

defenisve

conditioning

conditional stimulus

medial geniculate nucleus

auditory cortex

lateral nucleus

• short term adaptive changes that help animal respond to sressor
• long term: maladaptive changes

anterior pituitary adrenal cortex system

adrenocorticotropic hormone

glucocorticoids, adrenal cortex

the level of circulating glucocorticoids

adrenal medulla

cytokines

when conspecific threat becomes an enduring feature of daily life

study of interactions among psychological factors, nervous system, and immune system

receptors that are synthesized by many cells of the innate immune system for the purpose of detecting generic pathogens

cells, like macrophages and microglia, that destroy and ingest pathogens

destruction and ingestion of foreign matter

lymphocytes

t and B

T/B

autoimmune disorders

innate/adaptive

• distress: stress that reduces health
• eustress: improves health

the dense population of glucocorticoid receptors in the hippocampus

• -reduces dendritic branching
• -reduces adult neurogenesis
• -modify structure of synapses
• -reduce performance of hippocampus dependent tasks

mediated by elevated glucocorticoid levels

major glucocorticoid, effects of stress induce this

males; because estradiol has neuroprotective effects that testosterone lacks

adrenal cortex

adrenal medulla

cytokines

subordination stress

stress

psychoneuroimmuniology

adaptive, innate

pathogens

• 1) cell mediated
• 2) antibody mediated

antibody mediated

glucocorticoid

glucocorticoid

hippocampus