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124 Cards in this Set

  • Front
  • Back
tumor
mass of cells w. uncontrollable growth, serves no function
malignant tumor
cancerous tumor, lacks defined border and may metastasize
benign tumor
noncanerous tumor, distinct border, cannot metastasize
metastais
process where cells break off a tmor and travel and grow elsewhere in body
glioma
cancerous brain tumor compoased of glial cells
(neurons don't divide)
meningioma
benign brain tumor composed of cells that make meninges
tumor can damage tissue by
compression - press and affect neural tissue, indirectly block CSF flow - hydrocephalus

filtration - cut off blood supply
epilepsy
1% of population
seizures due to abnormal electrical signal
partial seizure
does not involve whole brain
has definite focus, restricted t small part of brain
due to develop. abnormality or injury
generalized seizure
entire brain
simple seizure
no L.O.C
complex seizure
L.O.C
often in temporal lobes
automatism - compulsive and repeptitive simple behaviors
grand-mal
L.O.C
tonic-clonic convulsions
-rigid (tonus) 15s , all muscles contracted
- tremors (clonus) 30s , trembling and jerking , sweating,

hypoxia
absence (petit mal)
children
no convulsions
disruption of consciousness, unresponsive.. do not realize
status epilepticus
undergoes series of seizures w/o regaining consciousness
cause hipp damage
caused by excessive glutamate release during seizure (excess glutamate is toxic)
febrile seizure
infantile fever 105 F
3% of children under 5
Alcohol/sedative withrawal
alcohol is massive release of GABA activation, NMDA blocked
withdrawal > glutamate rebound, NMDA R activated
leave brain in hyperexcitable condition
seizure treatments (3)
anticonvulsant drugs - increase effectiveness of inhibitory synapses
brain surgury- remove region of brain around focus
biet - ketogenic diet - high fat, low carb
interictal inhibition
inhibitory neurons around focus become more active
seizure occurs when excitation overcomes inhibition
kindling model
kindling model of epsilepsy
- series of alternating bilateral brain stimulations elicits convulsions
neural changes perm.
change in amyg/hipp (stimulated repeatedly)
eventually animal seizures w/o artificial stimulation

~ to epilepsy development due to brain injury
stroke
3rd leading C.O.D
1-2% by 75
- amnesia, aphasia, paralysis, coma

- hemorrhagic and obstructive
infarct
area of dead or dying tissue produced by stroke
penumbra
dysfunctional arrea around infarct
goal of treatment -save penumbra
hemorrhagic stroke
rupture of blood v
bleeding in brain from multiple sources of major blowout
death of many neurons from lack of glucose and compression effect

bursting anuerysm
obstructive stroke
occlusion of blood vessel
thrombus
embolus

causes ischemia
thrombus
blood clot in blood v, occludes it
embolus
material forms in one part of vascular system, breaks off, is carried by blood until it reaches smaller artery
ischemia
interuption of a blood supply to a region of the body

most damage due to excess NT release - glutamate
- blood deprived neurons become overactive (no O2, gluc .: Na/K transporters stop working ...depolarization) & release glutamate (Na &Ca enter , activates enzymes, h2o follows causing swell)
burst, causing inflammation (astrocyte - scarring, microglia - phagocytosis, make free radicals- destroy N.As, proteins, fats)
= excitiotoxic
ischemia treatment (3)
clot dissolving drugs
- tPA - within 3 hrs, can be neurotoxic
- desmoteplase - fr vamp. bats, not toxic, up to 9 hrs

hypothermia

constraint-induced movement therapy - force animal to use damaged/affected limb,
increased dendritic complexity and length, change in primary motor cortex
fetal alcohol syndrome
abn facial development, deficient brin develop.
neural adhesion protein - guides growth of neuron in developing brain...dont work
PKU
lack enzyme that converts Phe > tyr
excess Phe in blood interferes w. myleination of CNS neurons

treat - low phe diet
Tay-Sachs disease
causes brain to swell, and damage itself inside skull and dura mater

metabolic storage disease
enzymes are missing .: lysosome cannot destroy waste products, lysosomes swell, neurons swell and die
down syndrome (4 causes)
.15% births
increases w. maternal age
- trisomy 21 - nondisjuction cause gamate w. extra chromo 21 ..95% of D.S. 88% from maternal gamete
- mosaicism - some cells in body normal, other cells have trisomy 21 ...1-2% D.S
- robertsonian translocation - parents has long arm of chromo 21 is attached to another chromo (chromo 14) = isochromosome....reproductionhigh chance of extra chrom 21.. 2-3% D.S
-duplication of a portion of chromo 21 - severity depends on genes duplicated
transmissible spongiform encephalopathy
contagious brain disease , degenerative > sponge-like appearance
BSE - caspase 12
CJD
due to misfolded prion

sporadic, familial, acquired (latrogenic, variant)
prion
protein that exist in 2 forms that differ only in 3D shape
PrPc - normal
PrPsc (scrapie) infected - protease & heat resistant - taken up by retrograde transport
cause normal PrP to become misfolded
apoptosis
programmed cell death
- small blebs form
nucleus breaks apart organelles in blebs
cell breaks in apoptotic bodies
organelles still functional

caspases - enzymes generated by cell intiating cell death
caspases
enzymes (proteases) that generated by cell initiating cell death

in apoptosis
human prion disease (4)
- CJD- dom mutation PRNP gene on short arm of chromo 20...vCJD - transitted from beef to person
- GGS - autosom dom, trouble talking, cerebellar damage
- Fatal familial insomia - autosom dom, cannot sleep
- Kuru - cannabalism, eat brain of infected
parkinson's disease
1% ppl over 65, muscle rigid, slow move, resting tremor, instable posture
degeneration of nigrostriatal sys - DA secreting neurons of substantia nigra > BG

decreases input from substantia niger causes decrease in inhibition from BG to globus pallidus which .: inhibits thalamus&premotor cortex....hypokinetic
Lewy body
Parkinson's disease
abnorm. circular structures w. dense core w. alpha-synuclein protein
mutated chromo 4, toxic gain on function (protein alpha-synuclein)
-alpha-synuclein accumulates in DAergic neurons
parkin protein
parkinson's disease fail to produce protein due to mutation of chromo 6
loss of function

- help ubiquinate/tag misfolded proteins to be destroyed by proteasome
.: defected proteins accumulate in DAergic neurons and damage
toxic gain of function
genetic disorder caused by domin. mutation that involves faulty gene that produces a protein w. toxic effects
Parkinson's treatment (4)
- L-DOPA, shortterm, side effects
- deprenyl - MAO agoist, blocks effects of MPTP , inhibits MAO-B enzyme (breaks down DAneurons by h202 oxidation)
-sterotaxic surgury - transplant fetal tissue/neural stem cells, lesion/electric stim. of subthalamic nucleus
MPTP
drug ~ parkinson's disease
decrease DA in nigrostriatal sys
pallidotomies
surgurical destruction of globus pallidus releases motor cortex from inhibition
parkinson's disease
Huntington's disease
dom chromo 4... abnormal htt gene w. long glutamine...aggregates
caspase 3, apoptosis
degeneration GABA ergic of caudate nucleus and putaman
uncontrollable movement, removes inhibition of motor cortex(hyperkinetic)
BDNF
factor critical for neuron survival
normal htt produces and transports to BG

huntingtons
inclusion bodies
accumulation of misfolded htt in nucleus
neurons w. i.b have lower lvls of abnormal htt elsewahere (neuroprotective)
huntington
Alzheimers
degenerative, progressive memory los, motor deficits and death
loss of Ach neurons in basal forebrain
10% of pop over 65, 50% over 85
amyloid plaque
extracellular deposit w. dense B-amyloid protein surrounded by degenerating axons and dendrites and activates microglia and reactive astrocytes
B-amyloid protein defective, gene APP cut by secretases (B- tail, gamma- tail)...too much long form, swells and dies. AB bind p75 receptor > caspases
alzeimers
neurofibrillary tangles
dying neuron w. intracellular accumulation of abnom tau-protein filaments (cell's internal skel)
excess phosphate ions changes structure, disrupts transport > death
Alzheimers
APP gene
chromo 21,
gene for amyloid B-precursor protein
Alzheimers
ApoE
ApoE4 - increase rish of late onset alzeimers..interfere w. removal of long AB

ApoE2 - protective ?
M.S
autoimmue demyleinating disease
sclerotic plaques - hard patches of debris
M.S treatment (2)
interferon B - slows progression, modulates responsiveness of immune sys

copaxone - peptides, stimulate anti- inflammatory response, suppress immune sys, decrease mylein attack
schizophrenia
1% of population
mental disorder w. disordered thought, delusions, hallucinations
positive, cognitive & neg symptoms
larger ventricles, loss of brain grey matter tissue at puberty (hypofrontality dlPFC), smaller hipp
D2 R hyperactive(butyrophenomes: haloperidol<spiroperidol drugs)
positive symptoms of Schiz
hallucinations
delusions - grandeur, paranoid, persecution
disorganizaed, irrational
thought disorder
cognitive symptoms of Schiz
attention
low psychmotor speed
poor abstract reasoning
poor problem solving
eficits in learning and memory
negative symptoms of Schiz
anhedonia - inability to get pleasure
flat affect
social withdrawal
susceptibility hypothesis
carry gene, not necessarily expressed, role of enviro

Schiz
epigenetics
mechs that control expression of genes (enviro, toxns)
dopamine hypothesis
+ symptoms of Schiz are due to overactive DA synpases in nucleus accumbens and amygdala (mesolimbic system VTA > amygdala)

chorpromazine, reserpine - DA r blocker
Amphethamine, cocaine, L-DOPA - DA agoist, cause + symptoms
- inject amphetamine > more DA release in SChiz ppl than normal
- greater DA release = greater + symptoms
- greater # D2 R
Problems with dopamine hypothesis
- mesolimbic VTA > amyg not altered
- drugs take 2- 3 wks to work
- fix + symptoms of schiz only
tardive dyskinesia -
canot stop moving
supersensitivity of DA2 r if blocked for a long, chronic time
hypofrontality
decreased dlPFC activity causes negative symptoms of Schiz
- decreases NMDA activation, decrease PFC output to VTA (no inhibition on DA release in NA, no DA release in PFC)
PCP ant ketamine (NMDA antag) cause hypofronatility

treat:
indirect antag ; glycine and serine- facilitate NMDA activity
Atypical Anti-schiz drug: aripozole - partial DA agoist, antag in N.A, agoist in PFC
bipolar disorder
serious mood disorder characterizs by cyclical periods of mania and depression
depression lasts longer

treat : lithium

mPFR subgenual ACC (increased activation)
MDD
serious mood disoder of unremitting depression, no mania

MOA-inhibitors( iproniazid breaks down mao, increases DA, NE, 5HT) TCAs(imipramine NE, 5HT)
ECT - brief shock, causes seizure, activate inhibitory NT systems
Deep brain stim
SSRI(prozac/paxil)/SNRI(5HT&NE, milacipran, venlafaxine)
Transmag stim.
Vagus nerve stim
Bright ligh therapy
Sleep depriv.(REM selective or total sleep depriv) depressogenic
monoamine theory of depression
underactivity of serotonin and NE synapses

reserpine (monoamine antag) causes symptoms
agoists reduces symptoms

BUT
-takes 2-3 wks for antidepres drugs to work
-some ppl nvr respond to drugs
- depletion of typtophan does not alters unhealthy ppl
treatment resistant depression
MDD whose symptoms are not relieved after several diff treatments
anxiety disorder
- tension, overactive autonomic N.S, expectation of impending diaster & continued vigilance of danger... in absence of threat
interfers with normal functioning
17%

short 5-HTT allele
decrease ACC and OFC activity, increased amyg activity( decrease vmPFC- suppresses amyg in control ppl)
treat:
benzodiazepines - GABA agoist, addictive
5-HT agoists - busprione
anxiolytics - D-cycloserine - indirct NMDA agoist w. cognitive behav therapy to extinguish fear responses
panic disorder
episodes of shortness of breath, irreg heartbeat, accompanied by intense fear
anticipancy anxiety- fear of having a panic attack
2%
Generalizes anxiety disorder
excess anxiety, worry, disrupts life
3%
social anxiety disorder
excess fear of being exposed to scruntiny of other ppl, avoid social situations
5%equal in men and woman
OCD
mental disorder w. obessions and compulsions
obession - unwanted thought of idea that will cuz person to be preoccupied, will not leave them
compulsion - feeling one must perform a behavior, even if pefers not to, cannot keep from performing
1-2%
damages: BG, cingulate gyrus, PFC
B-hemolytic streptococcal infection
OCD treatment
cingulotomy - detroy fiber bundles that connect BG > PFC & cingulum bundle (PFC > LC)
capsulotomy -destroy fiber bundle caudate > mPFC
DBS of BG/fiber tracts
drugs : D-cycloserine
autism
chronic disorder , failure to develop relations w. other ppl, impair develop of communication ability, lack of imaginative ability and repetitve, sterotypes movements
"self-absorption"
rett syndrome
autism
mutation in gene MeCP2
normal until 6- 18 months
girls
cannot control feet, wrings hands, do not respond, pulls away
Asperger syndrome
repetitive,stereotyped behavior
less severe
speech not delayed
PDD-NOC
progressive developmental disorder- not otherwise specified
child has some symptoms of PDD but not enough to meet specific criteria of ASD
savants
intellectually handicapped individuals w. specific cognitive or artistic abilities
left hemi damaged (communication) right hemisphere compenstation
ASD
autism spectrum disorders
social deficients
communication difficulty
stereotypes/repetive behavior


hereitable, role of enviro on genes
> abnormal synapse
neuroligins (protein of PostSyn) binds neurexin (presyn protein glue neurons together)
skank3 gene - role in synpase formation
autism brain
size smaller at birth, grows 10% larger
larger amyg w. less neurons
decreased activity in fusiform face area in response to face stimuli
increased short white matter axons
stress response
physiological rxn caused by aversive/threathening situation

increased NE release in noradrenergic neurons in hypo, FC, lateral basal forebrain...controlled by oathway CN(in amyg) > LC

glucocorticoid (cortisol) - from adrenal cortex...controlled by PVN, secretes CRH, stimulates pituitary gland to secrete ACTH
destroys CA1 neurons of hipp, memory probs, ltp&spatial learning deficits
PTSD
chronic stress response
-reexperience tramatic event
-avoid stimuli associated w. event
- increased arousal
- helpless
- interfer w. social abilities

short 5-HTT allele, decreased hipp volume (predisposing), greater amyg/less PFC (inhibits) activity
animal models of anxiety
submersion stress
predator odor
isolation stress
chronic, unpredictable stress
Fear conditioning
social defeat
Prader-Willi syndrome
deletion of chromo 15
insatiable hunger
slow metab
act as though starving
become obese and die frrom related-disorders
ghrelin
peptide hormone from stomach, increases eating
rise before meals; stimulates thoughts of food
controlled by receptors in S.I and stomach secretes
glucoprivation
fall in glucose lvls available to cells
stimulates eating
detectors in liver and brain
lipoprivation
fall in FAs available to cells
stimulates eating
detectors in liver
what stops a meal
H - head factors - R in eyes, tongue, nose, convey info about odor, texture, temp of food
I- intestinal factors - CCK, Peptide YY (PYY)
G - gastric factors - stomach R presence of nutrients
L- liver factors - R, send satiety signal to brain via vagus nerve
I- insulin - absorptive phase, allows entry of glucose, brain R detect insulin

longterm - adipose tissue signals- leptin
CCK
hormone secreted by duodenum regulates gastric mobility and causes gallbladder to contract
provides satiety signal
PYY
peptide released by G.I system after meal in amount proportional to size of meal
~ calories injested
Ob mouse
mutation, fat cells do not produce leptin
become obese
leptin
hormone secreted by adipose tissue
long-term satiety
metabolic rate increases, body temp rises, become more active, eat less
decerebration
surgurcal cut hind brain from forbrain
disrupts initiation of eating, does not approach food
VMH
satiety center
lesions produce overeating
stimulation supresses
LH
hunger center
lesions stop/inhibit
stimulations produce eating/drink
MCH, orexin
MCH
peptide NT stimulates appetite and reduces metab rate
LH
increase and preserve body's energy stores

recieve excitatory input from NPY
orexin
peptide NT stimulates appetite and reduce metabolic rate
increase and preserve body's energy stores
recieve excitatory input from NPY
NPY
peptide NT found in arcuate nucleus
stimulates feeding, insulin, glucocorticoid secretion & breakdown of TG& decrease body temp
project to LH to MCH and orexin & PVN - insulin secrete
neurons release AGRP

leptin inactivates
AGRP
peptideincreases food intake, increases ghrelin
antago at MC-4R, increases eating

leptin inactivates
endocannabinoids
THC - increases appetite
increase release of MCH and orexin
CART
anorexigens
suppress eating
inhibits MCH and orexin neurons
increases metabolic rate through connects with PVN

low food, low CART lvl
stimulated by leptin
alpha-MSH
released by CART neurons
agoisst of MC-4R, inhibits feeding
stimulated by leptin
health hazards of obesity
can dogs see all cats ears
CVD, diabetes, Stroke, Arthritis, Cancer, Endocrine
UCP
found in mitochondria
determine metabolic efficency
converts nutrients > heat
UP3 - in muscles
leptin increases UP3 expression, ncreases metab. rate, and burns more cals
rouz-en-Y gastric bypass
produce small pouch in upper end of stomach
jejunum is cut and attached to upper stomach, bypasses duodenum
disrupts grehlin, reduces hunger
increaes PYY, increase satiety
sexually dimorphic behavior
behavior that has diff forms or occurs in diff amounts/circumstances in males and females

behavior due to diff neurochem and neuroanatomical
primordial gonad
6 wks
dimorphic
cortex - ovary
medulla- testis
Sry gene
at 6 wks,
on Y chromo triggers primordial gonad medulla to become testis

if lack, ovaries develop
organizational effects
hormone effects on tissue differentiation and develop
permanent effects
influence person's sex organs and brain
activational effect
effect of hormone that occurs in fully developed organism
after sex organs developed
androgenic insensitivity syndrome
androgen receptors are unresponsive
testes release androgens...proceeds as though none was released
lack of masculinizing effect (bipotential precursor of genitalia does not develop or internal organs)
normal anti-mullerian hormone, defeminizing effect prevent internal female organs

externa genitalia female
persistant mullerian duct syndrome
fail to produce anti-mullerian hormone or lack of receptors
in males, defeminization does not occur, has both sets of internal organs
Turner's syndrome
1 sex X chromo
no ovaries (2 X needed)
develop normal internal and external
need estrogen at puberty
GnRH
at puberty, hypothal secretes
stimulates production and release of LH and FSH from anterior pituitary
stimulate gonads to produce their hormones responsible for sexual maturation (estrodiol & testosterone)
coolidge effect
restorative effect of introducing new female sex partner to a male that has been exhausted by sexual activity
refractory period decreases
lordosis
sexual posture of female rates
depends on P and E
E increases followed by P
Receptivity- willing/able
proceptivity - eager
attractiveness - affect male
behavioral defemination
organization effect of androgens that prevents animal from displaying F sexual behavior in adulthood
behavioral masculinization
organizational effect of androgens enables animales to have male sexual behavior as adult
lee-boot effect
estrous cycle stops w. no males
whitten effect
sync of menstrual cycles of a group of F when male is present
Vandenbergh effect
earlier onset of puberty in F when exposed to male phoneme in urine
Bruce effect
terminate pregnancy caused by odour in a male's urine, other then who impregnated