Term
|
Definition
masked by antipsychotics
long term blockage of DA receptors will cause increase in number of receptors and sensitivity
involuntary movements |
|
|
Term
| low potency side effects of antipsychotics |
|
Definition
1. sedation
2. anticholinergic effects
3. cardiotoxicity |
|
|
Term
|
Definition
| blockage of histamine receptors |
|
|
Term
|
Definition
bad for cognitive symptoms
constipation
dry eyes |
|
|
Term
|
Definition
blocks norepinepherine
bad for the heart |
|
|
Term
| high potency side effects of antipsychotics |
|
Definition
parkinsonism
tardive dyskinesia |
|
|
Term
| The Dopamine Hypothesis for Schizophrenia |
|
Definition
| positive symptoms of schizophrenia are caused by overactive dopamine system |
|
|
Term
| how is chloropromazine evidence for dopamine hypothesis? |
|
Definition
chloropromizine found to be an effective antipsychotic for reducing positive symptoms of schizophrenia
operates by blocking Dopamine receptors (DA-2 antagonist) |
|
|
Term
| How is dopamine release evidence for the dopamine hypothesis? |
|
Definition
| When people with schizophrenia are given small dse of amphetamines to stimulate dopamine release, they release more than normal people |
|
|
Term
| is there a positive correlation between blocking d2 receptors and effectiveness of medication? |
|
Definition
|
|
Term
| what is the 5HT hypothesis? |
|
Definition
5-HT and DA systems interact
by blocking 5-HT-2A receptors, you can decrease transmission of dopamine |
|
|
Term
| what kind of effect do newer antipsychotic medications have on different neurotransmitters? |
|
Definition
less d2 blockage in substantia nigra
high affinity for D4
partial agonist at 5-HT 1A
antagonist at andrenergic (increased heart rate), cholinergic (constipation), and histaminergic receptors (sleep)
chlozapine associated with 57% reduction in d2 receptors |
|
|
Term
| what happens if you block glutamate receptors? |
|
Definition
|
|
Term
| what is the problem with just giving straight up NMDA receptor agonists? |
|
Definition
| too much glutamate kills cells |
|
|
Term
| Describe neural circuitry |
|
Definition
decreased DA in prefrontal cortex
decreased GABA signal and dopamine neurons fire more in VTA
this causes increased dopamine in nucleus accumbens |
|
|
Term
|
Definition
decreased activity of the dorsolateral prefrontal cortex
less dopamine going on up there |
|
|
Term
| how do people with schizophrenia perform on the wisconsin card sorting task and why? |
|
Definition
-they suck
-damage to pfc impairs behavioral flexibility
-they show decreased activity in pfc |
|
|
Term
| describe the glutamate excitotoxicity problem |
|
Definition
1. too much glutamate
2. kills GABA cells in thalamus
3. excitatory response
4. glutamate cells sent to PFC
5.kills GABA cells in PFC
6.excitatory response
7.glutamate sent to temporal cortex
8.kills GABA cells in temporal cortex
8. excitatory response
9. glutamate cells sent to thalamus
thalamus...pfc... temporal cortex... thalamas
TPTCT
to put this candidly... trouble |
|
|
Term
| what are the three brain abnoralities in schizophrenics? |
|
Definition
enlarged ventricles
cerebral atrophy (in pfc and medial temporal lobe)
disorganized hippocampus |
|
|
Term
| how is nmda receptor dysfunction related to schizophrenia? |
|
Definition
PCP causes same effects as schizophrenia.
PCP is an indirect antagonist of NMDA.
inhibition of NMDA supresses functioning of dorsolateral PFC
decreased activation of PFC causes increase of dopamine in NA. |
|
|
Term
| how does cannabis affect shizophrenia |
|
Definition
earlier age of onset
possibly an enviornmenta risk for developing |
|
|
Term
| what is one genetic risk of developing shizophrenia |
|
Definition
polymorphism in COMPT
val x cannabis - lower aao |
|
|
Term
| give evidence for genetic basis of depression |
|
Definition
| family studies twin studies and heritability scores |
|
|
Term
| what are the lifetime rates of depression among family members |
|
Definition
5.1 in normal conrols
~15/100 in relatives of individuals with mild depression
~16.5 in relatives of individuals with severe depression |
|
|
Term
| what are the concordance rates in twin studies for depression? |
|
Definition
37% in MZ twins
24% in DZ twins |
|
|
Term
| what is the heretability score for depression? |
|
Definition
|
|
Term
| is concordance in twins for depression greater for males or females |
|
Definition
|
|
Term
| which better predicts whether a family member will also have depression, early onset or recurrence? |
|
Definition
|
|
Term
|
Definition
| people are depressed because they have too little monamines |
|
|
Term
| provide evidence for the monamine hypothesis |
|
Definition
-drugs that decrease monoamines increase depression
rawoolfia and resperine
early antidepressants all increased monamines in synapse
(TCAs block NE transporters; MAOIs inhibit breakdown of NE, Da, 5HT) |
|
|
Term
| What are some of the criticisms of the Monoamine hypothesis? |
|
Definition
-too simplistic (not enough to explain diversity of symptoms)
-no direct relationship (between amount and effectiveness)
-measurement of amines or metabolites inconsistent
-some drugs that boost monamines are not antidepressants
-delayed therapeutic effect |
|
|
Term
| monoamine receptor hypothesis |
|
Definition
monamine receptors down-regulate B-receptors, 5HT 2 receptors, and 5 HT 1a autoreceptors
takes 24 weeks
g protein receptors
antidepressants effective because they down-regulate serotonin and NE receptors |
|
|
Term
| what is the dexamethasone supression test? |
|
Definition
dexamethasone doesn't work to turn off cortisol
its supposed to give negative feed back to anterior pitutitary that inhibits acth and crh which reduces cortisol
1. people with depression produce too much CRH 2. they have impairment in turning off the HPA axis |
|
|
Term
| what part of the brain has less volume in depressed people? |
|
Definition
|
|
Term
| what do antidepressents do in terms of changing brain structure |
|
Definition
| normalize hippocampul volume |
|
|
Term
| how do antidepressants combat hippocampus problem? |
|
Definition
| they increase neurogenesis in the hipocampus by increasing proteins such as creb and bdnf (bending down naked and F can really excite boys) |
|
|
Term
| What do MAOIs do (simple) |
|
Definition
| inhibit mao-a and mao-b enzymes |
|
|
Term
| what things are considered scissors? |
|
Definition
|
|
Term
|
Definition
| its not a problem of having too many or too fw of any particular neurotransmitter, but instead a failure to have homeostatic regulation (AD restore?) |
|
|
Term
|
Definition
| shown to be effective for severe depression |
|
|
Term
|
Definition
lots of side effects
hypertensive crisis, drug interactions (cant take anything else that increases monamines like cold medicines), diatary restrictions (triptophan, tyrophene.... huge list of food that would increase monoamines) |
|
|
Term
| mechanism of action for tricyclics (TCAs) |
|
Definition
-blocks the reuptake of NE and 5HT (blocks the reuptake pumps)
-increase neurotransmitters for serotonin and NE in synapse |
|
|
Term
| effictiveness of tricyclics and uses |
|
Definition
| used for severe depression when people have aches and pains, also used for anxiety, bedwetting, psychotic depression, ocd |
|
|
Term
| what is the one tricyclic that blocks serotonin more than norepinepherine reuptakers |
|
Definition
|
|
Term
| side effects of tricyclics |
|
Definition
| weight gain, strongly block muscarinic receptors (which causes the drying up of bodily fluids), histiminergic receptors (casuses drowsiness), and alpha-noradrenergic receptors (these are what you need to activate sns) |
|
|
Term
| mechanism of action for SSRIs |
|
Definition
blockade of 5-HT reuptake
(dont affect norepinepherines as much, only blocks serotonin reuptake or DA reuptake)
down regulate NE-beta |
|
|
Term
| efficacy of SSRIs for depression |
|
Definition
mild to moderate (slightly better than placebo); preferred treatment for depression because fewer side effects; ocd effective; social phobia, panic disorder, alochol abuse small effectiveness
-no ssri more effective than other, some work better for some people, and better for mild emotional problems not physical |
|
|
Term
|
Definition
| oversold; placebo effect... 1/3 |
|
|
Term
|
Definition
-serotonin syndrome: cognitive impariment, agitation, nervousness, neuromuscular problems, autonomic dysfnction
-withdrawal
-sexual dysfunction
-30-75% show decreased libido |
|
|
Term
| mechanism of action for atypicals (3rd generation) |
|
Definition
not a single moa, but
SNRI: block 5-HT AND NE reuptake
do not have 3 carbon rings
dont have the receptor problems... less side effects
side effects more similar to SSRIs
some block 5-HT2 receptors
some block DA reuptake (welbutrin) |
|
|
Term
| what other disorder does ocd overlap with genetically? |
|
Definition
|
|
Term
| what gene is involved with ocd? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| basically, ocd involves a disrupted connection between ______________ and _______________ |
|
Definition
| basal ganglia ; prefrontal cortex |
|
|
Term
| efficacy of OCD treatments |
|
Definition
| 40% of patients are nonresponders for treatment |
|
|
Term
|
Definition
| thoughts, impulses or images that are intrusive and inappropriate and CAUSE ANXIETY/DISTRESS |
|
|
Term
|
Definition
| contamination, aggression, religion, safety, symmetry etc. |
|
|
Term
|
Definition
| repetitive behaviors or mental acts |
|
|
Term
| why do ppl engage in compulsions? |
|
Definition
| driven to perform them in order to suppress obsessions |
|
|
Term
|
Definition
| checking, cleaning, counting etc. |
|
|
Term
| what kind of brain damage is associated with ocd |
|
Definition
| degeneration of the basal ganglia |
|
|
Term
| name 3 diseases that are associated w degeration of the Basal Ganglia |
|
Definition
1.OCD
2.Huntingtons
3. Sydenham's chorea |
|
|
Term
| ocd involves increased activity in which regions? |
|
Definition
| frontal cortex and cingulate gyrus |
|
|
Term
|
Definition
| OCD is caused by underactive serotonin system |
|
|
Term
| evidence for 5-ht hypothesis for ocd |
|
Definition
-drugs that increase 5-ht are the most effective treatment for OCD
-drugs that decrease 5ht make symptoms work |
|
|
Term
| Dopamine hypothesis for OCD |
|
Definition
| ocd caused by too much dopamine |
|
|
Term
| evidence for dopamine hypothesis for ocd |
|
Definition
-stimulant abuse often causes ocd types of behavior
-correlation between OCD symptoms and other DA dysfunction kinds of disorders |
|
|
Term
| what kind of efficacy do drugs that increase serotonin have on ocd symptoms |
|
Definition
| 35% reduction of symptoms |
|
|
Term
| psychosurgery for ocd involves |
|
Definition
| one way to help ocd is to cut connection between prefrontal cortex and basal ganglia |
|
|
Term
|
Definition
hyper-arousal
hyper-vigilance
exaggerated startle respose
sleep distrubances
impaired concentration
CAVES concentration arousal vigiliance exaggerated startle sleep
PTSD from being stuck in a cave |
|
|
Term
| what is the yohimbine challenge |
|
Definition
| try to elicit some adreneline activation... if you have ptsd you will have symptoms when your NE is elevated |
|
|
Term
| how is npy related to ptsd |
|
Definition
|
|
Term
|
Definition
| NMDA partial agonist that reduces fear |
|
|
Term
| how is propranolol a treatment for ptsd |
|
Definition
| blocks reconsolidation of fear memories....memories no longer associated w fear |
|
|
Term
| describe what happens with the spider and finger shock experiment |
|
Definition
day 1: spider and finger shock paired together ... shock to remind of fear
day 2: only one pairing of spider and finger shock.... then paring of propanolol and spider
day 3 spider test! you see a spider, how do you react?
propanolol group did not startle as badly as control group.... showed less fear |
|
|
Term
| nerologically, what does propanolol do in the spider shock experiment |
|
Definition
|
|
Term
| what is the NE system like for people with PTSD |
|
Definition
| higher resting urinary levels of NE |
|
|
Term
| list three categories of ASD symptoms |
|
Definition
-communication
-social interaction
-repetitive/rigid/stereotyped behavior |
|
|
Term
| what did wakefield find (1998) to support idea that asd is caused by vaccination |
|
Definition
| -dev. regression associated with mmr vaccination |
|
|
Term
| what did brian deer find? |
|
Definition
| 10/13 authors on lancet study retract their interpretations of findings in 2004 |
|
|
Term
| whid did UK's general medical council decide about old wakefield? |
|
Definition
acted dishonestly and irresponsibly
lost his medical license
guilty of professional misconduct |
|
|
Term
| what was the theme of the jan 2010 british medical journal? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| twin studies with asd concordeance for mz and dz |
|
Definition
|
|
Term
| how many genes convey population risk for autism |
|
Definition
|
|
Term
| give evidence for high degree of polygenetic basis of asd |
|
Definition
| 10-15 genes convey population risk for asd |
|
|
Term
|
Definition
serotonin transporter
developmental genes: mp4, wnt2, hoxa1 |
|
|
Term
| describe neurochemical abnormaliteies in asd people |
|
Definition
increased stress-induced NE and ACTH
DA antagonists (anti-psychotoics) used for treatment (though mixed reviews of whether da / hva is different)
increased 5-ht levels in plasma
impaired central 5-ht function |
|
|
Term
| physical brain differences in people with asd |
|
Definition
enlarged brain/head circumfrence
amygdala disproportionately large
decreased white matter in adolescents |
|
|
Term
| whats different w limbic system of autism people |
|
Definition
decreased dendritic arborization
icreased density of neurons
enlarged amygdala
fusiform face area
prefrontal cortex |
|
|
Term
| major drug treatments for asd |
|
Definition
antipsychotics like risperidone and aripiprazole
antidepressants like ssris or atomoxetine
oxytocin |
|
|
Term
| what's weird about the fusiform face area in asd ppl |
|
Definition
| little or no activity there when they look at faces |
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|
