Term
| Drugs can be administered in which 4 ways? |
|
Definition
Orally ingested
Injection (subcutaneous, intramuscular, IV)
Inhalation
Via mucous membranes |
|
|
Term
| The actions of most drugs are terminated by ______ |
|
Definition
liver enzymes
*usually eliminates drug's ability to cross lipid membranes, & facilitates excretion |
|
|
Term
|
Definition
Decreased sensitivity to a drug developing from repeated exposure
Need higher dose to get same effect; same dose size produces less effect |
|
|
Term
| Tolerance developing causes what kind of shift in the dose-response curve? |
|
Definition
| TO THE RIGHT (need to take more drug to get same effect) |
|
|
Term
| Difference between metabolic & functional drug tolerance? |
|
Definition
Metabolic tolerance -- less drug gets to its site of action
Functional tolerance --drug has decreased reactivity at site of action |
|
|
Term
| Tolerance to most psychoactive drugs is largely _________ |
|
Definition
FUNCTIONAL
(decreased activity of drug at site - down regulate receptors, etc.) |
|
|
Term
|
Definition
Adverse physiological reaction that occurs when a drug is abruptly stopped after significant amounts have been taken for prolonged period
Symptoms typically complementary to the drug's effects |
|
|
Term
| What is it believed to be that causes the withdrawal effects? |
|
Definition
Think they are related to the SAME neural changes that underlie drug tolerance (compensatory mechanisms by body to counteract effects of the drug)
Compensatory mechanisms manifest as withdrawal symptoms when drug is no longer taken |
|
|
Term
| What is CONTINGENT drug tolerance? |
|
Definition
Demonstrations show that tolerance only develops to effects of the drug that are actually experienced!
(e.g. anticonvulsant effects of alcohol experiment; only before group developed a tolerance to the effects because they experienced them) |
|
|
Term
| What is CONDITIONED drug tolerance? |
|
Definition
| Demonstrations show tolerance is maximally expressed only if drug is administered in the same situation which it was previously administered (environment specific tolerance essentially) |
|
|
Term
| What is the correct CS, US pairing and mechanism in conditioned drug tolerance? |
|
Definition
US = effects of the drug (NOT taking the drug)
UR = compensatory effects from body
CS = environmental cues
CR = compensatory effects from body |
|
|
Term
| How is Pavlovian conditioning used to explain drug sensitization? |
|
Definition
US = drug effects
UR = complimentary effects from body (same as drug effects)
CS = environmental cues
CR = complimentary effects which are additive to drug effects, increasing strength |
|
|
Term
|
Definition
| Acts at nicotinic cholinergic receptors in brain |
|
|
Term
| Symptoms of Smoker's Syndrome? |
|
Definition
| Chest pain, dyspnea, pain breathing, increased susceptibility to infection, coughing |
|
|
Term
| Why do smokers claim that smoking reduces tension? |
|
Definition
Actually, have normal stress levels during smoking, but elevated levels in between cigarettes
Therefore, the smoking calms them down, but only to the baseline of the normal population |
|
|
Term
| Buerger's disease symptoms? Seen in...? |
|
Definition
Seen in SMOKERS
Vasoconstriction of BVs, especially in legs; leads to hypoxia and potentially gangrene |
|
|
Term
| EtOH poses a risk of respiratory death if blood levels reach _______ |
|
Definition
|
|
Term
| Alcohol has what effect on body temperature? |
|
Definition
| LOWERS it (alcohol induces hypothermia) |
|
|
Term
| Phases of full blown alcohol withdrawal? |
|
Definition
1 = 5-6 hrs; tremors, agitation, headache, nausea
2 = 15-30 hrs; beginning of convulsions
3 = 1-2 days; delirium tremens (can be lethal) |
|
|
Term
| Delirium tremens is part of which withdrawal syndrome? |
|
Definition
|
|
Term
| Symptoms of delirium tremens? |
|
Definition
| Convulsions, hallucinations, delusions, tachycardia, seizures, hyperthermia |
|
|
Term
| What neuropsych disorder can be caused by long-term chronic EtOH abbuse? |
|
Definition
| Korsakoff's Syndrome -> memory loss, dementia, thiamine deficiency |
|
|
Term
| What drug can be used to combat EtOH abuse? How does it work? |
|
Definition
Can use DISULFRAM (ANTABUSE)
Causes accumulation of acetaldehyde by slowing its metabolism (causes dizziness, nausea, flushing) |
|
|
Term
| Psychoactive effects of marijuana are largely due to _____ which is part of a class of chemicals called ______ |
|
Definition
| THC; which is classified as a cannabinoid |
|
|
Term
| 2 documented health hazards of marijuana: |
|
Definition
Develop respiratory problems in chronic smokers
Single large doses can trigger MIs b/c MJ causes tachycardia |
|
|
Term
| In men that smoked at least 5 joints/day for 20 years, what structural abnormalities were observed? |
|
Definition
| Reduced volume in the hippocampus & amygdala (only a correlational study doe) |
|
|
Term
| Memory deficits & chronic marijuana use? |
|
Definition
| Memory deficits appear to disappear once having abstained from use (acute) |
|
|
Term
| Therapeutic effects of THC? |
|
Definition
Suppresses nausea and vomiting in cancer patients
Stimulate appetite in AIDS patients
Bronchodilator, antiepileptic, decrease severity of asthmatics |
|
|
Term
| What type of receptor is the CB1 receptor? |
|
Definition
| It is the most prominent GCPR in the brain |
|
|
Term
| 1st endocannabinoid found = ? |
|
Definition
|
|
Term
| What is the typically refined, powdery form of cocaine known as? |
|
Definition
|
|
Term
| What effects of cocaine DO NOT develop a tolerance? |
|
Definition
| MOTOR and CONVULSIVE effects - can be sensitized with use, no tolerance |
|
|
Term
| Types of endogenous opioids? |
|
Definition
|
|
Term
|
Definition
| Pain relief, cough suppressant, anti-diarrheal |
|
|
Term
| What outlawed the use of opiates? |
|
Definition
Harrison Narcotics Act (1914) - made it illegal to use or sell morphine, opium or cocaine
DID NOT include heroin (was semisynthetic and convinced that it was not addictive) |
|
|
Term
| What drug was not included under the Harrison Narcotics Act? |
|
Definition
|
|
Term
| Why is heroin much more potent than other opiates? |
|
Definition
| Has 2 Me groups added to a molecule of morphine - makes it more permeable to BBB |
|
|
Term
| What is worse, opiate withdrawal or EtOH withdrawal? |
|
Definition
| EtOH withdrawal has the potential to be much worse than opiate withrawal |
|
|
Term
| Opiate overdose typically kills individuals by _________ |
|
Definition
|
|
Term
| Why is death from heroin overdose often misunderstood? |
|
Definition
Usually also have high levels of EtOH/benzo's in their blood as well (drug interaction)
Many of the recent deaths have been from legal synthetic opioids (Oxycontin)
Death from OD may be if heroin is cut with another drug or excessively pure |
|
|
Term
| Primary treatment for heroin addiction = ? |
|
Definition
| METHADONE = similar effects, but without pleasurable high; lowers positive incentive value for drug; used to wean off dose |
|
|
Term
| Physical Dependence Theories of Addiction |
|
Definition
| Believe users take drug to prevent compensatory withdrawal symptoms (self-administer drugs to minimize withdrawal symptoms) |
|
|
Term
| Positive Incentive Theories of Addiction |
|
Definition
| Primary factor in addiction is the craving for positive incentive value of drug - expected pleasure from taking the drug |
|
|
Term
| Evidence that DOES NOT support Physical Dependence Theories of Addiction? |
|
Definition
Severity of withdrawal syndrome does not correlate with addiction rates (cocaine & meth don't have bad withdrawals)
Relapse rates continue to remain high after withdrawal period; normal pattern of drug taking typically involves binges, then detox |
|
|
Term
| How do positive incentive theories of addiction explain difference between hedonic and positive incentive value of drugs? |
|
Definition
PI value increases over time, even as the hedonic value decreases as tolerance develops (incentive sensitization theory)
The ANTICIPATED pleasure derived from taking drug fuels drug seeking behaviours |
|
|
Term
| Sensitization of drug craving experiment - does craving increase beyond acute withdrawal phase? |
|
Definition
YES - increases continually up to 60 days after withdrawal
Operant conditioning with lever + cocaine; cue for delivery = tone-light signal pair
When cue appears with lever pull (but without cocaine) see craving continue?? |
|
|
Term
| What are the 3 fundamentally different causes of relapse in addicts? |
|
Definition
STRESS
DRUG PRIMING
ENVIRONMENTAL CUES |
|
|
Term
| In addiction, the same compensatory responses trigger both ___________ and ____________ for the drug |
|
Definition
| Relapse & craving for drug |
|
|
Term
| Why did researchers believe that ICSS was fundamentally different than lever pressing for food/water? |
|
Definition
Despite high response rates, stopped lever for ICSS immediately when current shut off (rapid extinction rate)
Experienced self-stimulators did not immediately recommence pressing when returning, needed to be primed first |
|
|
Term
| DA system connecting from the midbrain to telencephalon is called? |
|
Definition
| Mesotelencephalic DA system |
|
|
Term
| The nigrostriatal pathway projects from... |
|
Definition
from the SN to dorsal striatum
Degeneration of this path implicated in PD |
|
|
Term
| The mesocorticolimbic path projects from... |
|
Definition
| Primarily from VTA to Nacc (reward & addiction mediation); also projects to other cortical and limbic regions |
|
|
Term
| 2 different pathways within the mesotelencephalic DA system? |
|
Definition
1) Nigrostriatal (SN to dorsal striatum)
2) Mesocorticolimbic (VTA to Nacc) |
|
|
Term
| Many brain sites of ICSS are part of the _______________ DA pathway |
|
Definition
| Mesotelencephalic (VTA & Nacc) |
|
|
Term
| The 2 main nuclei where DA neurons are located are the... |
|
Definition
Substantia nigra (beginning of nigrostriatal path)
VTA (beginning of mesocorticolimbic path) |
|
|
Term
| DA levels in Nacc are increased by (4 things) |
|
Definition
Natural reinforcers
Addictive drugs
Cues that predict reward
Stress |
|
|
Term
| Differences between cocaine induced and morphine induced place preference: |
|
Definition
Cocaine induced - eliminate with VTA or Nacc lesion
Morphine induced - CAN'T eliminate with Nacc lesion |
|
|
Term
| Cocaine neuroimaging study - asked addicts to rate the high they got...what was intensity of high correlated with? |
|
Definition
| Intensity of high correlated with amount of DA binding to receptors on postsynaptic membrane (needed at least 50% binding to achieve high) |
|
|
Term
| Mechanism of action of COCAINE vs. AMPHETAMINE |
|
Definition
COCAINE - block DA reuptake (DA reuptake blocker)
AMPHETAMINE - make reuptake pump run in reverse to pump more DA into synaptic clefts |
|
|
Term
| What are the 3 main theories of the purpose of DA release in the Nacc? |
|
Definition
1) Release codes for EXPERIENCE of reward (when reward is given)
2) Release codes for ANTICIPATION/EXPECTATION of reward
3) Release codes for reward value, based on discrepancy between expected and actual rewards |
|
|
Term
| What 3 areas of the brain mediate each trigger of relapse? |
|
Definition
HYPOTHALAMUS - for STRESS induced relapse
PFC - for DRUG PRIMING induced relapse
Amygdala - for ENVIRONMENTAL/CUE INDUCED relapse |
|
|
Term
| Structures in dorsal vs ventral striatum? |
|
Definition
DORSAL = caudate + putamen
VENTRAL = Nacc |
|
|
Term
| Relative abundance of DA-D2 receptors in striatum of cocaine & meth addicts? |
|
Definition
Have a LOWER abundance of D2 receptors
Don't know if this is down regulation due to addiction, or vulnerability factor to addiction |
|
|
Term
| What effect does long term cocaine use have on D2 receptor density in the striatum? |
|
Definition
| It DOWN REGULATES the # of receptors present in striatum |
|
|
Term
| Evidence for D2 receptor density as a vulnerability factor in addicts? |
|
Definition
| Note that in healthy humans, D2 receptor density negatively correlates with how much subjects liked cocaine-like drug (fewer receptors = like drug more = more potential to become addict) |
|
|
Term
| When comparing dominant vs. submissive monkeys, what were the differences in D2 receptors? |
|
Definition
DOMINANT - had a substantive increase in D2 receptor density
SUBMISSIVE - more vulnerable to reinforcing properties of cocaine; fewer D2 receptors = greater intake of cocaine |
|
|
Term
| What are neurotoxic effects of methamphetamine in animal models? |
|
Definition
Note that it damages DA and 5-HT neurons
Decrease in levels of DA and 5-HT, decrease in ENZ used in their synthesis as well |
|
|
Term
| What effect does chronic cocaine use have on glucose metabolism in the brain? |
|
Definition
Reduces glucose metabolism, get weaker BOLD signal in fMRI in chronic cocaine abusers
With longer period of abstinence from cocaine use, have increased glucose metabolism (recovery) |
|
|
Term
| Darwin's theory of the evolution of emotions? |
|
Definition
Emotions evolve from behaviors that can be used to indicate what an animal is likely to do next
If signals benefit animal, communicative fashion is enhanced and original function may be lost
Principle of antithesis = opposite messages have opposite movements/postures |
|
|
Term
| What is the principle of antithesis as believed by Darwin? |
|
Definition
| Opposite messages have opposite movements/postures |
|
|
Term
| James-Lange Theory of Emotion |
|
Definition
Sensory stimuli interpreted by cortex, triggers changes in visceral organs & muscles by autonomic/somatic NS, then these changes are fed back and perceived as experience of emotion in the brain
Causal pathway --> sensory stimuli to autonomic/somatic NS to feedback to brain to perceive emotions
Emotional event is caused by autonomic & somatic changes in the body |
|
|
Term
| Cannon-Bard Theory of Emotion |
|
Definition
Emotional stimuli have 2 independent effects:
- Excite feeling of emotion in brain
- Excite expression of emotion in autonomic/somatic NS
Says that emotional experience is split into emotion in the brain and emotion in the viscera/body |
|
|
Term
| Differences in predictions of feedback in J-L and C-B theories of emotion? |
|
Definition
J-L - emotional experience is entirely dependent on feedback to the brain from autonomic/somatic processes
C-B - emotional experience is INDEPENDENT of any feedback |
|
|
Term
| What are the 3 principal factors in an emotional response? |
|
Definition
Perception of stimulus
Autonomic & stimulus responses
Experience of emotion |
|
|
Term
| How is the modern view of emotional responses different than the J-L and C-B theories of emotion? |
|
Definition
Modern view is intermediate along the spectrum of the two
States that any one element of an emotional response can influence the other two, as none are completely independent |
|
|
Term
| What is "sham rage"? How can it be eliminated in animal models? |
|
Definition
Seen in decorticate cats (cats w/o cortex), respond aggressively to any provocation; aggression is general and not at any target in particular
Can eliminate sham rage by removing hypothalamus in addition to cortex |
|
|
Term
| What structures are found within the limbic system? |
|
Definition
| Amygdala, fornix, mammillary body, hippocampus, septum, cingulate cortex, olfactory bulb, hypothalamus |
|
|
Term
| What is Kluver-Bucy syndrome? Symptoms? |
|
Definition
Seen in monkeys w/o anterior temporal lobes - seems to be due to amygdalar damage
Symptoms - increased sexual activity, consumption of anything, repeatedly investigate familiar objects, investigate with mouth, lack of fear |
|
|
Term
| What is the "mock-crime procedure" and what technique is it used in? |
|
Definition
Used in POLYGRAPHY (lie detection)
Used to test validity of the test; have subjects involved in "mock crime" then interviewed by blinded examiner
About 80% success rate |
|
|
Term
| How is the "guilty knowledge" technique used in polygraphy? |
|
Definition
Examiner needs to know piece of information only guilty party would know
See how subject responds to actual vs. contrived details of crime scene - only a guilty individual would know true details and respond specifically (can't just ask if they committed the crime b/c everyone would have physiological response to that)
Shown to be 88% effective |
|
|
Term
| What are the primary facial expressions? |
|
Definition
| Surprise, anger, sadness, disgust, fear, happiness |
|
|
Term
| What is the facial feedback hypothesis? |
|
Definition
Theory that facial expressions influence our emotional experience (happy faces make us feel happier, e.g.)
This holds true even if people are not told what the face presented is supposed to be conveying |
|
|
Term
| What are 2 ways to distinguish true and false facial expressions: |
|
Definition
1) Microexpressions - last < 0.05 sec; break through false ones
2) Slight differences (e.g. smile of enjoyment produced by orbicularis oculi & zyg major - two muscles unique to sincere smiles) |
|
|
Term
| What name was given to the "genuine smile"? |
|
Definition
|
|
Term
|
Definition
| Emotional reaction to threat |
|
|
Term
| In the experiment regarding social interactions between cats & mice, what happened to the cats' behaviours when they were given anxiolytics? |
|
Definition
| Behaviours became more aggressive (those who hunted did so more aggressively, those who played now hunted) |
|
|
Term
| What is the "target-site concept" of aggressive & defensive animal behaviour? |
|
Definition
| Believes that these behaviours are designed to attack specific sites on the body of the prey, while still protecting sites of own body |
|
|
Term
| What is the difference between social aggression & defensive attack and their relation to testosterone? |
|
Definition
Social aggression - related to testosterone levels in individuals
Defensive attack - unrelated to testosterone
Have still not delineated this in human studies of testosterone & aggression |
|
|
Term
| Bilateral lesions to the ___________ can block fear conditioning to a tone |
|
Definition
| MEDIAL GENICULATE NUCLEUS (MGN = auditory relay nucleus) |
|
|
Term
| Lesions to the _____________ did NOT block fear conditioning to shock-tone pairing |
|
Definition
Auditory cortex
ONLY MGN lesions blocked fear conditioning |
|
|
Term
| Fear conditioning circuit involves projections from __________ to __________ |
|
Definition
| From medial geniculate nucleus to amygdala |
|
|
Term
| What are the 2 fear conditioning pathways that exist? |
|
Definition
DIRECT - MGN to amygdala (fine for fear conditioning to simple sounds)
INDIRECT - MGN to amygdala via auditory cortex (needed for complex sounds; can do simple also) |
|
|
Term
| What part of the brain, other than amygdala, is important for contextual fear conditioning? |
|
Definition
HIPPOCAMPUS
Contextual fear conditioning = animals learn to fear certain context/environment due to presentation of noxious stimuli in that environment |
|
|
Term
| What part of the brain is believed to be able to suppress conditioned fear? |
|
Definition
Prefrontal Cortex
PFC projects to lateral nucleus of amygdala and is believed to act here to suppress fear conditioning |
|
|
Term
| Differences in glucocorticoids in primates vs non-primates? |
|
Definition
Primates = have CORTISOL
Non-primates (e.g. rats) = have CORTICOSTERONE |
|
|
Term
| Hypocortisolemia is also known as.... |
|
Definition
Addison's disease
Hypocortisolism can be fatal; stressful event can lead to Addisonian crisis |
|
|
Term
| Where does the negative feedback for stress occur? |
|
Definition
| At the level of the HIPPOCAMPUS |
|
|
Term
| What type of receptors mediate negative feedback for glucocorticoids? What are their affinities for glucocorticoids? |
|
Definition
Mineralocorticoid receptors (MCRs) - HIGH affinity for glucocorticoids; regulate BASAL glucocort levels
Glucocorticoid receptors (GCRs) - LOW affinity for glucocorts; regulate increased glucocort levels
Exist in the hypothalamus |
|
|
Term
| What is the negative feedback loop for glucocorticoids as mediated by hippocampus? |
|
Definition
| Glucocorticoids bind to MCRs and GCRs in the hippocampus, causing it to inhibit the PVN (of hypothalamus) in production of CRH |
|
|
Term
| What limbic system structure is VERY vulnerable to stress? |
|
Definition
The hippocampus
Stress leads to loss of hippocampal neurons, impairing the negative feedback loop which increases cortisol levels, contributing to more stress (vicious cycle) |
|
|
Term
| What happens to hippocampal neuronal morphology in chronic stress conditions? |
|
Definition
See reduced # of branch points in dendrites, and decreased length of dendrites
Damage could be blocked by adrenalectomy or preventing corticosterone production |
|
|
Term
| Shrew stress experiment... |
|
Definition
Looking at effects of chronic stress on corticosterone levels
In "subordinates" - increased urinary cortisol levels, reduced weight |
|
|
Term
| In chronic stress conditions, the degree of hippocampal atrophy observed is ___________ |
|
Definition
Dose-dependent
More stress = more atrophy & possibly apoptosis |
|
|
Term
| Chronic stress can induce _____________ and suppress _____________ of cells in hippocampus |
|
Definition
induce APOPTOSIS
suppress NEUROGENESIS |
|
|
Term
| What typically happens to hippocampal volume in stress related disorders (e.g. PTSD)? |
|
Definition
| Typically see a reduced hippocampal volume |
|
|
Term
| What effect does stress have on the immune system? |
|
Definition
| Causes increased cytokine levels (responsible for inflammation & fever) |
|
|
Term
| Relationship between stress & gastric ulcers? |
|
Definition
Used to think stress caused them - now know causative agent is H pylori infection
However, seems like stress makes individuals more susceptible to infection from H pylori |
|
|
Term
| The innate immune system is activated by ______________ receptors |
|
Definition
|
|
Term
| Where are toll-like receptors located in immune system? |
|
Definition
| On the membrane of phagocytes (microglia, monocytes) - responsible for activating innate immune system |
|
|
Term
| What are 2 functions of phagocytes in the innate immune response? |
|
Definition
Engulf and phagocytose the material
Attract cytokines to the area of infection to trigger inflammatory response |
|
|
Term
| What immune cells are cytokines responsible for activating? |
|
Definition
| LYMPHOCYTES - part of the adaptive immune system |
|
|
Term
| What are the 2 main classes of lymphocytes in the adaptive immune system? What types of immunity is each responsible for? |
|
Definition
T cells - cell mediated immunity
B cells - antibody mediated |
|
|
Term
| What types of diseases to regulatory T cells help combat? |
|
Definition
| Help combat autoimmune conditions that involve T cells attacking the body's own tissues |
|
|
Term
______________ is stress that disrupts health
______________ is stress that enhances health |
|
Definition
DISTRESS disrupts health
EUSTRESS enhances health |
|
|
Term
| What types of stress are there and what effect does each have on immune function? |
|
Definition
ACUTE STRESS (< 100 minutes) - is EUSTRESS; enhances immune function, mainly innate system
CHRONIC STRESS (several days) - DISTRESS; negatively affects immune function |
|
|
Term
| What results were observed in the bonnet macaque mother-infant dyads under different foraging conditions |
|
Definition
Had low (LFD), high (HFD), and variable (VFD) conditions
Highest amount of conflict seen in VFD condition; made infants hyperresponsive to stress (less socially competent, more fearful, higher CRH levels in CSF) |
|
|
Term
| The mother-infant rat grooming experiment conducted by Liu, what was observed? |
|
Definition
Infants with a higher time spent being groomed were less responsive to stress when older
In high grooming (HG) group - infants had lower anxiety (measured by defensive burying); lower ACTH, CORT responses to stress |
|
|
Term
| What neurological changes were observed in the Liu rat grooming experiment in the rats raised by high grooming mothers? |
|
Definition
Less CRH in PVN (less stress response)
More glucocort receptors in hippocampus (better -'ve feedback)
Less CRH in amygdala (reduced fearfulness) |
|
|
Term
| Is amygdala more involved in our own fear or perception of fear in others? |
|
Definition
| More involved in perception of fear in others |
|
|
Term
| What is Urbach Weithe Disease? |
|
Definition
Caused by calcification of amygdala bilaterally
Lose ability to recognize facial expressions of fear
Poor use of others' eyes to infer emotion; dont' spend as much time looking at eyes (may be an attentional deficit); perform as well as controls if instructed to look at eyes |
|
|
Term
| What part of the face is a critical stimulus for amygdala activation in recognition of fearful faces? |
|
Definition
The EYES
Get the greatest amygdalar response with direct eye contact
Also sensitive to eye shape - largest response to wide-eyed fear |
|
|
Term
| In looking at individuals in love, romantic love caused increased activation of _____________, and decreased activation of ______________ |
|
Definition
Increased activation - insula, ACC, striatum
Decreased activation - amygdala, PCC |
|
|
Term
| How are the mPFC lobes involved in human emotion? |
|
Definition
| See activity in mPFC in tasks of both emotional suppression (inhibit emotional rxns) and reappraisal paradigms |
|
|
Term
| More activity is seen in the amygdala on which side of the brain? |
|
Definition
| L amygdala has higher activity |
|
|
Term
| Where does most expression usually begin? What does this suggest? |
|
Definition
Usually begins on L side of face and is more pronounced there, this suggests R hemisphere dominance
Also, judge others more based on R side of observed face (L visual field = R hemisphere) |
|
|
Term
| How do you conduct a fear potentiated startle task? |
|
Definition
Need to pair light with shock - so tone becomes CS for startle response
Then play tone by itself (startle alone)
Then show light, then play tone (fear-potentiated startle; light induced fear as CS, tone induced startle) |
|
|
Term
| In the fear-potentiated startle task, what effect did amygdalar lesions have? |
|
Definition
Tone alone (only startle) - amygdala lesion had NO effect
Tone + light (fear potentiated) - lesions REDUCED fear potentiated startle
Amygdala involved in fear conditioning |
|
|
Term
| What regions of the amygdala are important for fear conditioning? |
|
Definition
Lateral amygdala
Central amygdala |
|
|
Term
| What activity is observed in the lateral amygdala during fear conditioning? |
|
Definition
During acquisition of CS, get increased activity
As trial # increases, get larger and larger responses (similar to LTP) |
|
|
Term
| What are 3 of the main projections of the central amygdala which mediate the responses to fear conditioning? |
|
Definition
Central grey - mediates freezing behaviour
Lateral hypothalamus - mediates increased BP
PVN - mediates HPA axis |
|
|
Term
| In testing innate fear with septum vs. amygdala lesions, what was observed? |
|
Definition
Used elevated maze & defensive burying as tests
Elevated maze - only septal lesions increased time spent in open arms
Burying - septal lesions decreased defensive burying; amygdalar lesions decreased passive avoidance (shocked more often) |
|
|
Term
| What does "schizophrenia" mean in Greek? |
|
Definition
Schizen = split
Phren = mind |
|
|
Term
|
Definition
20-25 in males
25-30 in females; see 2nd peak after menopause |
|
|
Term
| Positive Symptoms of Schizophrenia |
|
Definition
| Hallucinations, delusions, inappropriate affect, disorganized speech/thought |
|
|
Term
| Negative Symptoms of Schizophrenia |
|
Definition
Anhedonia/Avolition, Asociality, Apathy, Alogia, Flat Affect
Alogia = lack of speech
Avolition = lack of motivation |
|
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Term
| Schizophrenia concordance in monochorionic vs dichorionic MZ twins |
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Definition
Concordance is 60% in mono, vs 10% in dichorion MZ twins
Monochorionic = twins share 1 placenta |
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Term
| How do maternal and paternal age affect schizophrenia incidence? |
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Definition
Maternal age = NO effect
Paternal age = increased age has a higher incidence of schizo |
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Term
| During what part of pregnancy are fetus' most susceptible to risk factors that increase incidence of schizophrenia? |
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Definition
2nd trimester
Risk factors - influenza, stress, malnutrition |
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Term
| What kind of neurodevelopmental errors are seen in neurons in the brains of those with schizophrenia? |
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Definition
See ECTOPSIA - error in cell migration
See DYSPLASIA - error in cell differentiation |
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Term
| What was the 1st antipsychotic developed? |
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Definition
| Chlorpromazine (typical anti-psychotic) |
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Term
| What did Carlsson and Lindqvist show in their experiments testing the effect of chlorpromazine on ECF DA levels? |
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Definition
Showed that DA levels were UNCHANGED when adminsitered, and DA metabolite levels increased
Deduced that chlorpromazine was DA receptor blocker |
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Term
| What are the different mechanisms of DA antagonism by chlorpromazine vs reserpine? |
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Definition
Chlorpromazine - D2 receptor antagonist; block at post syn membrane
Reserpine - breakdown DA in synapse |
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Term
| What anti-psychotic that treated schizophrenia was initially shown to have a low affinity for DA receptors? |
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Definition
| HALOPERIDOL - believed to have low affinity, but this was before they discovered different types of DA receptors |
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Term
| _________ is part of a group of anti-psychotics known as _______________ that bind with high affinity to D1 and D2 DA receptors |
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Definition
| Chlorpromazine - part of a group called phenothiazines |
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Term
| _____________ is part of a group of drugs classified as _____________ that bind only to D2 DA receptors efficiently |
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Definition
| HALOPERIDOL - part of the butyrophenones |
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Term
| The ability of ____________ to reduce symptoms of schizophrenia was proportional to their ability to __________ |
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Definition
Ability of "neuroleptics"
Ability to "bind D2 DA receptors" |
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Term
| What are some of the limitations of the DA theory of schizophrenia? |
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Definition
- Have linked other receptors also (5-HT, glutamate, GABA)
- Takes weeks of neuroleptic therapy to see effects, even though binding occurs within hrs
- Schizophrenia associated with widespread, diffuse brain damage
- Neuroleptics only marginally effective; only treat positive symptoms |
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Term
| What other transmitters have their receptors linked with schizophrenia? |
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Definition
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Term
| What drug is successful in treating schizophrenia that does NOT act on D2 DA receptors? |
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Definition
Clozapine - atypical antipsychotic
Acts on D1, D4, 5-HT receptors |
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Term
| In schizophrenia, abnormalities in brain are ______________, not neurodegenerative |
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Definition
| Abnormalities are "neurodevelopmental" (typically occur at onset, not progressive through course) |
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Term
| Schizophrenia cases that occur after traumatic brain injury are mainly characterized by _________________ only |
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Definition
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Term
| 2 different types of depression - based on cause... |
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Definition
Reactive depression
Endogenous depression (no apparent cause) |
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Term
| What is the lifetime prevalence for clinical depression? Ratio M to W? |
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Definition
About 10%
W diagnosed 2x as often as men |
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Term
| Which affective disorders have higher concordance rates - bipolar or unipolar? |
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Definition
| BIPOLAR disorders have higher concordance rates |
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Term
| 1st type of MAO inhibitor = ? Mode of action? |
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Definition
Iproniazid
Inhibits MAO in cytoplasm of neuron, reduce monoamine breakdown |
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Term
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Definition
| Side-effect of MAO inhibitors; can't eat anything containing TYRAMINE - could have a hypertensive crisis |
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Term
| What is the mechanism of action of tricyclic antidepressants? |
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Definition
They block reuptake of 5-HT and DA from synapses
Better than MAOI b/c o fewer side fx |
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Term
| Prozac is an example of a ...... |
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Definition
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Term
| Imipramine is an example of a ...... |
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Definition
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Term
| Iproniazid is an example of a ...... |
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Definition
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Term
| What was the 1st mood stabilizer found? |
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Definition
| Lithium (unknown mechanism) |
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Term
| Which mood stabilizer is best for MANIA and which for DEPRESSION? |
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Definition
MANIA - carbamazepine
DEPRESSION - lamotrigine |
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Term
| Two abnormal brain structures typically seen in affective disorders (esp depression)... |
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Definition
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Term
| What does the Monoamine Theory of Depression state? |
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Definition
| States that depression is due to a lack of activity at serotonergic (5-HT) and noradrenergic (NE) synapses |
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Term
| Evidence for Monoamine Theory of Depression: |
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Definition
1) Antidepressants all involve metabolism of monoamines
2) In brain of depressed individuals, see higher levels of 5-HT and NE receptors w/o treatment (were upregulated due to lack of transmitter production)
3)Tryptophan depletion results in symptom relapse |
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Term
| What does the Neurogenesis Hypothesis of Depression state? Evidence? |
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Definition
Depression involves impaired neurogenesis in the hippocampus
Support:
1) Stress = risk factor for depression (reduces hipp.neurog.)
2) Stress impairs hipp. neurogenesis
3) Antidepressant treatments increase neurogenesis
4) Blocking hipp. neurogenesis blocks antidepressant fx |
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Term
| What are indications from evidence that individuals with an s/s or s/l genotype (5-HT promoter gene) are at a higher risk of developing depression? |
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Definition
1) s/l and s/s individuals have 1/2 as many 5-HT binding sites
2) s/l and s/s individuals score higher on depression & anxiety scores
3) s/l and s/s individuals more at risk for depression with childhood stress & w/ multiple adulthood stressors (genotype makes them more susceptible) |
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Term
| In DBS treatment for depression, where is electrode implanted? |
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Definition
| Near anterior cingulate gyrus - create functional lesion here |
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Term
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Definition
| Chronic fear persisting in the absence of any direct threat; only a disorder if it interrupts normal functioning |
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Term
| What two types of disorders have a 2:1 female to male ratio? |
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Definition
| Depression & anxiety disorders |
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Term
| What are the 5 major classes of anxiety disorders? |
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Definition
GAD
Phobic Anxiety Disorders
Panic Disorders
OCD
PTSD |
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Term
| Valium is an example of a ...... used to treat ....... |
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Definition
| Benzodiazepine, used to treat Anxiety Disorders |
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Term
| What are the most widely prescribed psychoactive drugs in N America? |
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Definition
| Benzodiazepines - can be used as anxiolytics, hypnotics, anticonvulsants |
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Term
| What is the mechanism of action of most benzodiazepines? |
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Definition
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Term
| What class of drugs, other than benzos, can be used to treat anxiety disorders? |
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Definition
Serotonin agonists (e.g. buspirone)
Agonistic effects at 5-HT (1A) receptors |
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Term
| Main symptom of Tourette Syndrome? |
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Definition
| TICS = involuntary repetitive movements/vocalizations that are stereotyped |
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Term
| What are coprolalia and palilalia and what disorder are they associated with? |
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Definition
Coprolalia - saying obscenities
Palilalia - repeating own words
Associated with Tourette syndrome |
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Term
| What is the gender ratio of distribution of Tourette disorder? |
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Definition
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Term
| Most research in looking at Tourette syndrome is focused on which area of the brain? |
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Definition
CAUDATE (tend to be smaller)
Also see reduced volume in sensorimotor cortex to control larynx, face, mouth |
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Term
| What are the tics in Tourette syndrome treated with? |
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Definition
| Treated with neuroleptics (D2 receptor antagonists); can reduce tics in 70% of patients, would be higher with better compliance |
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