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clinical psychopharmacology > slides > Flashcards

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1
Q

What are the 9 steps of neurtransmission?

A

(1) NTs are synthesized in vesicles in pre-synaptic cell (2) AP reaches presynaptic terminal
(3) Ca2+ channels open because of depolarization
(4) Ca2+ flood presynaptic cell
(5) vesicles containing NTs fuse to the cell wall
(6) NTs released into the cleft via exocytosis
(7) NTs bind ot receptors on the post-synaptic cell
(8) channels on the post-synaptic cell either open/close (9) inhibitory/excitatory signal is sent in the post-synaptic cell

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2
Q

What is an agonist?

A

a ligand that binds to a receptor and mimics the effects of a NT

includes both molecular and behavioral changes

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3
Q

What is an antagonist?

A

a ligand that binds to a receptor and blocks the binding of a NT

does not include molecular change, but does have behavioral changes

for example, caffeine

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4
Q

What is tolerance/cross-tolerance?

A

when the body, over the timecourse of drug administration, slowly needs more and more of the drug to have an effect

cross-tolerance refers to the ability of one drug to cause tolerance for another drug

for example, alcohol and cocaine/amphetamine

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5
Q

What is sensitization/cross-sensitization?

A

when the body needs less of a drug over time to have the same effect, the effects become stronger with the same doseage

cross-sensitization refers to the ability of a drug to also cause sensitization for another drug

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6
Q

What does pharmacokinetic refer to?

A

refers to everything that happens in the body before/ after the drug reaches the recpetor

kinetic = movement

for example, how the body transfers, reabsorbs, inactivates and excretes the drug

also, half -life research falls under this umbrella

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7
Q

What does pharmacodynamic refer to?

A

this is what happens when the drug takes action at a site

for example, both physiological and biochemical interactions of the drug at a site

like caffeine being an antagonist at a a recpetor site

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8
Q

What does the elevated plus maze model?

What does an animal do once given the (targeted) medication?

A

anxiety model

if a rat is given anti-anxiety medicaiton, they will spend more time in the open arms of the maze

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9
Q

What does the conditioned place preference procedure model?

What does an animal do once given the (targeted) medication?

A

drug addiction model

if a drug with highly addictive properties is administed in one room, then the rat is more likely to spend time in that room because of the associated positive stimuli (even if that stimuli is no longer there)

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10
Q

What does the animal self-administration procedure model?

What does an animal do once given the (targeted) medication?

A

drug addiction model

if a drug with more addictive properties is adminstered, the lab rat is more liekely to self-administer often

depending on how many times the rat presses a lever, they will recieve different doses

a progresive ration model (more presses are required for drug distribution over time) can help model a drugs ‘breaking point’ (when the costs outweigh the benefits)

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11
Q

What does the pre-pulse inhibition (PPI) model?

What does an animal do once given the (targeted) medication?

A

schizophrenia/neuroleptic model

if a person has schizophrenia, they will have decreased PPI after given a cue that a startle stimuli will be presented (they will be just as startled even if they know the stimuli is coming)

if a neuroleptic is effective, it should increase PPI (less startled)

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12
Q

What does the learned-helplessness procedure model?

What does an animal do once given the (targeted) medication?

A

depression model

if anti-depressants are effective, the dog should be more willing to try and escape shocks that the previously would not have avoided (because of learned-helplessness they developed from not being able to escape initially)

if a dog is depressed, they will give up more quickly on trying to avoid shocks

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13
Q

What does the 8-arm-raidal maze and the Morris water maze model?

What does an animal do once given the (targeted) medication?

A

memory and cognitive function model

if a drug improves memory and cognitive function, a lab rat will be able to find the correct arm of the maze/platform in the water more quickly

if an animal has cognitive or emmeory impairments, they will be slower

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14
Q

(1) What kind of molecule is glutamate?
(2) Which kinds of cells contain glutamate?
(3) What is the role of glutamate?
(4) What is the precursor to glutamate?
(5) What enzyme synthesizes glutamate from its precursor?
(6) Where is glutamate found in the brain?

A

(1) excitatory amino acid NT
(2) glial cells and all neurons contain glutamate
(3) has 2 main functions: excitatory NT to excite post-synaptic cell, protein synthesis/ metabolism
(4) glutamine
(5) glutaminase
(6) everywhere - because it has 2 very important functions

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15
Q

What is unique to the glutamate neuron-astrocyte interaction?

Why?

A

Glutamate is synthesized from glutamine by glutaminase in the presynaptic cell

it is then released into the cleft and binds ot receptors on the post-synaptic cell

after it is released into the cleft, astrocytes recycle the glutamate by deactivating it back into glutamine (with glutamine synthetase)

glutmaine transporters then transport glutamine back into the pre-synaptic cell

this system is important because glutamate is an excitatory NT that needs to be deactivated quickly, or the post-synaptic cell will keep being excited

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16
Q

(1) What are the 2 glutamate receptors?

(2) What is important about the way these 2 receptors work together?

A

(1) NMDA and AMPA
(2) NMDA is an ion channel that needs 2 NTs to open: glutamate and glycine/D-serine

NMDA is often blocked by magnesium that is released if the membrane is previously activated (depolarized)

this prior activation which releases the magnesium is only possible due to AMPA receptors

NMDA also acts as a Ca2+ channel to activate 2nd messenger systems

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17
Q

What is Long Term Potentiation (LTP)?

How is it relevant to the glutamate receptor systems?

A

(1) when a signal is sent frequently enough, there are long lasting increases in the signal transmission between 2 neurons
(2) in the glutamate receptor system, NMDA is relevant during short-term/acute glutamate transmission

however, once 2nd messenger systems are activated (thanks to the Ca2+), NMDA is less relevant

for example, glutamate release can now be increased from the pre-synaptic cell, AMPA receptors are up-regulated, and AMPA receptors are now more sensitive to glutamate

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18
Q

(1) What kind of molecule is GABA?
(2) Where is GABA found in the brain and what is its role there?
(3) What is the precursor to GABA?
(4) What enzyme synthesizes GABA from its precursor?

A

(1) inhibitory NT
(2) most often found in: substantia nigra/ dopamine inhibition, cortex/ glutamate inhibition, hippocampus/glutamate inhibition

overall, it is expressed more highly than other NTs in the cortex/ most prominent

(3) glutamate
(4) GAD, glutamic acid decarboxylase

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19
Q

What are 2 GABA receptors and what kind of receptors are they?

A

1) GABA- A /ionotropic
2) GABA-B/ metabotropic

we focus mostly on GABA-A

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20
Q

(1) What is GABA-A mostly a target for?
(2) What kind of channel is it?
(3) What molecule is it a channel for?

A

(1) psychoactive drugs: like benzodiazepines and barbiturates
(2) ionotropic
(3) chloride channel

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21
Q

(1) What is the effect of benzodiazepines on the GABA-A channel?
(2) Which disorder is benzodiazepine helpful in addressing?
(3) What are the side-effects?
(4) What are the psychoactive effects of benzodiaszepine?
(5) What are 2 other names for benzodiazepines?

A

(1) acts as an agonist that increases the potency for GABA to be able to open the GABA-A channel, but only works in the presence of GABA
(2) anxiety disorders
(3) sedation, has long-acting compounds which cause bad withdrawal effects, and the drug stays in the system for a long time
(4) effects include: anxiolytic/anxiety reducing and anticonvulant, without excessive sedation or respiratory depression. has low tolerance, less withdrawal and is relatively safe.
(5) diazepam/ valium

22
Q

(1) What are 3 types of anxiety disorders in the DSM-IV?

(2) What are the 2 updated disorders in the DSM-V?

A

(1) generalized anxiety disorder, panic disorder, and phobias
(2) obsessive-compulsive disorder, trauma/stessor related disorders (like PTSD)

23
Q

(1) What does the PFC inhibit?
(2) Which disorders are characterized by an underactivity in the PFC?
(3) Which disorders are characterized by an overactivity in the PFC?

A

(1) amygdala/fear processing
(2) underactivity of the PFC fails to inhibit emotions/fear processing so this leads to more disorders involving fear and panic, such as: PTSD, phobias, panic disorder
(3) overactivity of the PFC leads to an over-regulation of emotions and causes more disorders that involve worry and ruminations, such as: generalized anxiety disorder, OCD

24
Q

(1) What are 3 types of catecholamines?
(2) What is the core structure of a catecholamine?
(3) What is the chain of catecholamine synthesis (3 steps)?

A

(1) dopamine, norepinephrine/NE, epinephrine (mostly hormonal)
(2) catechol + amine group

(3)
[tyrosine] —tyrosine hydroxylase —> [L-DOPA]
[L-DOPA] — AADC —> [dopamine]
[dopamine] — dopamine ß-hydroxylase —> [NE]

25
Q

Which 2 enzymes break down catecholamines?

A

COMT (catechol-O-methyltransferase)

MAO (monoamine oxidase) A and B

26
Q

What are 3 dopaminergic pathways and what purposes do they serve?

A

1) nigrostriatal pathway

substantia nigra —-> caudate putamen & globus pallidus/ striatum

striatum is location for D2 receptors

this pathway regulates motor behavior, so too much dopamine can cause motor disorders

2) mesolimbic pathway

VTA —-> NAcc

pathway for reward/addiction

3) mesocrotical pathway

VTA —-> frontal cortex/ hippocampus

involved in working memory

27
Q

(1) How many main usbtypes of DA recpetors are there?

(2) Which are the 2 primary ones of interest and what kind of receptors are they?

A

(1) 5: D1-D5
(2) D1 and D2 and metabotropic receptors that allow for 2nd messenger systems (longer lasting effects/ physical changes over time to adjust to DA levels)

28
Q

What are 4 drugs that act on the dopaminergic system, what areas do the target, and what is their effect?

A

1) DOPA

prcursor to dopamine used to increase DA levels in the brain

helps treat the nigrostriatal pathway in patients with parkinsons disease/ substantia nigra is not producing enough dopamine (uninhibited motor movements because dopaminergic neurons are understimulated)

2) reserpine

reduces dopamine and NE in the system by inhibiting vesicular uptake

acts as a sedative and HBP regulator, can be used for highly agitated patients (such as schizophrenic patients)

3) amphetamine/meth/cocaine

amphetamine releases more catecholamines while cocaine inhibits their reuptake

acts as stimulants that have the potential for cross-tolerance

meth and esctasy are neurotoxic

4) haloperidol

blocks D2 receptors/antagonist

used in the treatment of schizophrenia since it helps relieve positive symptoms caused by excess dopamine

29
Q

(1) Where is noradrenaline (NA) synthesized?
(2) What are noradrenaline receptors called and what kind are they?
(3) What is unique about subtype receptor alpha 2?
(4) What are the 3 main functions of NA?

A

(1) locus coeruleus, with projections throughout the cortex
(2) adrenergic /adreno-receptors, metabotropic, alpha/beta subtypes
(3) alpha 2 receptors are autoreceptors, therefore noradrenaline action is reduced it it binds to a2
(4) vigilance, arousal and alertness

locus coeruleus shows higher activity in mice when they are awake and alert

30
Q

(1) What is the early view of drug addiction?
(2) Why did there need to be a shift in this view?
(3) What is the newer model of drug addiction?

A

(1) an emphasis on physical addiction, such as the presence of withdrawal symptoms during abstinence
(2) some drugs that are abused do not show strong withdrawal symptoms, like cocaine
(3) an emphasis on behavior such as the compulsion to seek and use drugs

such as cravings and chronic relapsing disorder

31
Q

(1) What are the 2 main components of the Incentive-Sensitization Model?
(2) Which component is involved in the dopamine system?
(3) What is incentive salience?

A

(1) drug wanting/ motivation and drug liking/ pleasure

so, the act of seeking out drugs and the act of recieving

(2) drug wanting involves the dopaminergic mesolimbic pathway by increasing dopamingeric activity whenever the individual is reminded of the drug

VTA —> NAcc

this pathway is then sensitized over time, so less stimuli is required for dopamine to be released and for the user to want to use the drug

drug liking or the pleasure derived from drug use does not involve dopamine

(3) incentive salience is the sensitization to drug paraphenelia over time caused by dopaminergic sensitization in the striatum

32
Q

(1) What are 7 hallucinogenic drugs?
(2) What does psychotomimetic mean?
(3) What does psychedelic mean?
(4) What is a pro to hallucinogenic drugs?
(5) What are 3 cons to hallucingenic drugs?
(6) Which NT and receptor is important in hallucinogenic drug action?

A

(1) mescaline, psilocybin/magic mushrooms, DMT, 5-MeO-DMT, salvinorin- most potent, LSD- synthetic, dissociative anesthetics
(2) mimics psychosis, but mostly visual hallucinations

in real psychosis its mostly auditory hallucinations- not appropriate to use as schizophrenia model

only dissociative anesthetics mimic schizophrenia more accurately

(3) mind opening
(4) no addiction- no binges, cravings, physical dependence
(5) bad trips, flashbacks/hallucinations persist, psychotic breakdown
(6) 5-HT (serotonin) because they act as agonists, 5HT2a is the most important receptor

33
Q

(1) What is a dissociative anesthetic?
(2) What are 2 examples of a dissociative anesthetic?
(3) What is a K-hole?
(4) Which disorder can dissociative anestehtics model?

A

(1) a class of psychedelic drug that is characterized by distortions in perception and feelings and have depressant effects such as sedation
(2) PCP and ketamine
(3) separation from the body, similar to a near-death experience
(4) positive and negative symptoms of schizophrenia

administration of these drugs worsen pre-existing symptoms in schizophrenic patients

34
Q

(1) What are 3 classes of symptoms in schizophrenia?
(2) What is the older model for schizophrenia?
(3) What is the newer model for schizophrenia?

A

(1) positive/hallucinations, negative/withdrawal, cognitive/memory impairment
(2) prefrontal model

DA underactivity in the PFC reduces inhibitor feedback that then causes DA overactivity in limbic and ventral areas

the mesocortical function is overall reduced (VTA –/–> PFC)

(3)
The site of error is not the PFC, but rather the Nucleus Accumbens

the NAcc should normally not inhibit the ventral pallidum which inturn inhibits the VTA

in schizophrenia, this inhibition from the NAcc —> ventral pallidum decreases inhibition of the VTA which in turn increase DA production

35
Q

What are 2 classes of drugs to treat schizophrenia?

A

1) classic/typical

targets D2 receptors in the PFC
like haloperidome/DA antagonist
helps with positive symptoms

2) atypical

targets other receptors or acts as a less potent DA agonist
more effective at treating negative symptoms

36
Q

(1) What are 2 methods to make an animal model for schizophrenia?
(2) What do we do with the information from these studies?

A

1) drug induced psychosis: using amphetamine or PCP/ketamine

behavioral models: PPI

2) identify neurochemical and genetic action, screen for new drugs

37
Q

(1) What is the precursor to ACh (acetylcholine)?
(2) Which kind of psychological effects is ACh directly correlated with?
(3) Where in the brain is ACh focused and projected to?

A

(1) ChAT: choline acetyl-transferase

breaks down choline and acetyl CoA into ACh and coenzyme A

(2) ACh is directly correlated to attention/learning and memory
(3) this is because the most relevant ACh pathway is the basal forebrain (ie hippocampus) with projections to the PFC

another pathway is from the dorsolateral pons to the cortex which is hypothesized to be a site of integration of information

38
Q

(1) What are reversible ACHE inhibitors?
(2) What is their main purpose?
(3) What are muscarinic antagonists?

A

(1) ACHE is the enzyme that breaks down ACh

therefore, if ACHE is inhibited, ACh will increase

(2) physostigmine is an ACHE that is only used in anticholinergic drug overdoses (medication used for movement disorders/ reduces involuntary movement/sedative) because it has adverse effects with long-term use

clinically used compunds llike Donepezil help with alzheimers and memory by acting on the hippocampus

(3) muscarinic receptors are a type of ACh receptor that when antagonized impair memory

39
Q

What are 2 types of ACh receptors?

A

1) nicotinic

nicotine can act as an agonist
is ionic

2) muscarinic

reponds to muscarine
is metabotropic

40
Q

(1) Where are serotonin projection neurons most likely to be found?
(2) Where are glutamate/GABA projection neurons most likely to be found?
(3) Where are norepinephrine projection neurons most likely to be found?
(4) Where are dopamine projection neurons most likely to be found?
(5) Where are cholinergic projection neurons most likely to be found?

A

(1) raphae nuclei
(2) cerebral cortex
(3) locus coeruleus
(4) substantia nigra
(5) basal forebrain

41
Q

(1) What are the 2 steps for serotonin (5-HT) synthesis?
(2) Where in the brain is it synthesized?
(3) What are the 2 disorders associated with 5-HT?

A

(1)
tryptophan —tryptophan hydroxylase—> 5-HTP
5-HTP —-AAD—-> 5-HT

(2) raphae nuclei/ median raphe
(3) anxiety and depression

42
Q

(1) What is the method or reuptake for 5-HT?
(2) What is a drug that acts on these sites and which disorder does it treat?
(3) Which enzyme breaks down 5-HT?
(4) What is a genetic risk factor for depression?

A

(1) 5-HT transporter
(2) SSRI (selective serotonin reuptake inhibitors)

act as antidepressants

cocaine and MDMA also act on this transporter but also act on the DA transporter

(3) MAO

thats why MAOIs also help alleviate symptoms of depression by allwoing serotonin to stay in the system for longer

(4) a polygenetic risk factor can contribute to problem in the serotonin transporter

2 shorter alleles cause higher rates of depression/ healthy people with 2 short alleles also show more amygdala activation to emotional faces

this was not reproduced, however and rather the connectivity between limbic and visual regions was implicated

43
Q

What are 2 categories for depressive disorders?

A

1) major depression/ unipolar

recurring episodes of dysphoria and negative thinking

2) bipolar depression

mood swings from depression to mania

44
Q

(1) What is often a precursor to depression?

(2) How do we know?

A

(1) Stress: like intense environmental stress and anxiety

(2) cortisol is a stress hormone that is found in higher amounts in depressed patients

45
Q

What is the cortoid stress pathway?

A

Hypothalamus in the brain releases NE, ACh and GABA

CRF/corticotropin realeasing factor is sent from the Hypothalamus to the pituitary gland

the pituitary gland releases ACTH/ adrenocorticotropic hormone

ACTH reaches the adrenal gland and cortisol is secreted into the blood stream

cortisol acts in a negative feedback loop with the hippocampus and hypothalamus to prevent further secretion

46
Q

What is a common symptom seen in depressed patients?

A

sleep disturbance

categorized by:

long period before sleep onset
decreased deep sleep stages
alterations of REM
perhaps, altered internal clock

47
Q

(1) What is the serotonin hypothesis?

(2) What are 4 pieces of evidence to support this model?

A

(1) idea that the neurochemical basis for depression is a decrease in serotonin levels
(2) evidence for this:

low tryptophan levels - precursor to 5-HT

in post mortem studies, there is an increased density of 5-HT2 receptors

PET scans show decrease in 5-HTT/transporter

animal models show that antidepressants change the 5-HT system

48
Q

(1) What is a prominent structural change seen in depressed patients?
(2) What is the functional change associated?

A

(1) in MRIs, you can see reduction in grey matter in the amygdala
there is also limbic structural changes

(2) amygdala is shown to be hyperactive/fear reaction

the limbic system/emotional processing center is shown to have higher rates of glucose metabolism

49
Q

What does the early-stressor procedure model?

A

depression/stress model

models how stress early in life can be a precursor to depression

50
Q

What are 3 pharmacological treatment approaches for depression?

A

1) MAOIs
2) SSRIs - first choice

like fluoxetine/prozac
has no cardiovascular side effects because it does not interact with DA transporters
sexual dysfunction is the least liked side effect

3) tryciclic antidepressants - if SSRIs don’t work

clinical psychopharmacology (1 decks)

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