PSYC 304 Drugs and Addiction

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109 Terms

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criteria for NTs

  • endogenous

  • synthesized in presynaptic axon terminal

  • released when AP reaches terminal

  • recognized by specific receptors on the postsynaptic membrane

  • blocking release of NT prevents presynaptic activity from affecting postsynaptic activity

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types of amine NTs

ACh, DA, NE, E, 5-HT

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types of amino acid NTs

glutamate, aspartate, GABA, glycine

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types of peptide NTs

opioids (enkephalins, endorlphins), oxytocin, vasopressin

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types of gas NTs

nitrous oxide - difuse freely and signal retrogradely

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glutamate function

excitation, learning, memory

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GABA function

inhibitory, anxiety modulation

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ACh function

motor control, learning, memory (loss = Alzheimer’s)

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DA function

  • motor control (mesostriatal pathway)

  • reward and reinforcment (mesolimbocortical, involved in schizophrenia)

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5-HT function

mood, sleep, sexual behaviour, anxiety

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NE function

arousal, mood, sexual behaviour, fight or flight

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opioid function

analgesic and reward

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NO function

vasodilation and synaptic plasticity

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agonist

mimics NT and activates recpetor more

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antagonist

blocks receptor without activating, preventing the NT from working

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inverse agonist

produces the opposite effect of the NT

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partial agonist

produces a medium effect regardless of dose

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competitive ligand

bind at the same site as the NT, blocking its access

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noncompetitive ligand

bind to a different site on the target (modulatory), can still affect the cell

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ligand + receptor procedure

  1. ligand binds, so receptor changes shape/activity

  2. leads to ion flow, or second messenger cascade

  3. signal ends when the ligand dissociates

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binding affinity

strength of the ligand-receptor binding

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binding efficacy

ability to activate a receptor once bound

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dose-response curve

determines potency (how much dose to create an effect), efficacy (max response), and safety margin

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routes of drug administration

  • oral, intravenous, intramuscular, inhalation, transdermal, sublingual, etc

  • must cross BBB - administering closer to brain = more effective

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adaptations to drug presence in body

  • metabolic tolerance: faster breakdown

  • functional tolerance: receptor up/downregulation

  • cross-tolerance: developing tolerance to a full class of chemically similar drugs

  • sensitization

  • withdrawal

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3 ways drugs alter presynaptic processes

  • production

  • release

  • clearance

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production of drugs (presynaptic process)

inhibit enzymes that synthesize NT

  • this prevents NT storage in vesicles

  • eg: blocking DA synthesis enzymes results in less DA

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release of drugs (presynaptic process)

  • blockage of Na+/Ca2+ channels prevents AP-triggered release

    • eg: Novocain, TTX

  • prevents vesicle fusion/release

    • eg: botox blocks ACh → cause paralysis

    • tetanus: blocks inhibitory ACh release → sustained muscle contraction

  • also alters autoreceptor activity

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clearance of drugs (presynaptic process)

  • block reuptake transporters so the NT stays in the cleft longer (more effective)

    • eg: SSRIs

  • inhibits degrading enzyme for prolonged action

    • eg: acetylcholinesterase inhibitors stop the breakdown of ACh

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direct receptor effects of PSP

  • antagonists block receptors

    • eg: curare blocks nicotinic ACh, leading to paralysis (no ACh)

  • agonists activate receptor

    • eg: LSD activates 5-HT receptors in visual cortex

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cellular effects of PSP

  • alter number of receptors (eg: up/down regulation)

  • alter intracellular signalling (eg: gene expression, secondary messengers)

    • eg: lithium chloride is a mood stabilizer, via intracellular changes

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DREADDs

Designer Receptors Exclusively Activated by Designer Drugs

  • selectively activate/inhibit specific neurons for research

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autoreceptors

type of receptor located on a neuron thatbinds to the NT released by that neruon (basically activates itself)

  • triggers a feedback loop to inhibit further release of NT

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function of autoreceptors

  • stimulation decreases NT release (bc autoreceptor senses NT in the cleft already)

  • inhibition increases NT release (bc no longer downregulating)

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caffeine and autoreceptors

  • caffeine blocks adenosine autoreceptors

  • this increases catecholamine release (DA, NE, E) release to create alertness

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NT reuptake

taking NT back into presynaptic terminal via transporters (eg: 5-HT reuptake using SER) to recycle the NT again

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enzymatic degredation

NT is broken down in the synaptic cleft (often wasteful, cannot reuse NT)

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diffusion

NT leaves synapse, gets swept off

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first-gen antipsychotics

  • DA D2R antagonists

  • reduce positive symptoms of schizophrenia, but not very effective for negative symptoms

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second-gen antipsychotics

  • affect both DA and 5-HT receptors

  • effective for both positive and negative symptoms of schizophrenia

  • show that both DA and 5-HT dysregulation results in schizophrenia

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mechanism of antidepressants

prolong the activity of monoamines (DA, NE, 5-HT)

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MAO inhibitor

  • monoamine oxidase

  • prevent enzymes from breaking down monoamines at the synapse

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tricyclics

block reuptake of NE and 5-HT

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SSRIs

block 5-HT reuptake so 5-HT stays in the synapse for longer

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SNRIs

block reuptake of both 5-HT and NE, works similarly to SSRIs

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antidepressants time frame

biological effects begin with hours at the synaspe, but clinical effects take 2-6 weeks

  • this delay is due to autoreceptors, which detect 5-HT in the cleft and reduce its release

  • weeks of using SSRIs lead to autoreceptor downregulation, so there’s less autoreceptors and sustains 5-HT release

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anxiolytics

reduce nervous system activity

  • eg: tranquilizers, depressants

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barbiturates

reduce anxiety, promote sleep, prevent seizures

  • narrow safety margin and high risk of overdose (respiratory depression)

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benzodiazepines

GABA-A receptor agonist, which enhance the inhibitory effects of GABA

  • safer and more specific than barbiturates

  • eg: Xanax, Ativan (Lorazepam)

  • bind to orphan receptor sites on GABA-A

  • no known endogenous ligand

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neurosteroids

modulate different GABA-A sites, which are elevated during stress to calm down the brain

  • eg: allopregnanolone

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source of opiates

opium, from poppy seeds

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examples of opiates

morphine, heroin, oxycodone, fentanyl

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opiates effect on body

potent analgesic and highly addictive

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brain mechanism of opiates

  • bind to metabotropic opioid receptors in:

    • PAG

    • locus coeruleus

    • amygdala

  • produces euphoria and analgesia, reducing arousal

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opiate effect on periaqueductal grey

pain reduction

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opiate effect on locus coeruleus

reduces NE system, regulating arousal

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opiate effect on amygdala

emotional processing, eg: reduced anxiety/fear response

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opiate dependence

chronic use leads to decreased emotional system activity, lowered cortisol, decreased arousal

  • so, body compensates and increases receptor sensitvity

  • withdrawal leads to massive NE release, high pain sensitvity, insomnia, jitteriness

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orphan receptor discovery

  • opioid receptors were first called orphan receptors because they didn’t know any natural ligands that bound to them

  • led to discovery of endogenous opioids (natural analgesics):

    • enkephalins

    • endorphins

    • dynorphins

  • shows that the brain has a natural system for pain relief and reward

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opiate antagonists

  • naloxone and naltrexone block opioid receptors

  • rapidly reverse opioid overdose

  • blockign therewarding effects help treat addiction

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function of naltrexone

used for alcohol use disorder by blocking alcohol-induced euphoria via endogenous opioid release

  • suggests that alcohol plays a role in releasing endogenous opioids to bring pleasure

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source of cannabis

cannabis sativa

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THC

active part of cannabis, gives psychoactive “high”

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CBD

provides medicinal, anxiolytic, non-intoxicating effects

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CB1 receptor location

CNS:

  • substantia nigra, hippocampus, cerebellar cortex, cerebral cortex

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CB1 receptor function

mediates rewarding properties of cannabinoids

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CB2 receptor location

immune system and periphery, eg: microglia

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CB2 receptor function

regulates nociception, reduce cytokine release, decrease immune activation, lower eye pressure in glaucoma

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endogenous ligand in cannabis

anandamide

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nicotine effects on body

increase heart rate/blood pressure, intestinal activity, skeletal muscle contraction, cortical activity

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mechanism of nicotine

agonist at nicotininc ACh receptors

  • receptors on VTA → NaCC, pleasure/reward pathway

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chronic use of nicotine

leads to downregulation of nicotininc ACh receptor, leading to tolerance

  • extremely addictive, 1 cigarette binds 88% of brain’s total incotininc receptors

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mechanism of cocaine

  • block monoamine transporters and prevents DA, NE, 5-HT reuptake

  • strong VTA → NaCC activation for pleasure pathway

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early cocaine effects

tolerance via DA receptor downregulation

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chronic cocaine use effects

sensitization of D1/facilitating pathways, and downregulation of D2/inhibitory pathways in PFC and dorsal striatum

  • leads to decreased executive control and increased habit bias

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risks of cocaine usage

addiction due to habit-formation via glu/LTP, increased impulsivity

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(meth)amphetamine structure

resembles catecholamines, but induce NT release without needing APs

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amphetamine mechanism

  • block reuptake, competing with breakdown enzymes

  • potentiate AP-triggered release to help trigger other NT action

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short-term effects of amphetamines

induced euphoria, stamina

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long-term effects of amphetamines

insomnia, weight loss, psychosis, brain damage (from toxic monoamine levels)

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alcohol effects in low doses

stimulates mesolimbic DA pathway via VTA disinhibition

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alcohol effects on high doses

widespread inhibition, especially in PFC (decreased executive function) and cerebellum (decreased motor coordination)

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mechanism of alcohol

  • activation of GABA-A receptors = inhibitory effects

  • inhibition of NMDA receptors = blocks LTP, impairing memory and learning

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chronic heavy use of alcohol

  • cortical atrophy, white matter lose

  • PFC dysfunction

  • cerebellar degeneration, ataxia (lack of movement)

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recovery from heavy use of alcohol

some brain volume and function can improved with prolonged abstinence, but some deficits may still persist

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psychedelics

alter sensory perception to produce unusual experiences

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serotonergic hallucinogens

LSD, psilocybin, mescaline

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mescaline

serotonergic and noradrenergic hallucinogen

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dissociative drug

ketamine

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muscarine

a cholinergic hallucinogen

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salvia

a hallucinogen acting on kappa-opioid receptor

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ketamine mechanism

blocks NMDAR in PFC, leading to depersonalization

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MDMA

a type of hallucinogenic amphetamine

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chronic use of MDMA

leads to serotonergic neuron damage

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MDMA mechanism

increases 5-HT, DA, oxytocin, empathy, euphoria

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mild severity of substance abuse

2-3 symptoms

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moderate severity of substance abuse

4-5 symptoms

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severe severity of substance abuse

6+ ssymptoms

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moral model of substance abuse

addiction is due to a lack of willower/morals, but this theory is not supported by evidence

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disease model of substance abuse

addiction is an illness, however there is no clear pre-existing pathology