Chapter 5 (L7)

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36 Terms

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Addiction

preoccupation with a drug that is compulsive despite harm

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Tolerance

The brain adapts to the same dosage, while increasing the risks for overdose

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Withdrawal

Symptoms that are the opposite of drug’s effects, occurs as the brain adapts without the drug

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Depressants

Reduce CNS activity, creating a sedative, anxiolytic, and hypnotic effect

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How do alcohol, barbiturates, and Benzodiazepines work in the brain

Enhances GABA and suppresses glutamate, creating a sedation effect

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The GABA-A receptor

Five-part complex with a binding site for GABA, barbiturates, and benzodiazepines; causes extreme risk when multiple are used at once

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What are the three main depressants

alcohol, barbiturates, and Benzodiazepines

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Stimulants

Increase CNS activity, causing arousal, alertness, and elevated mood

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What are the three main stimulants

Cocaine, amphetamines, and nicotine

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how do stimulants work in the brain (cocaine, amphetamines, and nicotine)

Cocaine: Blocks the reuptake of dopamine and serotonin, prolonging their effect at the synapse; Amphetamines: Both increases release and blocks reuptake, creating a bigger flood from multiple directions; Nicotine: Triggers dopamine release in the nucleus accubens to a different route

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Opioids

Mimic endorphnines, causing euphoria but also causes respiratory depression, which is the mechanism behind overdose

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What are the 3 main opioids

OxyContin, fentanyl, and heroin

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What is heroin so problematic

It’s lipid solubility lets it cross the blood-brain barrier, which makes its effects much quicker and more addicting

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Psychedelics

Distort perception rather than creating it; most act on serotonin rceptors

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What are the three main psychedelics

LSD, MDMA, and THC

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MDMA

Blocks reuptake of serotonin, dopamine, and norepinephrine

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THC

act on the brain’s own cannabinoid receptors, controversial on how addictive it is because of mild withdrawal symptoms

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Cannabinoid receptors

Dense in the frontal, hippocampus, and cerebellum, which is what ultimately causes marihuanas psychedelic effects

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The mesolimbic Pathway

Dopamine neurons run from the ventral tegmental area to the nucleus accumbens; With every abused drug, this pathway converges with the procress, causing dopamine to rise and triggering the reward system

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structural changes to brain with drug abuse

More dendrites and synaptic complexities in the nucleus accumbens and prefrontal cortex ultimately drop dopamine activity, decreasing pleasure for normal things in life

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Hypo frontality

Reduced activity in frontal regions that normally support impulse control and behavioral inhibition

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Cue triggered cravings

Environmental cues that are reinforced through drug use, creating a normality associated with the environment and drug; can persist years after withdrawls symptoms leave

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Agonist treatment

Replace the drug with a safer version of itself (Vapes to nicotine patches/gum)

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Antagonist treatment

block the drugs effects at the receptors (ex: naloxone)

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Naloxone

The emergency overdose reversal that is commonly required in schools and public places

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Aversive treatment

Make the drug unpleasant (ex: antabuse paired with alcohol causes rapid sickness)

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agonist drug

mimics or enhances the effect of a neurotransmitter

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Antagonist drug

blocks a transmitter from binding

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conditioned tolerance

tolerance that is tied to the place or circumstance one usually is in

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