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Addiction
preoccupation with a drug that is compulsive despite harm
Tolerance
The brain adapts to the same dosage, while increasing the risks for overdose
Withdrawal
Symptoms that are the opposite of drug’s effects, occurs as the brain adapts without the drug
Depressants
Reduce CNS activity, creating a sedative, anxiolytic, and hypnotic effect
How do alcohol, barbiturates, and Benzodiazepines work in the brain
Enhances GABA and suppresses glutamate, creating a sedation effect
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
What are the three main depressants
alcohol, barbiturates, and Benzodiazepines
Stimulants
Increase CNS activity, causing arousal, alertness, and elevated mood
What are the three main stimulants
Cocaine, amphetamines, and nicotine
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
Opioids
Mimic endorphnines, causing euphoria but also causes respiratory depression, which is the mechanism behind overdose
What are the 3 main opioids
OxyContin, fentanyl, and heroin
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
Psychedelics
Distort perception rather than creating it; most act on serotonin rceptors
What are the three main psychedelics
LSD, MDMA, and THC
MDMA
Blocks reuptake of serotonin, dopamine, and norepinephrine
THC
act on the brain’s own cannabinoid receptors, controversial on how addictive it is because of mild withdrawal symptoms
Cannabinoid receptors
Dense in the frontal, hippocampus, and cerebellum, which is what ultimately causes marihuanas psychedelic effects
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
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
Hypo frontality
Reduced activity in frontal regions that normally support impulse control and behavioral inhibition
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
Agonist treatment
Replace the drug with a safer version of itself (Vapes to nicotine patches/gum)
Antagonist treatment
block the drugs effects at the receptors (ex: naloxone)
Naloxone
The emergency overdose reversal that is commonly required in schools and public places
Aversive treatment
Make the drug unpleasant (ex: antabuse paired with alcohol causes rapid sickness)
agonist drug
mimics or enhances the effect of a neurotransmitter
Antagonist drug
blocks a transmitter from binding
conditioned tolerance
tolerance that is tied to the place or circumstance one usually is in