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Chapter 4 – Neurochemistry, Neuropsychopharmacology, and Drug Addiction

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two classes of monoamines
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1) catecholamines 2) indolamines
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catecholamines
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consist of dopamine, norepinephrine, and epinephrine
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indolamines
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consist of serotonin
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neuropsychopharmacology
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goal is to identify specific drugs that interact with the nervous system and alter behavior that has been disrupted by disease, injury, or environment factors
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psychoactive drug
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-a chemical substance that changes brain function and results in alterations in perception, mood, consciousness or behavior -any substance that has a psychological of physiological effect when introduced to the body -affects neural transmission by enhancing (agonist) or blocking (antagonist) the actions of natural neurotransmitters in the synapse -affects the way our brain send, receives, and reacts to neural signals -may effect many different neurotransmitters in different ways -utilize the neurobiological pathways typically involved in motivating animals to engage in behaviors necessary for species preservation
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mesolimbic pathway
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reward pathway (that is effected by addictive drugs)
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antagonist
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-block (which keeps normal neurotransmitters or agonists from interacting with the receptor site) or decrease the effects of specific neurotransmitters -blocks the receptor from being activated by other ligands -Specific functions: -block receptor sites -increase the speed of neurotransmitter removal from the synapse -decrease production of neurotransmitters -Ex. Beta-blockers
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what beta-blockers are and what they do
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-antagonist drug -decrease the effects of epinephrine, which is typically experienced during the stress response -this allows the cardiovascular responses during a stressful event to calm down
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agonist drug
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-mimic (initiates normal effects of the receptor) or enhance the effects of specific neurotransmitters -initiates the normal effects of the receptor -Specific functions: -mimic neurotransmitters at the receptor site -stop the removal of neurotransmitters from the synapse -increase the production of neurotransmitters -Ex. Alcohol
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how alcohol is an agonist drug
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-by activating the GABA neurotransmitter system (which is an inhibitory neurotransmitter), it then inhibits the activation of the nervous system
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ligand
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substance that binds to a receptor (including neurotransmitters) and has one of three effects: -agonist -antagonist -inverse antagonist
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inverse agonist
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initiates an effect that is opposite of the normal function
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goal for developing new drugs
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develop a drug that has an affinity for the targeted neurotransmitter’s natural receptors in the brain and also that has a high efficacy (ability to produce desired effects for a targeted condition)
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blind study
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-patients do not know which group they have been assigned to -used to test the efficacy of a drug -efficacy of the actual drug is compared to that of the placebo drug -ex. one group of patients receives the actual medication under the study, but the other group receives chemically inactive placebo as a control (both groups receive pills though, so they are unaware that they are getting different pills)
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double-blind study
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-neither the patients nor the researchers know the group assignments -prevents research outcomes being “influenced” by the placebo effect (if patient knew that they were given a placebo pill) or observe bias
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placebo effect
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a beneficial effect, produced by a placebo drug or treatment, that cannot be attributed to the properties of the placebo itself, and must therefore be due to the patient’s belief in that treatment.
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pharmacokinetics
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-the process by which a drug is absorbed, distributed, metabolized, and eliminated by the body -focuses on what the body does to the drug
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pharmacodynamics
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-focuses on what the drug does to the body – the effects of the drug and the mechanisms of how the drug works -the functional relationship between drugs and their targets
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Things to consider for a drug to be a safe and effective treatment option
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1) Route of administration (dose-response curves) -also, what is the lowest amount of drug necessary to produce optimal responses in the patient? 2) Absorption and Distribution -which areas of the brain and body does the drug effect? 3) Binding -where else does the drug bind to/is it stored as a temporary inactive substance? 4) Inactivation -What metabolic processes make the drug inactive? 5) Excretion -How are the final metabolites (substances produced by metabolism) of the drug eliminated from the body?
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dose-response curve
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-these are established to determine the lowest amount of drug necessary to produce optimal responses -***graph of the relationship between drug doses + the effects -very helpful tool for understanding pharmacodynamics (the functional relationship between drugs and their target) -most drugs have different dose-response curves for different outcome measures -X-axis – size of dose of the drug (potency) -Y-axis – drug efficacy (response)
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ED50 value
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-used to determine the potency and toxicity of a drug -relative potencies between two drugs can also be compared -***a drug that has comparable effects at lower doses is more potent -this value is the effective dose for 50% of people receiving the drug -this value is used to determine the therapeutic index of a drug
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therapeutic index
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-ratio of the dose of a drug that produces toxicity to the dose needed to produce the desired effect -separation between the effective dose of a drug and the toxic dose shown on a dose-response curve -determined by a drug’s ED50 value
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potency
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-a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity. -a drug’s ability to induce a given effect relative to other drugs (related to affinity and efficacy)
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efficacy
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ability of a drug to produce desired effects
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how drugs can effect the manufacturing, transport, and reception of neurotrasnmitters
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1) Synthesis of neurotransmitters (drug increases/decreases synthesis of neurotransmitters) 2) Action potential (increases/decreases the rate of firing or alters threshold for action potential) 3) Degradation of neurotransmitter in vesicles (increase/decrease) 4) Release (increases/decreases release of neurotransmitter) 5) Autoreceptors (increases/decreases binding of neurotransmitter to autoreceptors on presynaptic neuron – increase of binding lowers amount of neurotransmitter in the synapse) 6) Reuptake or degradation (increases/decreases reuptake or degradation of neurotransmitters) 7) Receptors on postsynaptic neuron (activates/blocks receptors or changes the 3 of proteins) 8) Retrograde transmission 9) Metabotropic receptors (affect response of G protein or second messengers)
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autoreceptor
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-a type of receptor located in the membranes of presynaptic nerve cells -affected by drugs in that there is an increased/decreased binding of neurotransmitters to this type of receptor -Serves as part of a negative feedback loop in signal transduction -increase of binding LOWERS the amount of neurotransmitter in the synapse -it is only sensitive to the neurotransmitters or hormones released by the neuron on which this type of receptor sits.
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retrograde transmission
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-when a retrograde messenger is released by a postsynaptic dendrite or cell body, and travels “backwards” across a chemical synapse to bind to the axon terminal of a presynaptic neuron -the same effects of drugs apply to this mechanism too
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metabotropic receptor
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-a type of membrane receptor of eukaryotic cells that acts through a second messenger -these receptors don’t actually have “channels” -when a ligand binds to this receptor, it activates a G-Protein -the G-protein then goes to activate another molecule, which is the second messenger -THEN second messengers travel elsewhere to open other ion channels -second messengers travel all throughout the cell and result in a much wider range of responses -it may be located at the surface of the cell or in vesicles
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metabolic tolerance
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organ systems become more effective at eliminating the drug
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functional tolerance
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target tissue may show altered sensitivity to the drug
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four major drug types
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1) Stimulants 2) Depressants 3) Narcotics 4) Psychedelics
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CNS stimulants
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drugs that facilitate arousal and general activation
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examples of CNS stimulants
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-amphetamine -cocaine -caffeine -nicotine -ecstasy
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CNS depressants
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drugs that suppress arousal and increase relaxation
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examples of CNS depressants
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-alcohol -barbiturates -benzodiazapines
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narcotics/analgesics
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-facilitate pain relief and an altered psychological experience (euphoria, feelings of pleasure, etc.) -also induces sleep
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examples of narcotics/analgesics
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-opiates (ex. hydrocodone, fentanyl) -morphine -codeine -heroin
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hallucinogens
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causes an altered perceptual experience
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psychedelics
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-have wide-reaching effects on thoughts, emotions, and perceptions -subset of hallucinogens -“mind-altering”/”mind-manifesting”
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example of hallucinogens
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-mescaline -LSD -psilocybin
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psychotherapeutics
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drugs that target mental illnesses (ex. depression, schizophrenia, bipolar disorder, etc.)
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the earth’s most widely used psychoactive drug
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caffeine
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caffeine
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-drug where a low dose produces increased energy, efficiency, creativity, self-confidence, alertness, and ability to focus on one’s work
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caffeine’s affect on the brain
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-caffeine (agonist) blocks adenosine receptors -adenosine is an inhibitory neurotransmitter (antagonist) – it inhibits the release of excitatory neurotransmitters) -activation of adenosine receptors makes you sleepy -BUT, when the adenosine receptors are blocked so adenosine can’t bind, there is in overall increase in EXCITATORY neurotransmitters
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most addictive drug
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nicotine
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nicotine
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-causes heightened tension and arousal in non-smokers -causes relaxation and calmness in regular smokers -the active ingredient in tobacco
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nicotine’s effect on the brain
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-activates the nicotinic cholinergic receptors (which is normally activated by acetylcholine) -these receptors are chemical destinations for nicotine molecules and are located in many areas of the brain -once these receptors are activated, sodium channels open to allow the influx of Na+ and depolarization of the neuronal membrane -most nicotine receptors are presynaptic -b/c of this, nicotine alters the release of acetylcholine and alters other neurotransmitter systems where nicotine receptors are located on the presynaptic terminal -nicotine inhaled from three cigarettes will occupy a majority of the brain’s nicotinic cholinergic receptors
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nicotine’s effect on the PNS (autonomic nervous system)
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-nicotine receptors are also found in the PNS -once the receptors are activated, the adrenal gland releases epinephrine and norepinephrine -also leads to increased heart rate and elevated blood pressure -also has a stimulating effect on the metabolic rate of humans
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part of the body that releases epinephrine
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adrenal glands (which are on top of the kidneys)
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part of the brain that releases norepinephrine
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locus coeruleus
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locus coeruleus
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-a brainstem area involved in arousal, and in sympathetic nerves -involved in increased vigilance, focused attention, and enhanced energy
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why nicotine is so addicting
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-nicotine delivery is reinforcing -high-affinity nicotinic receptors leads to increased firing of dopamine neurons and the release of dopamine from the nucleus accumbens
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nucleus accumbens
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brain area known for its role in reward and motivational responses
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dopamine
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neurotransmitter involved in reward, pleasure, and movement
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parts of the brain that release dopamine
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-***substantia nigra -***ventral tegmental area -nucleus accumbens and prefrontal cortex
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ventral tegmental area
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part of the brain involved in movement, reward systems, and increased vigilance
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serotonin
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neurotransmitter involved in: -mood regulation -sleep/wake cycles -temperature regulations -sexual activity -aggression -synthesized from the dietary amino acid called tryptophan
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part of the brain that releases serotonin
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raphe nuclei
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cocaine
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-a stimulant that fights against the feelings of hunger and fatigue -causes intense euphoria, a sense of increased energy, heightened mental alertness, and feelings of competence and power.
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crack
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a mixture of cocaine hydrochloride with baking soda
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cocaine’s effect on the brain
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-blocks the re-uptake of dopamine, norepinephrine, and serotonin -specifically, blocks re-uptake transporters by binding to them -b/c of this, the neurotransmitters stay in the synapse for longer (ex. makes dopamine more available to act in the synapse – longer feelings of pleasure) -dopamine will just continue binding to receptors on the postsynaptic neuron on the receiving neuron as long as it remains in the synapse -SHORT-TERM – effects dopamine in the reward system (effects of intense euphoria is short-lived because the dopamine quickly “floats”/diffuses away from the synapse) -LONG-TERM – overstimulation of receiving neuron→ causes receiving neuron to “adjust” itself to a moderate response -less dopamine receptors – less response to cocaine/dopamine -one can’t be as happy from reward as they used to
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re-uptake transporter
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proteins that act as transporters for neurotransmitter re-uptake back into the presynaptic membrane
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amphetamine
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-drug that boost alertness and produce a sense of well-being (ex. adderall) -also, confidence and diminished fatigue – similar to cocaine -“uppers” -can be used for treatment of ADHD and narcolepsy (disorder that causes overwhelming drowsiness)
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MDMA (ecstasy)
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-boost alertness -diminished fatigue -enhanced sensory perception -a desire for social interaction (can relieve social anxiety) -a type of amphetamine
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amphetamine’s effect on the brain
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-catecholamine agonist (blocks catecholamine re-uptake) -also enhances the release of catecholamine (specifically dopamine) from presynaptic neurons -aka increased release of dopamine
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MDMA’s (ecstasy’s) effect on the brain
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-affects more than one neurotransmitter system -monoamine agonist -leads tot he release of serotonin and dopamine -can result in depression, anxiety, sleep-disruptions, cognitive deficits, involuntary teeth clenching, etc.
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most abused drug
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-alcohol -since it is legal in most countries, people do not see it as a drug
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alcohol
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-LOW DOSES – -improves mood -causes drowsiness -increased self-confidence -impaired judgement and muscle coordination -HIGHER DOSES – -further cognitive and reflexive impairment -acute alcohol poisoning -The CNS slows down and leads to extreme confusion and disorientation (and slow/irregular breathing patterns)
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alcohol’s effect on the brain
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-increases GABA activity by binding to allosteric receptors (GABA is an inhibitory neurotransmitter) -by enhancing the effects of GABA, it is enhances it’s inhibitory effects -***this is what causes the sedative-like effects of alcohol (drowsiness and a sense of relaxation) -decrease Glutamate activity by binding to it’s receptors (Glutamate is an excitatory neurotransmitter) -receptors are blocked so glutamate can’t bind -by decreasing the activity of Glutamate, it decreases it’s excitatory effects -also effects the dopaminergic system (during alcohol withdrawal, there is a decrease in the release of dopamine) -this can lead to anhedonia
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GABA
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-main inhibitory neurotransmitter -“quiets” communication between neurons -inhibition of this neurotransmitter can lead to seizures and death
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glutamate
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-main excitatory neurotransmitter –> makes the next neuron more likely to transmit a signal -workhouse transmitter for excitatory signaling pathways in the brain -involved in brain plasticity mechanisms (ex. synaptogenesis – creation of synapses) when neural networks are being formed -strengthens existing synapses (which facilitates both learning and memory) -activate NMDA receptors and AMPA receptors
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function of neurotransmitters other than glutamate and GABA
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modulate/control glutamate and GABA
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anhedonia
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-the inability to feel pleasure -result of decreased activity in the brain’s reward center (esp. during withdrawal)
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Areas of the brain that alcohol effects
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CEREBELLUM – this is the correction center of the brain and when alcohol effects the correction center, that’s what results in being off-balance, dizziness, etc. VENTRAL STRIATUM AND PREFRONTAL CORTEX – when the responsibility of these areas are inhibited, you engage in more impulsive behavior HIPPOCAMPUS – when this area is affected, it results in a loss in memory
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function of the cerebellum
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-movement -balance -complex motor function
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function of the ventral striatum and prefrontal cortex
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-brain’s reward system -regulates impulsive behavior
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function of the hippocampus
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-stores memory
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benzodiazepines and barbiturates
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-function similarly to alcohol except that they bind to different receptors
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opiate’s effect on the brain
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-bind to opioid receptors (ex. mu, delta, and kappa receptors) -the peptide called enkephalin activates the opioid receptors (ex. endorphins)
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endorphins
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-hormones that are secreted within the brain/nervous system (endogenous) -endogenous variation of morphine -interact with the dopamine system by decreasing the inhibitory effects of GABA–> which leads to an increased secretion of dopamine -***involved in pain and reward processing
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heroin
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drug that causes an intense feeling of euphoria and the inability to feel pain
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heroin’s effect on the brain
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-when this drug enters the brain, it is converted into morphine -binds to opioid receptors in the reward center -decrease production of GABA – results increase in production of dopamine (causes the feeling of euphoria) -SHORT TERM effects – 1) Mesolimbic System (reward system) – causes huge feeling of euphoria -area that leads to addiction 2) Brainstem and Spinal Cord (pain pathway) – causes Analgesia–> this is what leads to death – breathing and heart function will slow down (this is the result of heroin interacting with the brainstem) -area that causes withdrawal symptoms -LONG TERM effects – 1) changes white and grey matter (because of low blood circulation) 2) the prefrontal cortex is affected – which is responsible for impulse control and reward -***this part of the brain being affected is what leads to tolerance/dependence
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analgesia
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inability to feel pain
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dependence
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what causes the withdrawal symptoms when you stop taking a drug
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how dependence occurs when taking heroin
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-when heroin is converted to morphine, the morphine mimics the brain’s natural endorphins -Since the body can’t distinguish between morphine and the natural endorphins AND because the brain has been re-wired to function with heroin – the brain thinks it’s producing a normal amount of endorphins (but that’s just the heroin/morphine) -As a result, the body stops producing natural endorphins and becomes dependent on the heroin
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fentanyl
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-heroin’s synthetic and much stronger cousin -enters the brain much more quickly than heroin, reaching and binding to its receptors before standard morphine -causes a very quick and intense sense of euphoria
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overdose of heroin
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-since heroin is a CNS depressant, it slows down heart rate and breathing
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Narcan
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-blocks the effects of opioids -reverses the effects of too many opioids binding to their receptors -but this is only a temporary solution
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LSD
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-altered emotions -enhanced introspection -sense of being in a dreamlike state -hallucinations -illusions -alterations in perception of time and space -synesthesia -not physiologically addictive -doesn’t act on the mesolimbic pathway -was once/is used for treatment of mental illnesses (b/c it alters thoughts and perceptual experiences)
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synesthesia
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-when someone’s senses are blended -ex. someone that sees music or hears colors
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LSD’s effect on the brain
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-widespread activity within the brain -enhances the effects of the serotonin system (system that maintains mood balance) -increases disorder/disorganization in the brain -areas of the brain that don’t normally communicate with each other now communicate with each other
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short term effects of LSD
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-neuroplasticity -synesthesia -rapidly shifting emotions ranging from terror and despair to joy and gratitude -experience many emotions at once -sense of connectedness with people and universe (ego dissolution) -increase in creative/associate thinking
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long term effects of LSD
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1) neuroplasticity (***recreational use/abuse***) -can trigger or worsen underlying psychological patterns -one-time use can cause irreversible changes in the user’s mental state (ex. emotional problems or emergence of psychosis/psychotic symptoms) 2) neuroplasticity (***clinical setting***) -therapeutic potential (ex. terminal-illness related anxiety, depression, PTSD, etc.)
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Marijuana
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drug that has diverse psychological effects: -altered sensations -increased appetite -euphoria -disinhibition -relaxation -impaired memory and motor performance -primary active ingredient = THC
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cannabinoid receptors
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-receptors activated by THC -concentrated in the basal ganglia, substantia nigra, cerebellum, hippocampus, and cerebral cortex – which are all involved in coordination, memory, and locomotor activity -can inhibit many neurotransmitters – ex. dopamine, norepinephrine, acetylcholine, glutamate, and GABA -Anandamide (an endogenous substance that mimics marijuana) can also bind to cannabinoid receptors
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why marijuana is hard to study
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-no standardized chemical components; harder to get in the lab than cocaine -controversy whether it constitutes a “drug of abuse” – the evidence is mixed (ex. gateway drug) -doesn’t appear to work in the same systems as many other drugs – the body has “endocannabinoid receptors”
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oxytocin + vasopressin
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-peptide hormones involved in prosocial behaviors (ex. trust, empathy, and altruism) -both released by the posterior pituitary gland
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acetylcholine
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-neurotransmitter involved in memory and cognition in the CNS -motor and parasympathetic functions in the PNS
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nitric oxide
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-neurotransmitter released by postsynaptic neurons to affect the axons of presynaptic neuron –> ***retrograde transmission*** (how a neurotransmitter travels “backwards”) -also, a gas that can act as a retrograde neurotransmitter –> can readily pass through the cell membrane to modulate neurotransmission
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drug dependence
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-how the brain changes in response to continued use of a drug -then leads to the need for the drug to maintain physiological functions
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tolerance
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-when increasingly larger doses of a drug are needed to achieve the same desired effect
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drug sensitization
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an INCREASE in drug efficiency on repeated use
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what caffeine does in the brain
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-involved with adenosine receptors -normally, activation of these receptors by adenosine slows down neural activity and makes you sleepy (as adenosine builds up as a buy-product of active neurons) -however, when this drug binds to the adenosine receptors, it blocks access of the adenosine to the receptors–> so neural activity speeds up