ligand (naturally in body) normally produced by the body that binds a receptor (neurotransmitters)
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define exogenous ligand
ligand introduced into the body (drugs)
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Define agonist
ligand that activates receptors
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Define antagonist
ligand that has no effect on its own but blocks binding of exogenous ligand (neurotransmitter receptor blocker)
\ \-competes w/ endogenous ligand
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Define non-competitive ligand
binds to site other than endogenous ligand binding site & modulates receptor activity (non-competitive inotropic neurotransmitter receptor blocker)
\ \-have agonist or antagonist properties
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Define affinity
The strength of attraction between drug and receptor at any drug concentration concentration or firmness w/ which drug binds to receptor
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Define efficacy
(intrinsic activity) is the ability of a drug to illicit a pharmacological response (physiological) when interaction occurs w/ a receptor (relationship between response & occupancy of receptor)
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define binding affinity
"strength" of binding between ligand and receptor
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A higher concentration for a low or high affinity drug/ligand?
LOW affinity drug/ligand
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A lower concentration for a low or high affinity drug/ligand?
HIGH affinity drug/ligand
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if high & low affinity are both at equal concentration...?
higher affinity drug binds to more receptors than low affinity
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Kd (Affinity constant)
Dissociation constant. On graph it is the ligand concentration at which 1/2 receptors bound
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low Kd = ___ affinity & why?
high affinity cuz need less concentration of ligand
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high Kd = ______ affinity & why?
low affinity cuz need higher concentration to reach 100% binding
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Define efficacy simpler def
max effect a drug can produce regardless of dose; ability of drug-bound receptor to produce a full response
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EC50 stands for?
Concentration of the drug required to produces 50% of maximal effect; measures efficacy
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a full agonist has a _____ efficacy & produces _____
response while occupying a relatively low proportion of receptors
a full agonist has a high efficacy & produces a full response while occupying a relatively low proportion of receptors
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a ____ agonist has ___ efficacy then a ____ agonist
a partial agonist has lower efficacy than a full agonist
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explain selectivity of a drug
\-common for some drugs to bind to many receptor types or bind to several members of same neurotransmitter receptor class
\-less common for drugs to selectivity bind to 1 or 2 receptors
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Why are relative affinities of a drug at diff receptors exploited?
to adjust the dose down so only highest affinity receptors are bound & activated ("targeted") minimize side effects
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Evaluate dose response curves.
linear segment starts low, increases then levels off as it approaches max value (sigmoidal relationship) between dose & effect
\-structurally similar to morphine (convert to morphine in brain) \n -produces euphoria, highly addictive
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Heroin mechanism \n -opioids
\-(agonist) acts on μ-opioid receptors in VTA (ventral tegmental area) & nucleus accumbens, parts of mesocorticolimbic DA pathway involved in reward/reinforcement \n \n -activates μ-opioid receptors hyperpolarizes (Cl- in) GABAergic neurons & inhibits GABA release onto DA neurons=increase DA in VTA (inhibits inhibition)
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Nalaxone
opioid antagonist that rapidly reverses overdose
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Cannabinoids: cannabis effectiveness
therapeutic uses: anxiety, pain (chronic>acute), chemotherapy side effects, glaucoma, epilepsy, MS (multiple sclerosis), spasticity
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Cannabinoids: cannabis side effects
feelings of relaxation, hunger, sometimes paranoia
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Cannabinoids: cannabis mechanism
agonist at CB1 & CB2 cannabinoid receptors (GPCRs)
Increase DA & NE, levels at the synapse (by acting w/in axon terminals) and decreasing reuptake \n \n -DAT reverse transport send NT out instead of back
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Stimulants: Cocaine
creates euphoric state, increases endurance
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Stimulants: Cocaine side effects
long term use lead to psychosis, neurodegeneration, altered brain activity
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Stimulants: cocaine mechanism
\-DAT (transporter) antagonist \n -blocks monoamine NT reuptake (especially DA)
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Empathogen: MDMA
promising treatment for PTSD
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Empathogen: MDMA side effects
\-social, empathic, visual, euphoric (pos) \n -neurotoxic to thermoregulatory systems (risk of hyperthermia; neg)
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Empathogen: MDMA mechanism
\-agonist at 5-HT2a receptors, 5-HT1B & SERT (transporter) \n -inc release of DA, NE, 5-HT, oxytocin
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psychedelics: LSD (lysergic acid diethylamide) side effect
\-distorts visual perception, induces feeling of creativity \n -may cause long term changes in mood/personality
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psychedelics: LSD mechanism
agonist at 5-HT2a receptor which is highly expressed in visual cortex
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Dissociative: PCP and Ketamine
developed as anesthetics in 1960s \n -used in vet clinics & children in hospitals
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Dissociative: PCP and ketamine side effects
produce dreamlike state, detachment from reality, separation between consciousness & sensory inputs