Chapter #4: How do drugs affect our behavior? Flashcards
Agonist
an endogenous ligand (a naturally occurring molecule such as a transmitter that binds to the receptor) that activates its cognate receptor
Receptor Agonist
an exogenous ligand (a drug or toxin) that resembles the endogenous ligand and is capable of binding to the receptor and activating it
Competitive Antagonist
substances that bind to the receptor, but do not activate it; they block agonists from binding to the receptors
Noncompetitive Antagonist
agonist or antagonist drugs that bind to target receptors at a site that is different from where the endogenous ligand binds
if a particular drug has low affinity for a receptor…
-it will quickly uncouple from the receptor
-to bind half the receptors at any given time, a higher concentration of the drug is needed
if a drug has a high affinity for a receptor…
-the two will stay together for a longer time
-a lower concentration of drug will be sufficient to bind half the receptors
if equal concentrations of the two drugs are present…
-the high-affinity drugs will be bound to more receptors at any given time
-if the drugs have an equivalent effect on the receptors, then the higher-affinity drug will be more potent
Effective Dose (ED50)
the dose at which the drug shows half of its maximal effect
How can we assess the relative potencies of 2 drugs?
by comparing their ED50 values, whichever drug has effects at lower doses is more potent than the other (whichever drug is left on the x-axis)
How can we compare drug efficacies?
by evaluating maximal responses rather than dose, whichever drug goes higher up on the y axis has a much greater maximal effect
Partial Agonist/Antagonist
a drug of only moderate efficacy
Phencyclidine
-PCP or Angel Dust
-NMDA receptor antagonist
-Mind-altering drug that may lead to hallucinations
-PCP is a non-competitive NMDA antagonist, while PCP is bound, no other ligand can activate the NMDA receptor
NMDA Antagonists
-Loss of responsiveness (not consciousness)
-Loss of sense of self/identity
-Dissociation
-Psychotic thoughts
-Sensory aberrations
-Aggression and agitation (rare)
-relation to Susannah’s psychosis
Another drug with similar effects to PCP
Ketamine (special K) – also a NMDA antagonist
Psychotomimetic
elicit psychotic symptoms in people
NMDA & Schizophrenia
Because NMDA receptor antagonists, such as PCP, are psychotomimetic, it may be reasonable to assume that NMDA receptors are naturally sub-functional in people with psychotic disorders
GABA A Receptor
-GABA A receptor is a Cl- channel
-Has multiple binding sites for other substances
-These are involved in allosteric regulation/modulation
-inhibitory
Positive Allosteric Modulators
-Targeting different sites on the receptor
-Ex. AmBien used for sleeping
-Clonazepam
-Diazepam → used as a seizure medication to enhance GABA A receptor
Ethanol
-beverage alcohol
-Calming, anxiolytic and sedative/hypnotic effects of alcohol depend upon GABA-A receptor positive modulation
Dark Side of Positive Modulators
-Drugs violate homeostasis
-Receptor desensitization
o Fewer functional receptors = less drug-induced
inhibition
o Doesn’t always involve fewer receptors…
-Tolerance
Norepinephrine/Dopamine & ADHD
-All medications for ADHD influence the norepinephrine (NE) and dopamine (DA) systems
-Some block NE and/or DA reuptake via the transporter (Ritalin, Focalin, Strattera)
-Some cause NE and/or DA release (Adderall, Dexedrine, Vyvanse)
Selective Serotonin Reuptake Inhibitors examples
fluoxetine [Prozac], paroxetine [Paxil],
citalopram [Celexa], sertraline [Zoloft]
and fluvoxamine[Luvox]
What do SSRIs do?
These drugs enable serotonin to stay in
the synapse longer
Opioids
-Morphine, heroin, oxycodone, fentanyl
→ Analgesic and addictive properties
-Delta, kappa, mu opioid receptors
-Endogenous opioids = enkephalins, endorphins, dynorphins
-Naloxone and naltrexone
-Indirectly increases dopamine release
Nicotine
-Stimulant
-Nicotinic acetylcholine receptors (nACh)
-Increases dopamine release, may also affect other
neurotransmitters (e.g. norepinephrine)
Cocaine
-Stimulant
-Dopamine transporter (DAT)
-Prevents dopamine reuptake to increase dopamine levels in synaptic cleft (also norepinephrine,
serotonin)
Amphetamine/Methamphetamine
-Stimulant
1. Enters presynaptic terminal via DAT
2. Packaged into vesicles in place of dopamine
3. Excess dopamine pumped out of cell via DAT
4. Increases dopamine release into synaptic cleft (also norepinephrine, serotonin)
Alcohol
-Initial stimulant, prolonged depressant, sedative
-Enhances GABAA receptor activity
-Reduces NMDA receptor activity
-Low dose alcohol stimulates dopamine
release
