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Psych 115 Midterm 2 Exam Questions and 100% Correct Answers

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Drug action cellular/molecular changes that occur as a result of a drug binding to a receptor Drug effect widespread physiological or psychological changes as a result of the drug action Potential drug effects on neuronal conduction and synaptic transmission conduction: local - block na+ channels to prevent action potentials Storage of nt in vesicles Release of nt (exocytosis) Reuptake (interfere with transporters) Nt degradation (synaptic enzymes) Binding affinity the degree of chemical attraction between a ligand and a receptor (how much does this drug really want to bind) Efficacy/intrinsic activity the ability of a bound ligand to activate the receptor (likelihood of biological response after binding) How is drug potency proportional to affinity and efficacy? the higher the ligand's affinity, the more drug will be bound to receptors at any given time because they stay bound for longer (requires less drug to elicit the same effect as a drug with lower binding affinity). Greater biological response with greater potency and higher affinity. (pharmacodynamics studies these relationships) How can a drug have high affinity but no efficacy? drug antagonists - bind to receptor but do not elicit a response and can block agonist or inverse agonist activity How can the drc and ed50 tell us relative drug potencies? the less of a dose a drug requires to elicit the same ed50 (dose at which drug shows half its maximal effect), the more potent the drug How does the drc (dose-response curve) and ld50 (median lethal dose) tell us about the safety of a given drug? the closer the median effective dose is to the median lethal or toxic dose, the more dangerous the drug is (pay attention to the gap, the therapeutic index) - we want a wide therapeutic index, i.e., you can take pretty far beyond what is effective for a drug and not die

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Institution
PSYC 115
Course
PSYC 115

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Psych 115 Midterm 2 Exam Questions
and 100% Correct Answers
Drug action ✅cellular/molecular changes that occur as a result of a drug binding to a
receptor

Drug effect ✅widespread physiological or psychological changes as a result of the
drug action

Potential drug effects on neuronal conduction and synaptic transmission ✅conduction:
local - block na+ channels to prevent action potentials
Storage of nt in vesicles
Release of nt (exocytosis)
Reuptake (interfere with transporters)
Nt degradation (synaptic enzymes)

Binding affinity ✅the degree of chemical attraction between a ligand and a receptor
(how much does this drug really want to bind)

Efficacy/intrinsic activity ✅the ability of a bound ligand to activate the receptor
(likelihood of biological response after binding)

How is drug potency proportional to affinity and efficacy? ✅the higher the ligand's
affinity, the more drug will be bound to receptors at any given time because they stay
bound for longer (requires less drug to elicit the same effect as a drug with lower
binding affinity). Greater biological response with greater potency and higher affinity.
(pharmacodynamics studies these relationships)

How can a drug have high affinity but no efficacy? ✅drug antagonists - bind to receptor
but do not elicit a response and can block agonist or inverse agonist activity

How can the drc and ed50 tell us relative drug potencies? ✅the less of a dose a drug
requires to elicit the same ed50 (dose at which drug shows half its maximal effect), the
more potent the drug

How does the drc (dose-response curve) and ld50 (median lethal dose) tell us about the
safety of a given drug? ✅the closer the median effective dose is to the median lethal or
toxic dose, the more dangerous the drug is (pay attention to the gap, the therapeutic
index) -> we want a wide therapeutic index, i.e., you can take pretty far beyond what is
effective for a drug and not die

, Frequency ✅number of cycles per second of vibration (hz), perceived as pitch (higher
frequency means more waves in a second)

Sound amplitude ✅the height of a sound wave, how high or low determines loudness

Compression and expansion of sound waves ✅compression corresponds to the peaks
of waves and expansion corresponds to troughs of sound waves

Pinna ✅your earlobe, part of the outer ear, funnels sound inside

Ear canal ✅part of outer ear that looks like a tube and carries sound to middle ear

Tympanic membrane ✅eardrum, where sound waves get transformed into physical
vibrations

Ossicles ✅malleus (hammer), incus (anvil), stapes (stirrup). Stirrup pushes on oval
window (which connects to inner ear ), stapes taps on the oval window to transmit
vibrations. All ossicles responsible for transmitting sound vibrations from the eardrum,
but ultimately the stapes is what tells the oval window to vibrate to the inner ear

Inner ear ✅location of sound transduction from vibrations to neural signals

Cochlea ✅fluid filled structure within the inner ear that holds primary auditory sensory
cells, with base close to oval window and apex in the center of the spiral. Divided into 3
parallel canals

Organ of corti ✅sits in the middle of the cochlea and takes fluid motion and makes it
~neural~. Composed of hair cells (the auditory sensory cells), supporting cells, and the
basilar membrane

Basilar membrane ✅located in the organ of corti within the cochlea and vibrates in
response to sound. Tuned for frequency so base is thicker where it vibrates the most at
high frequencies and the apex is thinner so it vibrates at low frequencies

Hair cells of the organ of corti ✅inner hair cells for sensation (afferent to the brain after
transducing sound), outer hair cells for modulating incoming sound (equal afferent and
efferent signaling), a also embedded in tectorial membrane, a jelly-like membrane

Process of sound transduction via hair cells ✅stereocilia (the wavy hair part of the cell)
bend when sound waves travel through -> tip links connect between top of stereocilia
and cap of ion channels on neighboring stereocilia -> tip links stretch with sound and
pull open ion channels -> hair cell depolarizes -> calcium channels open up at base of
cell, ca ions come inside -> nt releases from base —> triggers aps in afferent nerve
cells

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