test 2 Flashcards
pharmacokinetics
what the body does to drugs
absorption, disruption, metabolism, excretion
pharmacodynamics
what drugs go to body/behavior
site and mechanism of action
neurotransmitter vs. neuromodulator
neurotransmitter
-act by directly transmitting signals between neurons
-released in localized manner at synapse
-specifically influences activity of target neurons
-has shorter-lasting effect
neuromodulators
-act by modifying response of neurons to other neurotransmitters
-released in diffuse manner throughout brain
-modulates overall activity of neural circuits
-generally has longer-lasting effect
ionotropic vs metabotropic
ionotropic
- direct; NT opens channel
- effect is immediate but short-lived
- affects polarity
- 1 chemical meesenger NT
metabotropic
- indirect: activates cascade of events
- effect is variable but generally longer
- primary NM + internal 2nd messenger
- broader effects on metabolism
agonist
add NT or precursor
induce release
block reuptake
block metabolic breakdown
mimetic (direct agonist)
antagonist
prevent synthesis
deplete release
stimulate autoreceptors; inhibit release
direct/indirect
principles of drug action
- drugs have multiple effects (central vs peripheral)
- receptor distribution often determines selectivity of drug action
- drugs modify (do not create) cellular processes (agonist vs antagonist)
- any agonist can become antagonist (ex increasing dose)
non-competitive inhibition
change shape of enzyme so it cannot bind to substrate
ex. lithium
direct antagonist
interferes with active site of enzyme so substrate cannot bind (like an outlet cover)
ex. naloxone
competitive agonist (mimetic)
interact directly with the receptor and activate it, producing the desired effect
ex. morphine
indirect agonist
do not directly activate the receptor but enhance its response to the natural molecule work by increasing the availability or effectiveness of the natural molecule
ex. cocaine
short-term vs long-term
short-term and reversible act as agonists ex. donepezil for alzheimer’s disease
long-term and irreversible are initially agonistic but then become antagonistic and render cell refractory ex. DFP
functions of ACh (acetylcholine)
in PNS inhibitory (slows HR)
in CNS general arousal (being awake), learning and memory
functions of DA (dopamine)
motor regulation/movement, pleasure/reinforcement
functions of NE/NA (norepinephrine/noradrenaline)
selective attention, stress response (fight/flight)
functions of 5-HT (serotonin)
regulation of emotion and mood
control of appetitive
firing increase during repetitive motor responding (walking, grooming)
functions of GLUT (glutamate)
principle excitatory NT in brain
plays major role in learning and memory
functions of GABA
principle inhibitory NT in brain
known as “calming” NT
involved in sleep, relaxation, anxiety regulation and muscle function
functions of GLY (glycine)
principle inhibitory NT in spinal cord
functions of endocannabinoids (lipids)
natural anxiolytic
reward
appetite stimulant
suggested functions of opioid peptides
natural analgesic: released during fighting, mating
involved in mediation of reward (with DA)
subtypes for cholinergic receptors
nicotinic: ionotropic
muscarinic: metabotropic receptors
adrenergic receptors
alpha: higher affinity for NE than E, vasoconstriction
beta: higher affinity for E than NE, vasodilation
serotonin receptor subtypes
5-HT3 is ionotropic
others are metabotropic
5-HT often acts as inhibitory neuromodulator: diffuse effect
glutamatergic receptor subtypes
ionotropic: NMBA receptor (special role in memory), AMPA receptor, kainate receptor
metabotropic GLUT recpetor
GABA receptor subtypes
GABA-A: ionotropic - linked to Cl- channel
GABA-B: metabotropic - linked to K+ channel
endogenous opioid receptor subtypes
all metabotropic and inhibitory
endorphins: bind to Mu
enkephalins: bind to Delta
dynorphins: bind to Kappa
presynaptic heteroreceptors vs autoreceptors
autoreceptors are activated by NT released by same neuron
heteroreceptors are activated by NT released by another neuron
presynaptic inhibition
suppresses the release of neurotransmitters from axons by binding chemical messengers to inhibitory receptors at transmitter release sites on the axon
ex. GABA
biological base for schizophrenia. evidence? specific drug treatment? action of these drugs?
hyperactive DA mesolimbic pathway (pos symptoms) underactive DA mesocortical pathway (neg/cog symptoms)
evidence that dysregulation of serotonin and glutamate also involved
DA antagonists only treat positive symptoms
-abilify - partial DA agonist has mixed agonist-antagonist prop.
biological base for ADHD. evidence? specific drug treatment? action of these drugs?
impairment of both DA and NE NTs which mediate exec functions including attention, cognitive control of behavior
ritalin/adderall DA/NE agonists (stimulants)
biological base for BPD. evidence? specific drug treatment? action of drug?
maybe manic phase assoc. with over-active NE think this from high MHPG (another NE by-product) in urine/blood
historically, lithium is effective “mood stabilizer” in direct NE antagonist
biological base for MDD. evidence? specific drug treatment? drug action?
genetic/environment interaction
monoamine hypothesis (low NE and/or 5-HT)
revised monoamine hypothesis (focus on receptor regulation rather than NT level
must be more to it than chemical imbalance if atypical meds don’t affect monoamines
SSRIs, 5-HT and NE reuptake inhibitors
neurogenic hypothesis of depression and evidence consistent with it
stress inhibits adult neurogenesis and increases vulnerability
evidence: hippocampal volume in depressives/PTSD patients is reduced
what does C4 gene synaptic pruning have to do with schizophrenia? can this line of research explain some things we know to be true?
C4 gene accelerates/intensifies pruning
shows that pruning is delicate process that we don’t really understand
mechanism of function: nicotine
agonist
mechanism of function: methanphetamine
agonist- induces DA release (and block reuptake)
mechanism of function: cocaine
agonist - blocks reuptake (induces DA release)
mechanism of function: ritalin+adderall
DA/NE agonists - stimulants - induce release
mechanism of function: lithium
indirect NE antagonist
mechanism of function: valporate
GABA agonist (inhibits breakdown)
mechanism of function: benzos, alcohol, barbiturates
indirect GABA-A agonists
