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126 Cards in this Set

  • Front
  • Back
Santiago Ramon y Cajal
dendritic spines
Henry Dale, Otto Loewi
mid 1930's, synaptic transmission
1) docking 2) priming 3) exocytosis (VDCC) 4) endocytosis 5) recycle
SNARE proteins
SNAP-35, syntaxin, synaptobrevin interrupted by botulinium neurotoxin
Synaptobrevin interrupted by tetanus toxin
alpha-latroxin- neurexin 1, acH at NMJ
vesicular NT transporters- require proton-ATPase
plasma membrane NT transporters- require Na+/H+/K+ transport relying on Na+ gradient
radioligand binding
H3, C14, I125
nonspecific binding
binding of ligand to things other than receptors, no limit to these places
specific binding
binding of ligand just to receptors; total-nonspecific binding
dissociation constant, the probability of it dissociating
100% of ligand bound
when 50% of drug specifically bound
more than one direction; u-shaped curve (ex: valium)
excitatory neurons
pyramidal cells in cortex and hippocampus, usually spiny
inhibitory neurons
inhibitory interneurons, usually non-spiny, Factor I - GABA
Ca++, Na+
Kd= 3-8nM (high potency)
can desensitize
Kd= 200nM (low potency)
AMPA agonists
glutamate and AMPA
AMPA antagonists
competitive: CNQX, NBQX
noncompetitive: GYKI53655
NMDA agonists
glutamate, NMDA
NMDA antagonists
competitive: APV
non-competitive: MK-801, PCP, ketamine
GABA-A agonists and inverse agonists
competitive: GABA, muscimol
non-competitive: benzodiazepines (i.e. diazepam, lorazepam)
inverse agonists: beta-carboline
GABA-A antagonists
competitive: bicuculline
non-competitive: picrotoxin, zinc, flumazenil
GABA-A sites in channel
barbiturates (i.e. pentobarbital- increase channel open time), steroid (anasthetics, anxiogenics), ethanol (increase channel open time)
GABA-B agonists
GABA, baclofen
GABA-B antagonists
necessary cofactor to NMDA
synthesized from glucose via serine
flux Cl-
antagonist: strychnine, picrotoxin
4 types of signal transduction
1) gated ion channels
2) g-protein coupled receptors
3) tyrosine kinases (neurotrophic factors)
4) steroid hormones- translocate and change gene expression
G-protein coupled receptor types
Gs= activate adenylyl cyclase, toxin is cholera
Gi/o= inhibits adenylyl cyclase and K+ channels, toxin pertussis toxin
Gq= phospholipase C, no toxin activates
Gt= transducin (photoreceptors)
Gg= gustducin (taste cells)
cAMP pathway
ligand binds to receptor->G-protein->adenylyl cyclase->cAMP->PKA->CREB
one way to block cAMP
phosphodiesterase (Viagra- Sildenafil- and caffeine at high doses inhibits this)
Metabotropic Glutamate receptors
Group I- Gq
Group II- Gi/o
cAMP response element binding protein
binds to CRE
phosphorylated at ser133 by PKA, CaMKII, CaMKIV, Rsk2 (can cross nucleus)
immediate early gene, expression regulated by CREB
cFos activated by depolarization and cellular activity so marker for recent activity in neuron
D2 antagonists
haloperidol, striatopallidal neurons
D1 agonists
amphetamine, cocaine; striatonigral neurons
dopamine- substantia nigra pars compacta
serotonin- raphe nuclei of brainstem
precursor molecule to catecholamines
actively transported across BBB
tyrosine hydroxylase
makes DOPA->dopamine->NE->Epi
presence of this indicates catecholamine
tells cells to transcribe only certain areas of gene
transcription factor
regulates how much of gene gets transcribed
most in LC at brainstem
regulates sleep-wake cycle (more firing, more alert)
activated by fearful, stressful stimulus (PTSD)
G-protein function
1) G-protein has 3 subunits bound with GDP
2) ligand binds->alpha physically associates which releases GDP and binds GTP
3) GTP causes alpha to break from beta-gamma and both directly regulate ion channels, adenylyl cyclase, etc.
4) GTPase converts GTP on alpha to GDP and all re-associate
G-protein inwardly rectifying K+ channel
rgulate opening of Ca++ channels in response to membrane depolarization
AMPA v. kainate
cyclothiazide- relieves AMPA desensitization
concavalin A- relieves kainate desensitization
routes of drug administration
oral and parenteral (SC, IP, IV, IC, ICV, smoking)
radioligand binding assay
1) grind up tissue= substrate
2) isolate membranes
3) 20 test tubes full of equal amount of membrane suspension
4) 10 test-tubes add hot radioligand with different concentrations and other 10 test-tubes with hot radioligand of different concentrations + cold ligand excess
5) let it site
6) wash well
7) expose suspension to film, hot ligand will be black spots
8) plot amount of ligand v. concentration; nonspecific, total and then specific
NMDA being depolarized not enough to have ion flux
Need to have positive enough charge inside to cause electromotive force to kick Mg++ out of channel
Why have inhibitory neurons?
need to stop excitatory signals at some point (otherwise excitotoxicity and also save metabolic resources)
GABA shunt
in glia, GABA goes through multi-step process to strop it of its amine group to be reconverted into glutamate and shipped back to neurons to be reconverted into GABA
EPSP- small positive bump in voltage due to Na+, K+, Ca++ ions entering
IPSP- small negative dip in voltage due to Cl- ions entering (GABA-A) or K+ leaving neuron (GABA-B)
synergistic effects
drugs simultaneously doing same thing (ethanol and barbiturates increasing GABA-A channel open time); can be exploited for cross-dependence
efflux of K+ and discourage influx of Ca++
dopamine neurotoxin, designer heroin (making merperidine) , caused Parkinson's disease ("frozen addict")
Oliver Sacks
treated people with encephalitis lethargica with L-DOPA
dopamine's function in CNS
1) movement- Parksinson's nigrostriatal DA)
2) executive function- psychosis normal executive function (mesolimbocortical DA system)
3) reward/pleasure- ICSS paradigm, cocaine, amphetamine (mesolimbocortical system)
4) endocrine control- prolactin from anterior pituitary (tuberoinfundibular tract)
5) sensory periphery- amacrine cells, periglomular cells
dopaminergic cell locations
1) substantia nigra
2) VTA
3) arcuate nucleus
3 main dopaminergic systems of brain
1) nigrostriatal DA system
2) mesolimbocortical DA system
3) tuberoinfundibular DA system
Nigrostriatal Tract
substantia nigra pars compacta in midbrain->caudate and putamen ("neostriatum")
Parkinson's Disease
- loss of nigral cells, may be caused by alpha-synuclein changing VNT's (because of toxins, mutations, aging) so that dopamine not put into vesicles and made into reactive O2 by MAO or COMT
-treated with L-DOPA + carbidopa
Mesolimbic Tract
VTA->NaC and cingulate/prefrontal cortex
major pathway for reward and reinforcement
sampling dopamine or other chemical in brain (ex: medial prefrontal cortex)
Tuberoinfundibular Tract
controls prolactin release from anterior pituitary
mediated through D2 receptors
antagonize D2R's, can result in hyperprolactermia and lactation
D2 agonist
used to treat hyperprolactermia
blocks VMATs which depletes pool of releasable monoamine, can result in hypotension or decreased BP
dopamine PNT
cocaine and amphetamines function
block reuptake of monoamines, transport monoamines back out into cleft (reverse)
adrenergic receptors
alpha and beta subtypes
effects cardiac tissue ("beta blockers")
D1 v. D2-like receptors
D1-like: D1, D5 receptors, Gs
D2-like: D2, D3, D4, Gi (can be autoreceptors)
serotoninergic cell locations
nucleus linearis
raphe pontis
precursor for serotonin
tryptophan hydroxylase
produces 5-HT from tryptophan
can be activated by PKA and gene promoter can be activated by cAMP
more serotonin= more production of TPH
serotonin VNT
things that bind/inhibit SERT
MDMA (ecstasy), cocaine and amphetamines, SSRI's
fenfluramine and phentermine
causes rapid release of serotonin from terminals by altering SERT
used for weight loss, but people had heart problems from
serotonin receptors
14 receptors- all metabotropic but one (5-HT3)
opens to inwardly flux Na+ and K+
LSD and serotonin
LSD= lysergic acid
LSD agonizes 5-HT2A receptor
antagonizing this receptor= antipsychotics
acetylcholine functions
attention, arousal, alertness, REM sleep (active part of sleep= more ACh), learning and memory, Alzheimer's Disease, tobacco use and addiction
ACh localization
basal forebrain: nucleus basalis of meynert, medial septal nucleus->cortex and hippocampus

brainstem nuclei->thalamus, sup. colliculus
Alzheimer's disease
thought that there's cell loss in nucleus baslias which causes regional cortical atrophy (tangles, plaques)
choline acetyltransferase choline + acetyl-coA= ACh
Schema for NT/Modulators
See Above
alpha latroxin and ACh
alpha latroxin promotes LOTS of vesicular release of ACh and overstimulates postsynapse, uncouples Ca++ from release process
ACh clearance from cleft
isn't taken back into presynapse
degraded by acetylcholinesterase
inhibit acetylcholinesterase
Cholinergic Muscarinic Receptors
bind muscarine, extract of poisonous mushroom
5 subtypes, all G-protein coupled receptors (M1-M5)
Muscarinic Agonists
ACh (endogenous), muscarine, carbachol
muscarinic antagonists
atropine, some tricyclics
Cholinergic Nicotinic Receptors
bind nicotine (from tobacco)
ligand-gated ion channels, inward flux of Na+ and Ca++
rapidly desensitize
Nicotinic Agonists
nicotine, ACh, carbachol
IC perforated path recording
make holes in membrane to get drug in
nicotinic antagonist
mecamylamine, curare (at NMJ)
intracranial self-stimulation
gives electrical stimulation to medial forebrain fiber bundle
drug self-administration paradigm
ICV administration (into lateral ventricles) of drug based on lever presses
local anesthetic, vasoconstriction, tachycardia, nasal septum destriction, enlarged heart, increased DA tone (higher levels of DA during time of use), DAT compromised, causes euphoria, increased arousal, appetite suppression
ex: heroin, morpine, opium, codeine (narcotics)
antitussive properties, disinhibits VTA so more DA in Nac
euphoria, sedation and claming
opioid receptors
mu, delta, kappa
mu activation = euphoria
kappa activation= aversive
natural opioids
beta-endorphin, leu-enkephalin, met-enkephalin, dynorphin
opiate v. opioid
opiate= exogenous (morphine, codeine)
opioid= endogenous
aids 5-HT3
increases GABA-A Cl- flux
causes CNS depression
removes nicotine-induced increases in monoamine release (DA) to help people kick smoking habit (less reward from smoking than before)
IC v. EC recording
IC= mV or pA
EC= microV or nA
long-lasting stengthening of synapses, causes EPSC bigger than usual
state of extreme mental illness where person disconnected from reality (schizophrenia)
features: hallucinations, delusions, illusions, formal thought disorder
drugs that induce psychosis
LSD, mescaline, pot, PSC, ketamine, psilocybin
THC primary ingredient
receptos: CB1, CB2, CB3
endogenous cannabinoids (endocannabinoids)
2-AG and anandamides
said to be released retrograde due to postsynaptic elevation of Ca++
found in TMN
less histamine cells active= lower activity of brain
receptors: H1,2,3--metabotropic
REM-on neurons
pontine tegmentum cells
adenosine buildup theory of sleep
1) adenosine levels increase with amount of time awake and decrease as sleep caught up
2) more time awake, more ATP breakdown, and more adenosine (because breakdown product of ATP)
3) adenosine receptors found throughout brain
4) adenosine can be blocked by caffeine
adenosine receptors
adenosine is derivative of adenine
A1, A2, A3
G-protein coupled
antagonists: methylxanthines (caffeine, theophylline, etc.)
things used to treat ADHD
amphetamines: D-amphetamine, methamphetamine, methylphenidate (Ritalin), Adderall or pemoline
sleep rebound effect
modafinil (provigil)
no rebound sleep, but keeps awake
Cephalon makes
promotes wakefulness without generalized CNS stimulation (mostly just histamine neurons in TMN of hypothalamus)
time givers
cues from world to keep circadian rhythm going right
mostly light, but also internal clock (SCN)
2 main processing centers of amygdala
lateral nuclei- input area, receives axon from cortex and thalamus

central nucleus- output, sends projections to hypothalamus, LC, VTA, output activates fear responses
paraventricular nucleus of hypothalamus
increase in CRF increased glucocorticoids during stress
pain suppression via endogenous opioid, suppression of aggression caused by amygdala inhibiting this area
2 routes to amygdala
direct: thalamus to amygdala, but inaccurate

indirect: thalamus->cortex->amygdala
elevated plus maze test
to test anxiety in rats/mice
5-HT1A agonist
other anxiolytics
adenosine receptor agonists
monoamine hypothesis of depression
depression is result of imbalance in serotonin or NE levels- in particular hypoactivity (too low)
4 classes of antidepressants
miscellaneous antidepressants (lithium)