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Chapter 1: Terms Chapter 2: Basic Signaling Membrane transporters

CNS: processing (brain, spinal cord) Resting membrane potential is created by continual resting efflux of K through leak K channels
Neurotransmitters -Large
Biogenic proteins
Amines continuedthat maintain conc
sol
PNS: communication (spinal nerves, cranial nerves) Electrochemical equilibrium:
Agonist: binds and exact balancing between two forces: the concentration gradient and the opposing
activates receptor gradients,
Catecholamine usesynthesis:
ATP directly or indirectly.
-somatic motor system (motor nerves) electrical gradient.
Antagonist: No that
molecule net flux ofand
binds ions.
inhibits receptor or channel Actively
--Precursor: move ions against
tyrosine-large amino conc. gradient
acid transporter,
-visceral motor system (sympathetic, parasympathetic, enteric, autonomic ganglia & nerves) Equilibrium potential
Desenstitization: aka reversal
transition to closepotential
state in is the potential
presensce generated across limits
of neurotransmitters, membrane at electrochemical
ion flux Ion exchangers
energy dependent mechanism– dependtoon cross BBB
-sensory ganglia and nerves equilibrium – depends
Allosteric binding ondiff
sites: concentration
than binding gradient
site of ligand, modulates receptor or channel properties --Rate limiting step:gradient
electrochemical tyrosine Hydroxylase-converts
of other ions as
Planes – sagittal (left/right hemisphere), coronal (front and back), horizontal (top and bottom) In cell: higher conc. in cell: K || higher conc outside cell: Na, Cl, Ca
Acetylcholine tyrosine source.
energy to DOPA,Takes DOPA one decarboxylase
up gradient converts to L-
while
Afferent: carrying signals toward brain Acetyl from acetyl coA is transferred from choline by choline acetyl transferase (ChAT which is rate limiting DOPA which
taking one down crossesgradient
BBB and converted into Dopamine
Efferent: carrying signal away from brain step) Overshoot: The peak, positive-going phase of an action potential, --Dopamine Beta hydroxylase only in weight),
norepinephrine
caused(glucose
by high metabolism),
membrane permeability to a cation such as Na +
or to Structure> primary (molecular
Interneuron: local circuit neuron Acetyl coA precursor: derived from pyruvate must exit mitochondria to gain access producing neurons
Ca2+. move choline into neuron secondary (alpha helix, beta sheet) –
Neuron partstransmission
Synaptic ChAT. High affinity Na/Choline transporters --PNMT in Epinephrine neurons
rising(10,000
phase: molecules
The initial,into
depolarizing transmem prot, tertiary (inter &
Dendrite: long, thin,
Gap junctions: tubular,
channels taper at end,
physically branches
connect for ions
neurons, surface area,
flow 100s & 1000smade
is bidirectional, inputs
up of connexons which Packaging: vesicular cholingeric transporter vesicles) phase of an action potential, Catecholamine domains),
extracellular storage: VMAT 1 and VMAT 2 which
quaternary
-Spines: small protrusions
are hexameric, connexonsof dendritic
dock to form membrane, increase
channel. Seen surface area.of cortex, striatum, hippocampus,
in interneurons caused by(AChE)
Inactivation: enzyme called acetylcholinesterase the regenerative,
in synapticvoltage-dependent
cleft breaks downinflux of a cation
acetylcholine intosuch are also used for serotonin
Na+ or Caby2+ (subunits)
Convergence: Innervation
breathing, allow passage ofofalarge
targetmolecules.
cell by axons
Signfrom more than
preserving and one neuron. firing
synchronized acetate and choline where the choline isas conversed .reuptake. --blocked by resperine which depletes stores of
Axon: longer,
3 critera thinner,
of for tubular structure,
neurotransmitter: no taper,
1. Present minimal branching,
in presynaptic terminal 2.output structure
Released in response to AP and Ca Threshold: The level of membrane potential at which an action Na/K structure: 10 transmembrane
serotonin, DA, NE
Divergence: The branching
influx 3. Receptors presentofona single axon tocell
post synaptic innervate multiple target cells. potential is generated. domains, beta unit, ouabain binding site
Catecholamine inactivation:
Soma/perikaryon: cell body, golgi, nucleus (transcription), protein synth (ribosomes), signal integration
2 classes of neurotransmitter: Undershoot: afterhyperpolarizatoin, The final, hyperpolarizing phase Ca pump structure:
--Dopamine Transporter10 transmem
(DAT): binds to domains,
Dopamine and
-Nissl
Smallsubstance: endoplasmicsmall
molecule transmitter: reticulum, ribosomes
clear vesciles, synthesized in presynpatic terminal, released in response to of an action potential, typically caused by the voltage-dependent NB = ATPinto
transports binding,
presynapticP=Phosphorylation
terminal for re-use site
-reticulum
signal action– tubules,
potentialstrings of vesicles, large and flat cisternae efflux of a cation such as K+. voltage gated K channels are still open Ca Pump cycle:Transporter
--Norepinephrine 1. Ca binds (NET)to high
binds affinity
to Norepi and
-polysomal rosettes – clusters
Peptide neurotransmitter: largeofdense
ribosomes, “free” ofsynthesized
core vesicles, ER in soma and transported to presynpatic site 2. ATP
transports into binds/phosphorlation.
presynaptic termainal for reuse. 3. Confo
-Rough
terminal,ERreleased
– proteinin translation,
response to ribosomes attached||Smooth
a burst of repetitive APs ER – calcium storage, release change exposes
--degradation: Ca externally
MAO-happens (low affinity)
after re-uptake in
-Ribosomes: protein translation||Golgi:
Fast axonal transport: up to 400mm/day, post translation
used mod of proteins,
for neuropeptide packaging
transport, molecular motors such as kinesin mitochon, COMT-happens in cytoplasm
Action Potential ATPase pumps – hydrolysis
Axon hillock:
attach axon
vesicles originates, microtubules
to microtubules, and neurofilaments
all this requires ATP hydrolysis align Dopamine
Initial Capacitive current – instantaneous current flow due to redistribution of of ATP
Slowsegment: adjacent to
axonal transport: hillock,ofmicrotubule
transport bundles
enzymes needed forcalled
small fascicles,
molecule Most APs originate
neurotrans, here
.5-5mm/day. Location: substania nigraNa/K into statrium,
Node of Ranvier: gap in myelin sheath – generates electrical activity charge across membrane. pump –VTA projects to –
electrogenic
nucleus accumbans and prefrontal cortex:
Tubulin: protein constituent of microtubules Early influx of Na (causes early inward current) followed by delayed efflux pumps 2 K in for every 3
Function: activate G protein coupled receptors
Tau: microtubule binding protein, only in axon of K (causes delayed outward current). Na out, producing small
Role: in reward and addiction
Actin: in tips of growing axons & dendrites, enriched in spines Tetrodotoxin – neurotoxin found in puffer fish, blocks the Na current, no Norepi hyperpolarizing current
Glia: No synaptic interactions or electrical signal, glia to neuron ratio 3:1, 3 types: K current effect location: locus coeruleusNa/K pump cycle – 1. Na
-Astrocytes: Glial cells in CNS; regulating the ionic milieu, transmitter reuptake, developmental scaffold Tetraethylammonium ions- block K current, no effect on Na current Role: attention, sleep-wake from inside cell binds, 2.
cycle
-microglial: repairing damage following neural injury, secrete cytokines – modulate inflammation Na conductance – during depolarization, rapid activation of Na Epi ATP to ADP phosphorylates
- Oligodendrocytes: their major function is to elaborate myelin in CNS conductance
Plant alkaloids with a rapid inactivation (even in depolarized level) Location: medullary epicell. neurons, 3. Conformational
project into thalamus,
-Schwann cells: their major function is to elaborate myelin in PNS K-- conductance
Nictonia tabacum, activates nACh
– delayed receptorsbut does not inactivate like Na
activation, hypothal, medulla, project: changeadrenalcauses
medullaNa release
projection neuron: A neuron with long axons that project to distant targets. --Muscarine:
Both Na and posinous red mushroom,
K conductance areactvates muscarinic ACh
time dependent andreceptor
voltage dependent Role: fight or flight outside the cell and the
white matter: A general term that refers to large axon tracts in the brain and spinal cord --produce nausea, vomiting,
Depolarization due to: 1. mental confusionof Na conductance 2. Activation of K
Activation Histamine: binding of K 4.
ganglion (ganglia):group of hundreds to thousands of neurons found outside the brain and spinal cord Nicotinic ACh receptor
conductance structure: of Na conductance
3. Inactivation Synthesis: mast cells in Dephosphorylation
bloodstream causes
gray matter: regions of the CNS rich in neuronal cell bodies and neuropil --5 subunits: 2period
Refractory alpha subunits (ACh binding
– resistance to further site) and 3 subunits (usually 3 beta in neuron)
excitation Role: inflammation and conformational allergic response change
interneuron: a neuron whose relatively short axons branch locally to innervate other neurons. ---each subunit has 4 transmembrane
Action potential cycle: AP initiated domains by selective increase of Na Loaded into vesciles with VMAT
which leads to K release
local circuit neuron: neurons whose activity interaction b/w sensory & motor systems aka interneuron --long extracellular amino terminal has ACh binding
conductance, increases cause more Na to enter thus depolarizing the site, pore formed by 2 nd
TM Domain Degradation by histamine methyltransferase and MAO
motor neuron: nerve cell that innervates skeletal muscle. Muscarinic ACh is metabotropic receptor Ena (this is a positive feedback loop, Role: arousal and attention and reactivity of vestibular
membrane more as it approaches
motor system:describe all the central and peripheral structures that support motor behavior. Structure of Ligand gated receptor channels system
the regenerative/self supporting property of depolarization). Rate of
Nerve: A collection of peripheral axons that are bundled together and travel a common route. 5 subunits: nAChR, GABAA glycine, serotonin 3 types (metatabotrpic): antagonist to H1 prevents
Neuropil: dense tangle of axonal and dendritic branches, & synapses b/w them, lies b/w cell bodies in the gray depolarization then falls because electrochemical driving force on Na
4 subunits: glutamate receptor motion sickness, antagonist to H2 reduce gastric acid
matter of the brain and spinal cord. decreases
Some have 4 and Na conductance
transmembrane domains while inactivates.
others have At3 the same
TM and onetime, voltage
pore loop
dependent K conductance activates, because K conductance is higher secretion, diphenhydramine crosses BBB acts as sedative
peripheral nervous system: All nerves and neurons that lie outside the brain and spinal cord. Plant alkaloids: Nictonia tabacum, activates nACh receptors Serotonin
sensory system: all the components of the central and peripheral nervous system dealing with sensation. than at the
Structure resting condition,
of metabotropic receptors it becomes more negative than the resting
Synthesis: indoleamine-similar to LSD, precursor:
potential (this the undershoot). Hyperpolarization causes voltage
7 TM domains, single subunit, intracellular segment and 3-4 loop binds to GTP binding protein, extracellular tryptophan, rate limiting: tryptophan hydroxylase
dependent
loops 2-3 and K 6-7conductance
bind neurotransmitter to turn off and return to resting potential. SERT: binds to serotonin, transports it into the
Voltage
Amino Acid clamp: control –membrane
Transmitters potential and
Major neurotransmitters measure
in the CNS current flow presynapatic terminal for re-use. Loaded into vesciles by
Ii o n
Excitatory: glutamate and aspirate G i o =n VMAT. MDMA and ecstasy inhibit VMAT and SERT
Measuring techniques Inhibitory: GABA, glycine (V M − E R )
EEG:
Ca isaverage
trigger ofelectrical
neurotransactivity produced
release: depol causesby
Cawhole
currentbrain
and release of neurotrans Na/Ca exchanger – Role: uses Na regulates
gradientsleep wake
created bycycles, implicated
Na/K pump. 3 Nainfor 1 Ca
Synthesis: derived from glucose metabolism, alpha-keto glutarate is formed by Tricarboxylic acid cycle, psychiatric disorders.
Voltage clamp:
Differential internal
release: electrode
low frequency measures
stimulation Vm increase
–localized and is inconnected tomolecule
Ca and small voltagetransmitter
clamp amp. Permeability changes:
transanimated into glumate from alpha-oxogluarate transaminase (GABA-T), GAD forms GABA from Only 1 iontropic receptor; 5-HT3 = non selective cation
2 release.
voltage High freq stimulation-more
clamp amp compares diffuse
Vm toincrease in Ca and
command release of(designated
potential neuropeptide transmitter
by Ion channels
glutamate Calcium channels with Er of 0 mV
Transmitter secretion
experimenter) 3. If different, current injected through 2nd electrode. This causes mem Microscopic
Alternative current: glutamate
synthesis: current through is formedsingle fromchannel, parallel
glutamine, behavioristoproduced
glutamine macroscopic
in glial cells and -inward current, canPURINESgenerate AP (slower and wider than Na spike, adds to
potential to be the same as command potential. 4. Current flowing back into axon and current. Though
transported individual channels open and close randomly. Macroscopic current is
into terminals. depoloraization of spike.
2 main types: ATP-coreleased by all vesicles and
thus across membrane can be measured. aggregation
Vesicular of many
storage: thousands
vesicular glutamateof microscopic
transporter, NaGABA
currents, each representing
vesicular transporter a single L channel type: Long lasting (little to nofrom
adenosine-generated inactivation)
ATP by ,extracell
high threshold,
enzymes
Patch clamp: single channel recording voltage sensitive
Inactivation: channel. of by glia and neurons, 3 types of GABA transporters (GAT), excitatory decrease
via re-uptake amino in Ca leads3 to decrease
classes in cardiac contractions
of receptors:
--Whole cell: current across whole cell measured, sharp electrode method, low noise Ion transporters
acid selectivity – fordiscriminate
glutamate,between different ions
glia re-synthesize glutamine from glutamate T type channel: Transient (inactivation
--Iontropic: nonselectiveprominent), low voltage
cation chan, threshold,
2 TM domains
recording Voltage gated - opening
Glutamate – Amino acid transmitterand closing effected by membrane potential rhythmic bursts of Ap
--Metabotropic: adenosine preferring and ATP preferring
--outside out: extracellular side of membrane exposed to bath. Measure voltage and Depolarization increases the probability of channel opening where hyperpolarization N type channel: neither transient nor long lasting, some inactivation,
NEUROPEPTIDES
neurotransm response closes them. threshold between TPre-propeptides
and L type, Casynthesizeddependent releasein somaof(rough
neurotrans
ER) by
--inside out: intracellular side of membrane exposed to bath. Response to voltage and Voltage sensor – detects the potential across the membrane P type channel: purkinjeprotein cells, generate dendrite calcium spikes, similar to
translation
intracell substances L type Pro peptide created by cleavage of signal sequence (in
Voltage gated Ion channels Q type: similar to PRER),type secreted
--cell attached: Some channels in membrane encircled by pipette tip. Measure current
R type:residual, remainsPeptide after all else
created byblocked.
processing in golgi:
through single channel
Extracellular recording: potential next to neuron is compared to potential further away. --proteolytic cleavage-large pro peptides can be cleaved
Measure signal in response to behavior. into multiple active peptides
Intracellular calcium indicator dyes: flouresence depends on whether Ca is bound --glycosylation, phosphorylation, disulfide bond
Voltage sensitive dyes: floursensce indicates mem potential of large # of neurons Passive and activeformation.
propagation of AP
--packaging
simulatenously Requires subthreshold current: into vesciles.
All current
act on G protein coupled receptors
FRET:
Snare floursence depends
complex: proteins oninshape
involved dockingofand
molecule.
priming, synaptobrevin, syntaxin, SNAP-25 form complex -Passive current flow: flows axially, some current flows across the
Five categories:
--CFP: cyan flourscent
Synaptotagmin protein
associates and syntaxin binds Ca channels membrane, as charge is lost membrane potential decreases. This decrease
Brain gutsite
= found in brain and gut
Depol yellow
--YFP: causes Ca channels to open,
floursecent Ca binds to synaptotagmin and fusion occurs
protein happens with distance from of current injection and is exponentially
decaying. ResponseOpiod: morphine like activity
--CFP and YFP attached to molecule like calmodulin, if CFP is near YFP (when Ca binds), develops more slowly at greater distances from site of
then cyan emissions excite YFP producing yellow emission. current injection. Hypothalamic: release pituitary peptide hormones
Opoid receptors: colocalized with GABA and 5HT
Computerized Tomopgraphy: narrow x-ray beam and array of detectors, 2-d pic AMPA not preamble to Ca and faster response than NMDA Decay of potential:
receptors, analgesic , depressant , behaviors: sexual
Excitatotoxicity – caused by abnormal hgh levels of glutamate, dendrites of target neurons are swollen, effect r mand aggression/submission, involved in
attraction
λ =
AP propagation blocked by glutamate antagonist − x r
Conduction velocity depends on: time to depol Na channels, each instance of AP regen adds time to K channels: gate open with depolarization, gate closed with hyperpolarization V ( x ) = V 0 e λ addiction λ = ri m
propogation. To increase conduction speed, limit the locations where AP are generated and b/w these locations --current continues to flow with sustained depolarization Unconventional r i neurotransmitters
Na channel: Activation gate: open during depolarization, closes during Why?: not stored in vesicles, released post synaptic
allow passive propogation. This can be accomplished by saltatory AP condunction along myelinated axons
hyperpolarization terminals and act on presynpatic terminals
--Node of Ranvier= gap in myelin sheath along axon rm=resistance of membrane, ri=resistance of cytoplasm
--inactivation gate: closes with depolarization, opens with hyperpolarization Two classes: endocannabinoids, NO
---at the gaps is a high density of Na channels, this causes fast depol lamda = length constant or space constant, defined by 1/1-e of applied Volt
--current flows with both gates are open Endocannobinoid
--passive propagation b/w nodes rm decreases with axon radius because it iswith
inversely propgroup
to circum:
--deploarization causes activation gate to open quickly – current flows, then Unsaturated fatty acid polar head
Action potential generated at point A, inward current rapidly flows axially with limted loss to point B because 1
depolarization causes inactivation gate to close slowly –current stops flowing. rm ∝ Production stimulated by rise in Ca
of myelination
Repolarization required to de-inactivate channel, allow subsequent current flow 2 π r a d i Diffuse
u s from post synp to pre synp and bind to CB1
Diversity of ion channels: genes, alternate splicing, RNA modified, post translational receptor where it inhbits GABA neurotransmitter
--depol leads to Ca influx, endocan production, inhibition
Voltage Gated Ion channel Structure: Ri is inversely propoftoGABA cross sectional area so decreases
release, smaller IPSC with axon radius:
Na and Ca channels: 1 Receptors: cortex, cerebellum, hippocampus
ri ∝
4 homologous domains, each domain w/ 6 transmembrane domains S1-S6, total of 24 π r a d 2 i u Enrichs caudate putamen and substantia nigra, regions
transmembrane domains. Accessory proteins called Beta subunits can regulate function involved with addiction
Vesicle recycling K channels: Marijuana acts on endocannabinoid receptors, active
Clathrin coat: clathrin triskelion made of 3 legged protein -most subunits have 6 transmembrane domains, 4 subunits to form channel, total of 24 Lamda increases asingrident is THC better signal prop in larger axons:
radius increases,
Axial current depolarizes point B which cause a rapid iniation of AP
Dynamin: motor protein that promotes rapid retrieval transmembrane proteins, some have 2, 4, or 7 transmembrane domains λ ∝ r a d i uNOs
Glycine:
S4 voltagepredominantly inhibitory transmitter
sensor: one transmembrane domain hasinchargedspinal cord
amino acid, movement opens Synthesis: NO synthase produces nitric oxide
GABA:
pore. inhibitory transmitter in brain --NO synthase activated by Ca-calmodulin
Iontropic
StructureGABA receptors:
of Bacterial Cl permeable channels, Cl influx produces IPSP, stop firing, decrease firing
K channel: rateincreases rmNO
Myelin andfreely
thus diffuses
lamda because througheach membrane
wrap istoanother
activate pre and
--Structure: 2 GABA
2 transmembrane binding
domains and sites, 2 alpha subunits
connecting loop to form the pore membrane, which prevent post synapatic
current terminals
flow across membrane, thus better signal
Drugs acting on GABA receptor
4 subunits create functional channel
A prop in mylinated axons --spontaneously decays in seconds
--benzodiazepines:
Only non hydratedvalium, K can fitLibrium,
throughenhances
selectivity GABA
filter, current
collected at and dehydrated at Changes in membrane potential are not instantenous, this happens because
--barbiturates:
central cavity,phenobartial
4 K binding =sites, anti electrostatic
epeletic, pentobartial=anthestic
repulsion helps speed transit the membrane behaves as a capacitor, storing the initial charge that flows
--steroid metabolites of testorestone, corticosterone, progesterone
Mammalian channel: part of T1 domain and Beta subunit participate in inactivation at the beginning and end of current pulse
Inward current at point B flows to Point C which iniates AP, point A encounters a refractory membrane --strychine:
--additionalfrom
voltageseeds, blocks
sensor exerts glycine
forcereceptor,
on S4-S5overexcitation
linker to openoforbrainstem
close pore, and cord, seizures
paddlelike When current injection is stopped, membrane potential decays slowly:
Picrotoxin:
movement from anamerta
of linker cocculs, blocks
from extracellular GABA channels
to intracellular. −t
Excitatory actions of GABA in developing Brain V M (t ) = V ∞ e τ
Ligand Gated channels:

Tau=is time constant:


Receptor Function
Neurotransmitter increase the probability a channel is open
τ = rm c m
APIonjumps
flow from node
depends ontomembrane
node, fewer instances
potential of inward
relative Na current
to reversal implies less ATP to restore equilibrium
potential
Reversal potential of EPC is average of Na and K channels, below 0 mv: net influx of ions, above 0 mv, net
Macroscopic
efflux of ionsand Microscopic Current Myelin increases rm and decreases cm
Microscopic current is current
Action of transmitter through single
drives membrane channel
potential toward reversal potential Suprathreshold current:
AP initiated and AP shape independent of distance
= γ ⋅EPSP-increase
i Excitatory: (V M − probability
E R ) of AP, reversal potentialQauntal
> AP threshold
theory Time of AP depends on distance from iniation site
Inhibitory: IPSP-decrease probability of AP, reversal potential < AP threshold
end plate: The complex postsynaptic
Depolarizing IPSP possible if Erev is above Vres and below threshold --delay is proportional to distance
single channel current = single channel conductance Nerve gas and organophosphate instectides target AChE by
Summation of postsynaptic potentials: EPSPs may sum to produce specialization
AP whileatanthe of*nerve
sitecan
IPSP
driving potential
contact
prevent AP on --constant condunction velocity =measurable rate of transmission
Either channel is open=gamma or closed=0 removing inactivation which causes muscle defibrillation
Events of neurotransmitter release: skeletal muscle fibers.
Macroscopic current equals sum of microscopic current Families of Postsynaptic Receptors Neostigmine: inhibits AChE which increases ACh in synapse, this
end plate current (EPC): Postsynaptic current
I = N Fo i makes up for decreased Ach receptors due to auto-antibodies
produced by neurotransmitter release and Biogenic Amines: 5 types, 3 are catecholamines which ACh
are (dopamine, norepinephrine, epinephrine), 2 others
I=macro current N=# of channels Fo=fraction of channels openbinding (0 to 1) ati=single channel current attacking receptors in myasthenia gravis.
the motor end plate. are histamine and serotonin
G = N Fo g Myasthenia Gravis:: disease interfers b/w motor neurons and
end plate potential (EPP):Depolarization of
skeletal fibers. Auto antibody attack on ACh receptors
Potassium Channel Reserve pool: vesicles connected to each Firing Patterns Bungarotoxin: high affinity for nicotinic ACh receptors which
Regular firing: repetitive AP in response to sustained current injection,
to bindincreased
Types: voltage dependent, Ca dependent, hyperpolarization dependent, the membrane
other &leak
actin potential
cytoskel
channels of skeletal
by thinmusclecross links firing
preventsGlutamatergic
from ACh to receptors and thus no muscle
frequency with increased current amplititude,movement
time intervals APsNeurons
and b/w
fiber, caused
Shaker Family: delayed rectifier, Kv1.1-Kv1.8 (diff in voltage Readily
dependence by activation
releasable
and the action of
pool: the transmitter
closely
time), Role: spike are all similar 1. Sodium channels open locally, positive feedback loop of Na influx and
paralysis
Ubiquitous excitatory transmitter found in pryimadal
repolarization, Blocked by TEA and some subunits by dendrotoxin acetylcholine with at the presynaptic
neuromuscular membrane.
synapse. (interspike interval) more depol produces AP. 2. Inward current flows axially along axon to
associated Curare: blocks nicotinic ACh
cellsreceptors
miniature Adaptation: decrease in frequency with time, increaseneurons, granulemostly
spike interval, and thalamus
pyramidal,
types: end
Voltaged Gated: Kv2.1 (sustained activation) Kv4.1 ( transient 2activation) docked plate potential
and fusion (MEPP):Small,
competent --difficult to distinguish between glutamate andneighboring
aspartate. area causing depol in adjacent area. Depol opens Na channels
Transient K channel: (Kv1.4, Kv4.1, Kv4.2), rapid activation, minimalspontaneous
current depolarization
active both of
at resting the membrane
potential, role: cortical, hippocampal Developing brain: andEcl is
another AP is iniated.
--Synpasin: binds actin and vesc Glutamate
Delay: time delay b/w deplorization and firing, time delay calledreceptor
latency,types:
spiny all have 4 subunits
projection
greater than AP per channel,
threshold,
slow firing caused by inactivation by AP, de-inactivated by AHP, potential
--CamKII: of causes
activates skeletal
as muscle
Vm returns tocells,
synpasin spiketocaused by
threshold,
release subtypes distinguished by affinity of agonist, all have
slow return to threshold. 2nd role: allows arbitrarily low firing frequency. 3 rd
function: increase latency to spike neurons so GABA is excitatory.
vesc reversalpyramidal
Bursting: cluster of APs, short & long interspike intervals, potential & of thalamic
0 mV Olderbrain:
relay Ecl is lower
neurons with hyperpolarized resting potentials, depol activates 1.Docking:
Athecurrent,
releaseno ofspike occurs
a single until
quantum current
of
inactivated.
movement of vesicle from Spontaneous firing: also called beating, AP generated--Glutmate, kainite,
regularly with NMDA, AMPA
no inputs than AP threshold and so
Ligand gated(iontropic)
acetylcholine.
reserve pool to associ metabotropic
with plasma mem NMDA type Glutamate receptor: glycine co agonist, Mg
KCNQ family: similar structure to shaker channel, slowly activating andwere
non-inactivating, family epiplesy GABA is inhibitory
Ligand
-MEPP
2. gated:
Priming: 2 funcall domains,
rxnthe multimers
sameconverts
that size because of ato from
vesc blocks pore unless depolorized (below -40mV), lets
Ca depedent K channels: control freq of repetitive firing, spike frequency
of 5that
release of adapation,
individual subuints
single repol
which
quanta of APpore,
form
of neurotrans, through Ca and Na
can fuse with membrane
2 types: large conductance and small conductance usually rapid postsynaptic
amplitude oflocal
EPP appearseffects
to be multiple
3. fusion: evalvation of Ca conc
Inward rectifier K channel: 2 transmem domains Metabotropic:
mEPPs. vesc g protein coupled receptors, 3. inward current flows axially in both directions from point B but point A
causes to fuse with the membrane
thought of astheory:
Quantal tranducers. Usually
neurotrans slowerin
released is refractory because K channels are open and Na channels are inactive

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