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lipid
predominant species on membrane
phospholipids
cholesterol
what are 3 types of phosphatidyl?
phosphatidylcholine (PC)
phosphatidylethanolamine (PE)
phosphatidylserine (PS)
phosphatidylinositol (PI)
what does cholesterol do to membrane fluidity
increase fluidity
makes membrane more flexible & dynamic
mem can’t be dull
phosphatidylcholine (PC)
phosphatidylethanolamine (PE)
phosphatidylserine (PS)
what do phospholipids do in water
form lipid bilayers w/ polar heads outside w/ np inside
creating order
do not permit polar moc to get acx bilayer
what lipids are key signaling lipids?
phosphatidyllinositol (PI)
participate in communication, signal process
PLC splits PIP2 > DAG & IP3
PI3 kinase adds Pi on PIP2 → PIP3
what does PIP3 do?
lipid 2nd messenger
triggers cell growth, survival, movement
huge cancer target
growth promoting signal
IP3
2nd chemical messenger
triggers rel of in ER Ca2+
membrane proteins
make up most part of membrane
allows things to move in/out
fluid-mosaic model
mix of protein & lipids
accommodate motion, neurons are very active
what are 2 types of membrane protein
intergal & peripheral
peripheral mem protein
water soluble
inner / outter of membrane or on top of a integral protein
not embedded in np core
regulate mem struc & fuction
integral mem protein
integrated in the bilayer
help transport solute
continuously undergo shape change
major drug target receptors, transporters, ion channels
selective permeability of mem
cells controls what gets in& out via integral proteins
channels, pumps, carrier/exchangers
what are 2 types of solute transport
diffusion
ion channels
no energy, travel down conc gradient, fast
active transport
pumps, exchangers
need energy, move solute against conc gradient, atp hydrolysis, slow
Na+/ K+ ATPase/ pump
maintain high [Na+] out & [K+] in
stabilize potential
enable neurons to fire action potential
steps of Na/K pump
for 1 ATP —> 3 NA+ out & 2K+ in
ATP binds pump —> promotes 3 Na+ binds to pump
ATP → ADP & Pi, Pi binds to pump and changes shape
shape change allows pump to rel Na+ out & 2K+ binds to pump
Pi gets released → back to normal shape → 2k+ gets rel
what contributes to resting membrane potential
an unequal distribution of charged ions inside and outside the cell & the selective permeability of the cell membrane
ion conc gradeint
K+ leak channel
Na/K pump
Na+
higher conc outside the cell → want to go back in the cell
K+
more inside cell → favors the leaving of K+
Ca2+
very very large conc outside
strong driving force to enter cell when channel opens
a rush of calcium inside the cell can cause cell death
Leak Channels
Passive transport: Ions move down their concentration gradient
Always open: non-gated pathways
Creates the charge: Potassium leak channels let K⁺ flow out of the cell faster than Na⁺ leaks in —> inside more (-)
ex: 1 using ion gradient to transport solute
na+ gradient
secondary active transport
MAT uses Na+ gradient energy to bring NT back inside cell
1. NT gets rel to synaptic cleft to signal postsynaptic neuron
2. once done, NT needs to be removed → needs MAT (transporter)
high sodium outside bc of pump → tendency to go back in side cell
MAT: binds to both, Na+ movement provides energy to help NT move in against its conc gradient
ex: 2 using ion gradient to transport solute
VAT & VMAT uses H+ gradient to bring NT into vesicle
proton pump uses ATP
brings H+ into vesicle → more proton in vesicle, wanna leave
transporter uses H+ gradient energy to bring H+ out and NT in
drug targeting key solute transporter
blocking serotonin (5-HT) transporter increases serotonin signaling
usually, SERT brings back serotonin into presynaptic neuron via Na+
inhibition: blocks movement, more serotonin stays in synaptic cleft, can bind to receptors on postsyn terminal
more serotonergic signaling
what establishes the resting mem Potential?
high selective permeability of K+ ion
electrical & chemical forces
2 factors of electrochemical gradient that drive movement of charged ions acx cell
resting membrane potential
electrical potential: -70 mV
K+ flow in & out are balance bc chemical gradient
electrical force = chemical force
restoring resting mem after stimulation
depolarization: more positive (-60), process not isolated point
inside became more positive —> smaller electrical force inside
cause
stimulus trigger voltage gated Na+ channels to open
Na+ rush in cell down conc grad → more (+) inside
Na+ gated channels close & K+ volatge gated channels open
repolarizes → restore membrane to resting
restoring resting mem after inhibition
hyperpolarization: more negative (-80)
larger electrical force
cause
too much k+ leaving via gated channels (until close)
passive leak channels bring K+ back in
K+ influx → depolarize membrane to resting