neurophysiology Flashcards
coulomb
charge of one electron (1.6E-19C)
faraday constant
total charge of one mole of charge
potential difference
work required to move a charge from point A to B
ampere
current (coulombs per second)
ohm
resistance (measured in ohms per cm^2)
ohms law
E = IR
siemen
conductance (reciprocal of resistance/ohm)
ionic equilibriam potential
balance between ion gradient and charge gradient
capacitance
storage of electric charge
nernst equation
E = (58mV/z) * log([outside]/[inside])
when is the nernst eq valid?
ONLY when the system is in equilibrium
what value does nernst eq. give?
the membrane potential at equilibrium
principle of electrical neutralitiy states
[cation]=[anion] in any compartment
donnan equilibrium means that?
the electrical potential across the membrane must balance the concentration gradient
donnan equilibrium equation
[K+]outside * [Cl-]outside = [K+]inside * [Cl-]inside
goldman equation accounts for
permeability (P)
permeability is expressed relative to ___
K+
3 things that affect transmembrane potential
transmembrane resistance; axial resistance; membrane capacitance
membrane resistance
measures how sensitive something is to an applied current LONGITUDINALLY; R(m)
internal resistance equation
R (in) = delta V / I
resistance durastically changes when..
radius increases (because the surface area of the cell gets way bigger and the charge diffuses across that area)
R(m) is proportional to
lambda. Since the membrane doesn’t take on the charge it travels farther down the axon
lambda equation
lambda = sqrt((Rm) / (Rin))
what does diameter do to lambda
lambda is inversely proportional to Rin which is inversely proportional to r. As diameter increases, so does lambda
membrane time constant
time needed for electronic potential to decrease to 37% of original
time constant depends on?
membrane resistance (Rm) and membrane capacitance (Cm)
larger time constant means?
less decay over time, so there is a larger chance for the impulse to trigger an action potential
hyperpolarization
an increase in membrane potential; proportional to the current increase; makes it harder to start an AP
hypopolarization
a decrease in membrane potential; makes it easier to start an AP
AP triggered by
depolarization; of 10-20mV from the resting membrane
all or nothing means
an AP is triggered, or it is not; the amplitude is the same no matter the strength of the trigger
stimulus strength dictates?
the frequency of the all or nothing AP
speed of AP
relatively slow
AP decrements?
no, it is regenerative and propagates without diminishing
overshoot
when the AP goes positive
undershoot
when the AP goes extra negative
absolute refractory period
you can’t over excite the cell during this period. Its impossible
inward current of AP is from
sodium, proved by nernst equation and tetrodotoxin and ion substitution
outward current of AP is from
potassium, proved by tetraethylammonium
seizures are from
defective sodium channel that leaks TOO MUCH and you get an unwanted AP; treat with phenotoitin
hyperkalemic periodic paralysis from
too much K so you lose muscle tone especially after a meal with high carbs or high K; this is due to a defective Na channel that responds to a high [K] by shutting down; treat with insulin and glucose
hypokalemic periodic paralysis from
low K that prevents generation of AP; treat by giving them K (bananas or strawberries)
driving force of ions across membrane?
ohms law says its due to the difference in membrane potential and the equilibrium potential
Na and K conductances depend on
voltage: the conductances increase as the neuron is depolarized
Which ion conductance peaks first?
Na before K
Why does the Na depolarization level out?
as Na enters the cell, the conductance of sodium increase and therefore, the cell loses its driving force
What causes the hyperpolarization?
voltage change opens pores so that K leaves the cell; conductance of K increases more than during rest and this causes hyperpolarization
why Is depolarization regenerative?
Na progressively depolarizes the cell, and when it runs out of energy, it activates K to release from the cell which repolarizes it back to the resting state voltage potential
the speed of an action potential depends on
the diameter and myelination of the nerve
relatively refractory period =
when membrane voltage is being changed by outward flow of K
relationship between myelin and Rm
myelination decreases the amount of lost energy, so Rm decreases
relationship between axon diameter and Ri
increasing diameter, lowers internal resistance of the axon
where are ion channels located?
in nodes of ranvir
saltatory conduction decrases
the amount of metabolic stress; otherwise, it would take to keep pumping ions out of the entire length of the axon
guillan-barre from?
circulating peripheral anti-myelin Ab, so the pt. loses their myelin, but the nerves are still alive
guillan-barre symptoms
peripheral neuropathy, usually had an intestinal virus 3-4 weeks prior
guillan-barre treatment
purified IgG to down regulate natural production of their IgG; plasmaphoresis to get their Ab out
multiple sclerosis from?
Ab against central myelin and the oligodendrocytes
multiple sclerosis symptoms?
progressive gait problems, loss of vibratory and proprioception, pale optic disk
multiple sclerosis treatment
selective immunosuppressive drugs that can enter the CNS; you cannot regenerate already lost myelin
two types of synapses?
electrical synapse (gap jxn) and chemical synapse (NT)
a gap jxn pore is not __
selective. If it fits through, it goes through.
gap jxns are made of?
connexons with 6 protein subunits
what types of things usually pass through gap jxn
sodium, potassium, cAMP
What can close a gap jxn
a lowering of cytoplasmic pH or an elevation of Ca2+ can make the conexxon parts rotate and close the pore
gap jxns are appropriate for?
cells that are directly adjacent that will work by passive electrotonic potentials; example: cardiac muscle, or something that needs synchrony
another cellular fxn of a gap jxn
passing nutrition; example: schwaan cell does this, also your cornea does this because it doesn’t have a blood supply.
drawback of gap jxn?
they are bidirectional. You can’t mandate the flow of something to only go one way
what signals a NT to release?
the action potential allows Ca2+ into the cell
end plate potential
transient depolarization of the post synaptic membrane
What blocks postsynaptic ach receptors
curare
result of increased extracellular [ca] in neuromm. Jxn
you hit the threshold more, there is a higher amplitude response (from extra quanta released) but the concentration within each quanta is the same
__ has the lowest threshold for AP
the axon hillock because the voltage sensitive Na and K channels are concentrated there
examples of excitatory NT. Cause?
ach, glu. Increase Na permeability @ postsynaptic membrane and depolarize it
What is the break even point for epsp?
the reversal potential. No net potential occurs at -11mV
what typs of NT for ipsp? Cause?
GABA. Increase the Cl permeability at postsynaptic membrane
where is the break even point for ipsp
reversal potential for this one is at -80 mV
2 pieces of info that cns carries
WHERE the info comes from, INTENSITY
What is the Ach binding site made of
a disulfide bond from cysteins in the N terminal domain
what lines the pore of Ach receptor
TM2 sections from the 5 protein subunits
what happens when Ach binds its receptor
the alpha helicies rotate and allow the kink in the TM2 to spin out of the way so that ions can pass through the pore
Ach receptor belongs to what category?
ionotropic. It directly lets ions through a pore
glutamate importance
most important NT in CNS. Almost all EPSPs in CNS are glutamatergic
two ionotropic receptors for glutamate
AMPA and NMDA
what does TM2 look like in glutamate receptor
it has a hairpin loop within the membrane and it reenters the cytoplasm
glycine receptors are
inhibitory ionotropic glycine gated Cl channels
which type of channel is most prevalent
chemically activated (vs. voltage activated)
crossbridge cycle: when is ADP released?
when the energized myosin binds to the actin
where is a voltage gated Ca channel
in the t-tubule that causes the calcium ion channels in the SR to open
what triggers smooth m contraction
variety of NT and hormones. This triggers a cascade of reactions with IP3, Ca, phosphorylation of MLCK and calmodulin
innervation ratio
number of mm that are activated by 1 neuron. Usually 10-10,000
size principle is due to
the fact that smaller cells are depolarized easier than bigger ones. If you have a small signal, only the small (slow twitch) muscles are activated to work
ryanodine receptor
regulates the release of Ca in skeletal muscle; diseased state is malignant hypothermia
muscle force depends on
the number of cross bridges being utilized
