3P03 REVIEW:

#3: YOU ultimately return to the same level after the actin
potential is over, so roughly equal amounts must be exchanged
over the entire action potential to make it return back to where it
startedit wouldnt make sense to explain it in this way: sodium
comes in during rising phase and leaves during falling phase for
example(no driving force for sodium to goback outthe only way
for sodium to get back out is to get pumped out through atpase,
and this cannot occur in the time scale necessary for the whole
action potential..this occurs during recovery or the refrectory
period)
#9: metabolic poisons inhibit ATP production.example of this
would include dinitrophenol, blockers of oxidative phos like
cyanide, etc. iT S INHIBIT THE SODIUM/POTASSIUM ATPASES IN
THIS CASE BECAUSE WE ARE NOT MAKING ENOUGH atp. Looking
at sodium, because in unmylinated axons it is a continuous
propagation along entire axon, so if we looka t any length of
membrane, the sodium is coming in through entire segment,
whereas unmylinated axon the sodium entry is discontinuous and
occurring at nodes of ranvier, so any given length of segment
theintracelualr sodium changes will be more sodium entry in
case of unmylinate acon because sodium entry is continuous
every time cviotn potential goes by only changing intracellular
sodim conc much more slowly in mylinated because only
occurring at the nodesdont need as much energy to pump
sodium outcan accumulate more actin potentials ebfor epump
really has to work..w.ay of conserving energy as well because it
is metabolically more efficient.pump has to do morework
because sodium conc are rising more rapidly in the unmylinated
axon..memrbane becomes so depolarized so it will fail a lot
sooner and will not be able to conduct after a certain amont of
time
#6(a): membrane current under voltage clampstpe
membrane potential from -70 to -65..between these values
nothing much is going to happen..may get a tiny bit of current
inward.close to resting membrane potential thoughoutward
current will be large at 0mV. At -65 there is littledriving force and
little conductance..but at 0 you would have nice sodium and
potassium currents. aT +65.IT IS MORE POSITIVE THAN
Ena.the early sodium current will be outward.little outward
current and then inactivate and then have large potassium
current because huge driving force.
#11: could have different G proteinsthe Gi vs Gs perhaps. Or
even what downstream effectors they activate depending on the
pathways they are connected to in the cell.

#13: -34mv and driving force for the exchanger at the cells
resting membrane potential is -26mV. The movements of the ions
then if dirivng force is negative are inward current.this means
that sodium is going inexchanger is 3 to 1..if net durrent is
inward, then more ins must begoing in than out. Echanger is net
positive charger. Exchanger is operating in normal mode. For
part 2, with elevated sodium levels, the reversal potential is
-64mV and +4 driving force so current is outward. By just simply
changing sodium conc inside in this case, we have changed the
direcint of the driving force and thus exchanger changes mod eof
operaiotn..bringin calcium in because net driving force is outward
and sodium is going outward. If situation is right, this could
happen to any eletrogenic exchanger.need righ concentrations
and gradients though and the voltage range.
#8: Muscarinic receptor with acetylcholine where beta/gamma
can open potassium channel and cause inhibitionso it can be
inhibition by both calcium and potassium ions. With relative
refractory period, you get increase in ptassiumconductance by
different mechanismcoltage instead oligand/receptor binding.
vOLTAGE VS NEUROTRANSMITTERS BEING THE CONTROLLING
AGENT.
#12: NO activates gunaylyl cyclase ot make cGAP from GTP and
cGMP can activate PKG which leads ot inhibition of actin/myosin
interactions and thus have muscle relaxation. Viagra blocks
phosphoidesterase that rbeaks down cGMP, elevating the levels
and favoring actiation of pkg and thus muscle relaxation. This
might affect visual defects because with rhodopsin receptor
cGMP is broken down by phsophdiesterase to cause
hyperpolarizaiotn when you are in the lightif you cannot break
it down then it will affect your vision.