most commonly rather than almost exclusively because they are found in a number of neurons.

However, I do agree that this question is probably about graded vs active transmission. use

chemical synapses to send info from one cell to next. Glia use gap junctions to communicate

with other glia in the CNS. However, the chapter doesn't really go into glia, so it leads me to

think they are talking about Graded potentials versus action potentials. They could also be

talking about Fast versus Slow chemical transmission between neurons. We will discuss the

graded versus action potential (AP). A graded potential is a potential that is not regenerative.

This potential will travel through the cell and eventually be reduced to nothing. The purpose of

this potential is either to elicit an AP or in some neurons to cause the release of transmitter at

their axonal synapse. An action potential is a regenerative electrical response that will travel

down the neuron to cause the release of transmitter.

2) AP's are slower than electricity in a wire due to the nature of the AP. That is the AP is

regenerated constantly along its journey down an axon to compensate for charge exiting the cell.

In a copper wire their is no current contributing to capacitance or exiting the wire.

3) Synaptic potentials (postsynaptic) are of the graded type and are therefore not regenerating

themselves. AP's do regenerate.

4) You are lowering the internal resistance and therefore more current will travel through the

inside of the axon. This is valid since the specific resistance of the membrane will stay relatively

the same. Actually the resistance of the membrane drops as well due to the increased surface

area. It's just that the internal increase drop is due to the increase in radius squared, while the

membrane resistance is just due to increase in radius (ie it's linear). Additionally, the

conductance increases, but it increases linearly as well. Thus, the conductance and Rm cancel

each other out (time constant=Rm x Cm). This ties in nicely with the next question.

5) See spotlight 6-2. The important information here is that an increased length constant will

also increase the speed of propagation of a signal (because at any distance x, there will be more

current to depolarize the membrane). They make a comment that the length constant, , is

proportional to k times the square root of r. This means the relative rate for a axon with

diameter of 10 uM (r=5) is 2.23, while the relative rate for d=25 (r=12.5) is 3.53.

6) Thanks to the increased membrane resistance from the myelin, more current will flow down

the axon, since the axons resistance is relatively much lower now. Additionally, the capacitance

has been greatly decreased, so that it takes less charge and time to "charge the capacitor" in the

membrane ahead, allowing current to flow more rapidly down the axon. Majority of the leak is

gone and only at the nodes will we have to deal with the slow regeneration.

7) In a myelinated axon there are only Na channels at the nodes. If the myelin is reduced or gone

then the signal will leak out of the cell without being regenerated between the 'nodes'. The point

here is that a current which is above threshold will rarely make it from node to node in the absence of myelination because the resistance across the membrane between the nodes is now much lower.

8) Injection of a dye into the postsynaptic neuron that can fit through the gap junctions but cannot

leave the cell through the membrane would work. If the dye showed up in the presynaptic cell

then it would be a gap junction. You could also try and send current from the postsynaptic cell to

the presynaptic cell. This would also show they were gap junctions.

9) The postsynaptic receptors.

10) First and foremost the receptors will open channels. Obviously Na channels will always

depolarize the cell. A Cl channel can do both. In this situation the cell is either depolarized

based on the initial Vm across the postsynaptic membrane or... you left out the other part of the

either. This is due to the fact that when Cl channels open the Cl will attempt to reach its

equilibrium potential which may be above or below the cells initial Vm.

11) The equilibrium potential for both species for potassium is roughly -55.5 Vm. (-54.9, L and -56, S) If K channels open in either system it would then depolarize the cells from -70 to

approaching threshold. It would appear that in this system the K conductance is excitatory. If

one uses 0.060, (T=37), then Limnaea would produce no effect, bringing the cell just below

threshold, and Sepia would definitely be hyperpolarizing. On the other hand, if one uses 0.058

(T=25) which would reflect room temperature and might be more accurate for cold-blooded

snails, then both L(-53) and S (-54) would be excitatory.

12) An inhibitory synapse is defined by one neuron inhibiting the activity of another neuron. At the synaptic level the presynaptic membrane will release a neurotransmitter that will act to keep the postsynaptic cell from eliciting an action potential. Two well-known ways of doing this are for the transmitters to open either Cl or K channels. If K channels open then the membrane potential will become more negative (ie it will hyperpolarize). If Cl channels open the net effect can be either depolarizing or hyperpolarizing. In both cases it is inhibitory. How can it be both inhibitory and depolarizing? It is important to remember that when Cl channels open that Cl will attempt to reach equilibrium potential for Cl. If the resting potential is at –90mV and E for Cl is –70 then the Cl will EXIT the cell as the membrane potential approaches E for Cl. So, this means the membrane potential, in this situation, will depolarize. The reason that this is inhibitory is because it will attempt to keep the membrane at E for Cl (-65). Therefore if Cl and Na channels are opened on the same dendrite (by different synapses) then the Cl will enter the cell to keep the cell depolarized near –65 (threshold at –55). Thus preventing the cell from reaching –55. Accommodation is another way that depolarizations and inhibition can coincide. Here a mild depolarization due to transmitter will open channels but will not reach threshold. At the depolarized state the Na channels will eventually close and they require a certain amount of time to change conformation back to resting. Because some of the channels are in a ‘refractory’ period the next depolarization is harder to elicit.

13) The evidence for this is the fact that most release from the presynaptic cell can be quantified

as a multiple of the unit of transmitter released. That is, the change in potential varies as a

multiple of the smallest change possible. They also discuss work done by showing that adding

the transmitter directly can not reproduce the stepwise depolarization.

14) The absolute limit is where the end plate has allowed Na to enter. This first sentence is

confusing. Just state that the equilibrium potential limits amplitude. That is the potential due to

the Na current is limited by the Na equilibrium potential.

15) ACh is broken down in the synapse by AcetylCholinesterase to give Acetate and choline.

Choline is then taken up by the presynaptic cell to make more Ach. Buildup of Ach in the

synaptic cleft can result in a postsynaptic cell that can not repolarize or a cell that has inactivated

receptors.

16) In the Soma, just prior to the axon hillock.

17) Both fast and slow transmissions are the result of the presynaptic cell releasing a chemical

into a synapse. From here the fast transmitters bind to receptors that are also ion channels.

Therefore the binding of neurotransmitter leads to ion channels opening. In slow transmission it

is the same except for the receptors (neurotransmitter may be different as well remember ACh is

involved in both fast and slow) that are involved. So here the ligand binds and the message is

transferred to a G-protein as opposed to an ion channel opening. The G-protein will then activate

a second messenger system to ultimately open channels. Fast transmission is faster but decays

quicker whereas slow is slower but has a longer lasting effect.

18) Neuromodulation is a term that generically refers to how chemicals can modulate or change

the way some neurons behave. A good example is that some neuromodulators can cause a

neuron to be more sensitive (easier to elicit an action potential).

19) In depolarization-release coupling Ca enters the cell due to an AP and binds to a regulatory

protein known as synaptotagmin. This event is believed to allow vesicular release. Facilitation

is believed to be due to increased calcium that has been unable to leave the cell prior to a second

AP. That is, a first AP lets Ca in and by the time a second AP appears not all of the Ca is gone.

In post-tetanic potentiation the train of impulses is believed to increase the Ca inside and

override the Ca buffering system. This increase in Ca is similar to facilitation. It differs in that

the short depression after tetanus is due to decreased transmitter release. In heterosynaptic

modulation a transmitter from will alter the presynaptic channels that allow Ca to enter. That is

they can allow more to enter the terminal. In long-term potentiation the NMDA receptor will

activate when both the cell is depolarized and glutamate is bound. When this occurs the Ca

concentration increases and second messengers are activated, resulting in a strengthening of the

synapse.

20) Reread the question - I think they just wanted to know how intensity was signaled in graded

potentials for the first part - ie there is a greater depolarization, or hyperpolarization.The

receptor potential can encode intensity through the presence of neuromodulators. These

modulators can alter the amount of current that can pass through the channel. Firing AP's at

close intervals can facilitate synaptic potentials. This is due to a presynaptic elevation of Ca and

thus more transmitter release. Intensity can only be encoded in AP's by increasing the frequency.

21) ACh at the heart is an inhibitory transmitter. Ach at the motor end plate in excitatory. This

is due to the difference in receptors that bind the transmitter.