REVERSAL POTENTIAL

lantomore

hi am sorry for the delay…the job was technical and have been researching on it.

Neuroscience3600 Problem Set 4

Please write neatly and give complete, but concise, answers. Point credit for each problem shown to
the left (total of 20 pts).

1. (6 pts) What’s the difference between an EPSP and an action potential? Compare and contrast

these two potentials. Consider the ions involved, types of channels, duration, amplitude,

triggering events, and mechanisms of depolarization.

2. (1 pt) Do EPSPs show an after-hyperpolarization? Why or why not?

3. (0.5 pt) True of False: The key determinant of whether a synapse is excitatory or inhibitory is
the identity of the neurotransmitter. Briefly explain your answer.

4. (3 pts) Measurements used to determine the reversal potential of a particular
synapse are shown below. Separate experiments confirm that changing Cl- and

Ca
2
+ concentrations have no effect on these results.

a) Plot the results on the I-V plot at right (approximate values are sufficient) and

identify the reversal potential.
Reverse potential is The point at which the I/V curve crosses the X-axis .-50mV

b) What can you say about the relative contribution of each permeant ion to

the reversal potential? Explain your reasoning.
Reverse potential is contributed by the four principle ion; potassium, sodium,
chloride and calcium. However conductance by calcium is slow and considered only it
plays a significant role. Relative contribution of the permeant ions to reverse potential
is dependent to their relative permeability and conductance ratios.
Potassium ions: PK (relative permeability of potassium) is set at 1.0. There are more
K

+
leak channels than any other type of channel. Actually this accounts 67%of the

current to reverse potential..
Sodium ion: PNa (relative permeability of sodium)is 0.04 compared to K+.Accounts to
3% of the current. Sodium equilibrium potential is +60Mv this is away from reverse
potential and membrane resting potential. Sodium channel are fewer than that of
potassium
Chloride: PCl is 0.45 (relative permeability of chloride ions) this translates to 30% of
the current. Again, its equilibrium potential is close to reverse potential.

c) Describe a manipulation that would shift the reversal potential downward to around 0 mV.

Tetraethylammonium+(TEA) is an ion that blocks K+but not Na+channels.this can bring

reverse potential to 0 M.Ths. increases the firing level of excitable cell

4-aminopyridine used to alleviate multiple sclerosis bringing down reverse potential to 0Mv

through increasing neuronal and axonal excitability!

5. (1 pt) The medial prefrontal cortex (mPFC) and striatum both receive a dopaminergic

projection from the ventral tegmental area (VTA). You hypothesize that the same VTA

cells that innervate the mPFC also send a parallel projection (also called a collateral axon)

to the striatum. The alternative hypothesis is that there are separate sub-populations in

VTA, with one group of cells projecting solely to mPFC and a separate group projecting to

NA. How would you test to discriminate between these two hypotheses?

Differential test

Medial prefrontal cortex (mPFC) mediates decision making. mPFC in support of hippocampus is

selectively involved in the retrieval of remote long-term memory. On other hand,

The striatum is thought to play a crucial role in value-based decision making.

I would carry animal studies; by injecting animals general dopamine antagonist and other as control

inject normal saline. Then subject the two groups to test of memory (conditional reflexes i.e. Pavlov’s

experiment) and reward and punishment experiments to test valued based decision.

Deductions: if animals can’t recall Pavlov’s ring bell, shown by salivation and at the same time not be

able to avoid or do certain action that will attract punishment or reward, then it is hypothetical that

both medial prefrontal cortex and striatum are innervated by parallel projection from ventral tegmental

area. If one functions of striatum are spared (ability distinguish a reward and punishment) then it

means that sub population of cell in VTA is specific for innervation of striatum.

6. (1 pt) The following electron micrograph shows a close-up of an axon (A) and

two dendrites, labeled D1 and D2. Is there anything unusual about these

dendrites vis-à-vis their ability to communicate? If so, what? Describe any

evidence you use to reach your conclusion.

Yes they have unusual; Cluster of polyribosomes is invariably present in the two dendritic points. The

axon is short and thin thus nerve signal can’t be efficiently to nearby cells. This could be as result of

degeneration and aging

These observations show that the fundamental differences in form and in the distribution of ribosomes

between axons and dendrites that is not similar to normal distribution in normal nerve cells

7. (1.5) Describe three mechanisms whereby an drug or toxin can enhance neurotransmission. For

each mechanism, cite a specific example (the drug and the affected neurotransmitter) and

briefly describe its mechanism of action.

8. (3 pts) The membrane potential, Em, of a post-synaptic cell can be calculated from the

following equation:

where grest is the leakage current which maintains the resting potential, Erest is the normal resting

potential, gE is the conductance due to excitatory post-synaptic channels (e.g., AMPA channels),

ErevE is the reversal potential for the excitatory channels, gI is the conductance due to inhibitory

post-synaptic channels (e.g., GABA channels) and ErevI is the reversal potential for the
inhibitory channels (this equation comes from the equivalence circuit discussed in Lecture 13

& 14, slide 21). Assume grest = 1 milliSiemens, Erest = -65 mV, ErevE = -10 mV, ErevI = -70 mV.
a) If gE at the peak of the EPSP is 2 milliSiemens, what is the height of the EPSP

without an IPSP (i.e., what is the change in potential from resting)? +36.3mV
b) If gI at the peak of the IPSP is 1 milliSiemens, what is the change in potential

from resting?
+23.3mV

c) What is the sum of the peak IPSP voltage change and the peak EPSP voltage
change?
+59.5mV

d) What is the net change in synaptic potential when an EPSP and IPSP occur

simultaneously?
134.6mV
Why is your answer different from the simple sum of potentials in part c?
Normally, in body EPSP and IPSP don’t occur separately and independently. These two take
place together and you can’t separate them. This explain why the net change is different
when each is determined separately as opposed to when are occurring together

Neuroscience 3600 Problem Set 4

9. (1 pt) A cell receives two synaptic inputs at adjacent locations on a dendritic branch. Each

synapse, when activated by a single pre-synaptic spike, produces a depolarizing EPSP. From

resting potential, these EPSPs create a peak voltage change of +18 mV. If the resting potential is

-80 mV and threshold for spike generation is -40 mV, can these two synapses ever cause a spike

in the post-synaptic cell? Explain.

10. (2 pts) The left two columns in the figure below (Fig 5.20 from your book) show ion

flow and net current during an EPSP at different clamp voltages in an ACh channel

that is equally permeable to both Na+ and K+. Now, assume that Na+ concentration

inside is equal to the outside Na+ concentration. In the right two columns, show ion

flow and net current during an EPSP under these new conditions.

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