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Chapter 12: Problem 14

The neurotransmitter acetylcholine is made in the cytosol and then transported into synaptic vesicles, where its concentration is more than 100 -fold higher than in the cytosol. When synaptic vesicles are isolated from neurons, they can take up additional acetylcholine added to the solution in which they are suspended, but only when ATP is present. Na \(^{+}\) ions are not required for the uptake, but, curiously, raising the \(\mathrm{pH}\) of the solution in which the synaptic vesicles are suspended increases the rate of uptake. Furthermore, transport is inhibited when drugs are added that make the membrane permeable to \(\mathrm{H}^{+}\) ions. Suggest a mechanism that is consistent with all of these observations.

Short Answer

Expert verified
A proton gradient across the vesicle membrane, maintained by ATP, drives acetylcholine uptake via a \(\mathrm{H}^+\)-antiporter mechanism.

Step by step solution

01

Understanding the Problem

The problem presents a scenario where acetylcholine (ACh) is concentrated in synaptic vesicles, over 100 times the concentration in cytosol, depending on ATP presence. Notably, Na \(^{+}\) ions are not essential, but a higher \(\mathrm{pH}\) and ATP enhance uptake, while drugs that increase \(\mathrm{H}^{+}\) ion permeability inhibit transport.
02

Interpreting pH Influence

A higher \(\mathrm{pH}\) means fewer \(\mathrm{H}^+\) ions, suggesting that uptake is inversely related to \(\mathrm{H}^+\) concentration. This indicates that the proton gradient (\(\mathrm{H}^+\) ion gradient) across the vesicle membrane is essential for the uptake of acetylcholine.
03

Analyzing ATP Requirement

ATP presence is required for ACh uptake, implying an active transport mechanism. ATP likely provides energy for a proton pump, producing a \(\mathrm{H}^+\) gradient across the vesicle membrane, contrasting with cytosolic \(\mathrm{H}^+\) levels.
04

Linking Proton Gradient and Acetylcholine Transport

The existence of a \(\mathrm{H}^+\) gradient supports the hypothesis of an antiporter transport mechanism, where acetylcholine influx into the vesicle is coupled with \(\mathrm{H}^+\) efflux. This antiport activity accelerates when the \(\mathrm{H}^+\) gradient is steepened, consistent with increased \(\mathrm{pH}\) or blocked when permeability to \(\mathrm{H}^+\) ions increases.
05

Proposing Mechanism

The synaptic vesicle likely employs a proton pump fueled by ATP to maintain a \(\mathrm{H}^+\) gradient. This gradient powers an acetylcholine/\(\mathrm{H}^+\) antiporter, enabling acetylcholine to be concentrated in vesicles when ATP is available and \(\mathrm{H}^+\) leaking (via membrane-permeable drugs) is inhibited.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Acetylcholine
Acetylcholine (ACh) is a vital neurotransmitter in the nervous system, responsible for carrying signals between neurons. Imagine it as a messenger that travels from neuron to neuron, ensuring that information is transmitted swiftly and effectively. It is synthesized in the cytosol of neurons before it makes its way to synaptic vesicles.
Here is why acetylcholine is essential:
  • It relays signals across synapses in the brain and between nerves and muscles.
  • It impacts functions such as muscle activation, memory, and attention.
  • It's a key player in both the central and peripheral nervous systems.
For acetylcholine to carry out its role efficiently, it must be concentrated inside synaptic vesicles, ensuring a rapid response upon release into the synaptic cleft.
Synaptic Vesicles
Synaptic vesicles play a crucial role in neurotransmitter transport. Consider them storage units for neurotransmitters like acetylcholine. They are tiny, membrane-bound compartments found within neurons. Whenever signals have to be passed on, these vesicles step up to release the required chemicals like acetylcholine into the synaptic cleft.
Synaptic vesicles:
  • Help in the storage and release of neurotransmitters.
  • Ensure neurotransmitters are protected until the right moment of release.
  • Facilitate rapid and controlled neurotransmitter release, crucial for efficient neuronal communication.
Understanding these vesicles is critical in comprehending how neurotransmission occurs and what factors affect its efficiency, such as the proton gradient or the presence of ATP.
Proton Gradient
A proton gradient is a difference in proton concentration across a membrane that drives many cellular processes. In the context of synaptic vesicles, this gradient is crucial for transporting neurotransmitters like acetylcholine.
The proton gradient's importance arises because:
  • It creates a stored form of energy that can be harnessed for active transport.
  • In synaptic vesicles, a steep proton gradient means fewer protons inside and more outside, which drives the exchange process.
  • The gradient's disruption leads to inhibited transport, as evident in the presence of drugs that alter \( \mathrm{H}^{+} \) ion permeability.
This gradient proves crucial because it powers an acetylcholine/\( \mathrm{H}^{+} \) antiporter system, efficiently concentrating acetylcholine within the vesicles.
ATP-dependent Transport
ATP-dependent transport is another key concept in cellular mechanisms, and it is vital in the neurotransmitter transport process. It refers to the active transport of molecules against their gradient, driven by energy derived from ATP.
In synaptic vesicles, the significance of ATP-dependent transport includes:
  • Maintaining the proton gradient through ATP-driven proton pumps, which is essential for efficient acetylcholine uptake.
  • Ensuring energy-dependent processes, such as the coupling of acetylcholine influx with the efflux of protons, are sustained.
  • Providing the energy required to maintain the concentration differential of acetylcholine within vesicles.
Thus, ATP is indispensable for neurotransmitter filling of synaptic vesicles, showing how bioenergetics play a part in cellular communication.

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Most popular questions from this chapter

We will see in Chapter 15 that endosomes, which are membrane-enclosed intracellular organelles, need an acidic lumen in order to function. Acidification is achieved by an \(\mathrm{H}^{+}\) pump in the endosomal membrane, which also contains \(\mathrm{Cl}^{-}\) channels. If the channels do not function properly (e.g., because of a mutation in the genes encoding the channel proteins), acidification is also impaired. A. Can you explain how CI' channels might help acidification? B. According to your explanation, would the Cl-channels be absolutely required to lower the pH inside the endosome?

Which of the following statements are correct? Explain your answers. A. The plasma membrane is highly impermeable to all charged molecules. B. Channels have specific binding pockets for the solute molecules they allow to pass. C. Transporters allow solutes to cross a membrane at much faster rates than do channels. D. Certain \(\mathrm{H}^{+}\) pumps are fueled by light energy. E. The plasma membrane of many animal cells contains open \(\mathrm{K}^{+}\) channels, yet the \(\mathrm{K}^{+}\) concentration in the cytosol is much higher than outside the cell. F. A symport would function as an antiport if its orientation in the membrane were reversed (i.e., if the portion of the molecule normally exposed to the cytosol faced the outside of the cell instead). G. The membrane potential of an axon temporarily becomes more negative when an action potential excites it.

Amino acids are taken up by animal cells using a symport in the plasma membrane. What is the most likely ion whose electrochemical gradient drives the import? Is ATP consumed in the process? If \(s o,\) how?

The resting membrane potential of a typical animal cell is about \(-70 \mathrm{mV}\), and the thickness of a lipid bilayer is about \(4.5 \mathrm{nm} .\) What is the strength of the electric field across the membrane in \(\mathrm{V} / \mathrm{cm} ?\) What do you suppose would happen if you applied this field strength to two metal electrodes separated by a \(1-\mathrm{cm}\) air gap?

In the disease myasthenia gravis, the human body makes-by mistakeantibodies to its own acetylcholine receptor molecules. These antibodies bind to and inactivate acetylcholine receptors on the plasma membrane of muscle cells. The disease leads to a devastating progressive weakening of the people affected. Early on, they may have difficulty opening their eyelids, for example, and, in an animal model of the disease, rabbits have difficulty holding their ears up. As the disease progresses, most muscles weaken, and people with myasthenia gravis have difficulty speaking and swallowing. Eventually, impaired breathing can cause death. Explain which step of muscle function is affected.
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