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Place these events in the order in which they occur after a presynaptic neuron releases acetylcholine into the synaptic cleft. a. Vesicles containing a neurotransmitter fuse with the cell membrane. b. Ligand-gated \(\mathrm{Na}^{+}\)channels open, causing an influx of \(\mathrm{Na}^{+}\)ions. c. Voltage-gated \(\mathrm{Na}^{+}\)channels open in the axon. d. Membrane depolarization triggers voltage-gated \(\mathrm{Ca}^{2+}\) channels to open. e. Local membrane depolarization in the axon triggers an efflux of \(\mathrm{K}^{+}\).

Short Answer

Expert verified
Order: a, d, b, c, e.

Step by step solution

01

Vesicle Fusion

After the action potential reaches the presynaptic terminal, vesicles containing the neurotransmitter acetylcholine fuse with the presynaptic membrane. This step is represented by option (a).
02

Calcium Influx

The fusion of the vesicles is triggered by the opening of voltage-gated \(\mathrm{Ca}^{2+}\) channels, which occurs due to membrane depolarization. This is described by option (d).
03

Neurotransmitter Release

Once the vesicles fuse with the presynaptic membrane, acetylcholine is released into the synaptic cleft.
04

Sodium Channels Open

Acetylcholine binds to ligand-gated \(\mathrm{Na}^{+}\) channels on the postsynaptic neuron, causing them to open and allowing \(\mathrm{Na}^{+}\) ions to flow into the neuron. This corresponds to option (b).
05

Voltage-Gated Sodium Channels Open

If the local depolarization is sufficient, it triggers voltage-gated \(\mathrm{Na}^{+}\) channels to open, causing further sodium influx. This is represented by option (c).
06

Potassium Efflux

Following this, the local membrane depolarization will generally lead to an efflux of \(\mathrm{K}^{+}\) ions as voltage-gated \(\mathrm{K}^{+}\) channels open, maintaining the action potential's progression. This is described by option (e).

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Key Concepts

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

Synaptic Cleft Interaction
In the grand process of neural transmission, the synaptic cleft is where information jumps from one neuron to another. This tiny gap separates the terminal of a presynaptic neuron from the surface of a postsynaptic neuron. It is the battlefield for neurotransmitters, the chemical messengers of the brain.
Neurotransmitters are packaged in vesicles within the presynaptic neuron. When action potentials ride down the neuron's axon, reaching the terminal, these vesicles are set to release their chemical contents into the cleft. Vesicle fusion with the presynaptic membrane is crucial for neurotransmitter release. This process is tightly regulated by voltage-gated calcium (\(\mathrm{Ca}^{2+}\)) channels. They open in response to membrane depolarization, allowing calcium ions to flood into the cell.
Post release, neurotransmitters dock onto receptor sites on the postsynaptic neuron. This interaction is the first handshake in neural communication and can excite or inhibit the neuron, depending on the neurotransmitter's nature and the receptor type.
  • Neurotransmitters are stored in vesicles within presynaptic terminals.
  • Calcium channels are key to vesicle fusion and neurotransmitter release.
  • Receptors on postsynaptic neurons determine the response to neurotransmitters.
Neurotransmitter Release
Neurotransmitter release is a classic example of cellular exocytosis tailored for swift communication. It begins with the arrival of an action potential at the presynaptic terminal. This electrical impulse prompts voltage-gated calcium channels to pop open.
Calcium ions rush into the cell, sparking the movement of neurotransmitter-filled vesicles towards the cell's membrane. In a burst of activity, these vesicles fuse with the presynaptic membrane, spilling their contents into the synaptic cleft.
Once released, the neurotransmitters are free to bind to receptors on the postsynaptic neuron, initiating either an excitatory or inhibitory signal. This event is crucial as it determines the ensuing electrical response in the postsynaptic neuron. The role of calcium is indispensable here—it acts like a key, unlocking the gate for neurotransmitter release.
  • Exocytosis allows vesicles to release their neurotransmitter cargo.
  • Calcium influx prompts vesicle movement and membrane fusion.
  • Receptor interaction leads to signals in the postsynaptic neuron.
Ion Channel Dynamics
Ion channels are the gates through which ions flow in and out of neurons. They are crucial for maintaining the delicate balance needed for neural activity. In our context here, the dynamics are centered around sodium (\(\mathrm{Na}^{+}\)) and potassium (\(\mathrm{K}^{+}\)) channels, which are essential for propagating electrical signals.
Ligand-gated sodium channels on the postsynaptic membrane open in response to neurotransmitters from the synaptic cleft, allowing sodium ions to enter the neuron. This influx causes a local depolarization.
If this depolarization is strong enough, it triggers voltage-gated sodium channels to open, causing a rapid influx of more sodium ions. This is the beginning of the action potential traveling down the neuron. Following this, to restore balance, voltage-gated potassium channels open, allowing potassium ions to leave the cell, returning the membrane potential to its resting state.
  • Ligand-gated channels respond to neurotransmitter binding.
  • Voltage-gated channels respond to changes in membrane potential.
  • Potassium efflux helps in resetting the neuron's membrane potential.

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