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Comparison of Action Potentials and Excitatory Postsynaptic Potentials (EPSPs)

  • TABLE 7.4: Comparison of Action Potentials and Excitatory Postsynaptic Potentials (EPSPs)

Characteristics

  • Amplitude

    • Action Potential: All-or-none response.
    • EPSP: Graded response.

  • Stimulus for Opening of Ionic Gates

    • Action Potential: Depolarization.
    • EPSP: Acetylcholine (ACh) or other excitatory neurotransmitter.

  • Initial Effect of Stimulus

    • Action Potential: Na+ channels open.
    • EPSP: Common channels for Na+ and K+ open, leading to a loss of intracellular positive charges over time and distance.

  • Cause of Repolarization

    • Action Potential: Opening of K+ gates.
    • EPSP: Not applicable (graded potential).

  • Conduction Distance

    • Action Potential: Regenerated over the length of the axon.
    • EPSP: Typically 1 to 2 mm; considered a localized potential.

  • Positive Feedback Between Depolarization and Opening of Na+ Gates

    • Action Potential: Yes.
    • EPSP: No.

  • Maximum Depolarization

    • Action Potential: +40 mV.
    • EPSP: Close to zero.

  • Summation

    • Action Potential: No summation; an all-or-none event.
    • EPSP: Summation of EPSPs can produce graded depolarizations.

  • Refractory Period

    • Action Potential: Yes.
    • EPSP: No.

  • Effect of Drugs

    • Action Potential: ACh effects inhibited by tetrodotoxin, not by curare.
    • EPSP: ACh effects inhibited by curare, not by tetrodotoxin.

Mechanism of Depolarization

  • d-Gated Channels:

    • Ligand-gated channels exemplified.
    • Inward flow of Na+ ions depolarizes the cell, leading to the generation of an EPSP.

  • EPSP Characteristics:

    1. Occur in dendrites and cell bodies.
    2. Results from the binding of several ACh molecules that can add together to produce a greater depolarization (graded).
    3. This can potentially reach the threshold for voltage-gated channels located in the axon hillock, which can lead to the generation of an action potential.

Acetylcholinesterase (AChE)

  • Definition: An enzyme responsible for inactivating ACh activity immediately after it binds to its receptor.
  • Function: Hydrolyzes ACh into acetate and choline, which are then taken back into the presynaptic cell for reuse.

Cholinesterase Inhibitors

  • Overview: These drugs inhibit the action of acetylcholinesterase (AChE), leading to an increased amount of ACh in the synaptic cleft, thus enhancing cholinergic synaptic transmission.

  • Clinical AChE Inhibitors:

    • Examples include neostigmine, physostigmine, and pyridostigmine, which are used in the treatment of myasthenia gravis and are significant in the treatment of Alzheimer's disease.

  • Nerve Gas:

    • Mechanism: Inhibits AChE, causing spastic paralysis and potentially lethal overstimulation of cholinergic synapses.

G-Protein Coupled Receptors (GPCRs)

  • Mechanism: The neurotransmitter receptor is coupled with the ion channel through a mechanism involving G-proteins.
    1. The binding at the receptor indirectly opens ion channels by utilizing a G-protein.
    2. Muscarinic ACh receptors operate through this mechanism, which affects ion channel functionality.