Ligand Operated Channels

This is the most direct mechanism by which chemically regulated gates can be opened. In this case, the ion channel runs through the receptor itself. The ion channel is opened by the binding of the receptor to the neurotransmitter ligand.

Such is the case when ACh binds to its nicotinic ACh receptor. This receptor consists of five polypeptide subunits that enclose the ion channel. Two of these subunits contain ACh-binding sites, and the channel opens when both sites bind to ACh (fig. 7.23). The opening of this channel permits the simultaneous diffusion of Na+ into and K+ out of the postsynaptic cell. The effects of the inward flow of Na+ predominate, however, because of its steeper electrochemical gradient. This produces the depolarization of an excitatory postsynaptic potential (EPSP).

Although the inward diffusion of Na+ predominates in an EPSP, the simultaneous outward diffusion of K+ prevents the

Extracellular Fluid

Extracellular Fluid

0 K+

■ Figure 7.23 Nicotinic acetylcholine (ACh) receptors also function as ion channels. The nicotinic acetylcholine receptor contains a channel that is closed (a) until the receptor binds to ACh. (b) Na+ and K+ diffuse simultaneously, and in opposite directions, through the open ion channel. The electrochemical gradient for Na+ is greater than for K+, so that the effect of the inward diffusion of Na+ predominates, resulting in a depolarization known as an excitatory postsynaptic potential (EPSP).

1 Fox: Human Physiology,

1 7. The Nervous System: 1 Text

© The McGraw-Hill

Eighth Edition

Neurons and Synapses

Companies, 2003


Chapter Seven

Table 7.5 Comparison of Action Potentials and Excitatory Postsynaptic Potentials (EPSPs)


Action Potential

Excitatory Postsynaptic Potential

Stimulus for opening of ionic gates


Acetylcholine (ACh)

Initial effect of stimulus

Na+ channels open

Common channels for Na+ and K+ open

Cause of repolarization

Opening of K+ gates

Loss of intracellular positive charges with time and distance

Conduction distance

Regenerated over length of the axon

1-2 mm; a localized potential

Positive feedback between depolarization



and opening of Na+ gates

Maximum depolarization

+40 mV

Close to zero


No summation—all-or-none event

Summation of EPSPs, producing graded depolarizations

Refractory period



Effect of drugs

Inhibited by tetrodotoxin, not by curare

Inhibited by curare, not by tetrodotoxin

Table 7.6 Drugs That Affect the Neural Control of Skeletal Muscles




Botulinum toxin

Produced by Clostridium botulinum (bacteria)

Inhibits release of acetylcholine (Ach)


Resin from a South American tree

Prevents interaction of ACh with the postsynaptic receptor protein


Venom of Bungarus snakes

Binds to ACh receptor proteins and prevents ACh from binding


Red tide (Gonyaulax) algae

Blocks voltage-gated Na+ channels



Blocks voltage-gated Na+ channels

Nerve gas


Inhibits acetylcholinesterase in postsynaptic membrane


Nigerian bean

Inhibits acetylcholinesterase in postsynaptic membrane


Seeds of an Asian tree

Prevents IPSPs in spinal cord that inhibit contraction of antagonistic muscles

depolarization from overshooting 0 mV. Therefore, the membrane polarity does not reverse in an EPSP as it does in an action potential. (Remember that action potentials are produced by separate voltage-gated channels for Na+ and K+, where the channel for K+ opens only after the Na+ channel has closed.)

A comparison of EPSPs and action potentials is provided in table 7.5. Action potentials occur in axons, where the voltage-gated channels are located, whereas EPSPs occur in the dendrites and cell body. Unlike action potentials, EPSPs have no threshold; the ACh released from a single synaptic vesicle produces a tiny depolarization of the postsynaptic membrane. When more vesicles are stimulated to release their ACh, the depolarization is correspondingly greater. EPSPs are therefore graded in magnitude, unlike all-or-none action potentials. Since EPSPs can be graded, and have no refractory period, they are capable of summation. That is, the depolarizations of several different EPSPs can be added together. Action potentials are prevented from summating by their all-or-none nature and by the refractory periods they exhibit.

B Jt Muscle weakness in the disease myasthenia gravis is due to the fact that ACh receptors are blocked and ^ destroyed by antibodies secreted by the immune system of the affected person. Paralysis in people who eat shellfish poisoned with saxitoxin, or pufferfish containing tetrodotoxin, results from the blockage of Na+ channels. The effects of these and other poisons on neuromuscular transmission are summarized in table 7.6.

Clinical Investigation Clue

Remember that Sandra had flaccid paralysis and difficulty breathing after eating mussels and clams gathered from the local shore.

■ Mussels and clams are filter feeders that can concentrate the poison in the organisms responsible for the red tide. How might eating these mussels and clams cause her flaccid paralysis?

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