Human Physiology, 14th edition (2016)

The Nervous System 187

activate a complex of proteins in the cell membrane known as

G-proteins —so named because their activity is influenced by

guanosine nucleotides (GDP and GTP). This topic was intro-

duced in chapter 6, section 6.5. Muscarinic receptors are thus

members of a family of receptors called G-protein-coupled

receptors.

There are three G-protein subunits, designated alpha, beta,

and gamma. In response to the binding of ACh to its recep-

tor, the alpha subunit dissociates from the other two subunits,

which stick together to form a beta-gamma complex. Depend-

ing on the specific case, either the alpha subunit or the beta-

gamma complex then diffuses through the membrane until it

binds to an ion channel, causing the channel to open or close

the receptors and the ion channels are different, separate mem-
brane proteins. Thus, binding of the neurotransmitter ligand to
its receptor can open the ion channel only indirectly. Such is
the case with the muscarinic ACh receptors discussed in this
section, as well as the receptors for dopamine and norepineph-
rine, discussed in section 7.5.
The muscarinic ACh receptors are formed from only a
single subunit, which binds to one ACh molecule while the
rest of the receptor protein forms intracellular and extracellu-
lar loops. Unlike the nicotinic receptors, these receptors do not
contain ion channels. The ion channels are separate proteins
located at some distance from the muscarinic receptors. Bind-
ing of ACh (the ligand) to the muscarinic receptor causes it to

Table 7.4 | Comparison of Action Potentials and Excitatory Postsynaptic Potentials (EPSPs)

Characteristic Action Potential Excitatory Postsynaptic Potential

Amplitude All-or-none Graded

Stimulus for opening of ionic gates Depolarization Acetylcholine (ACh) or other excitatory

neurotransmitter

Initial effect of stimulus Na^1 channels open Common channels for Na^1 and K^1 open

Cause of repolarization Opening of K^1 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^1 gates

Ye s N o

Maximum depolarization 1 40 mV Close to zero

Summation No summation—all-or-none event Summation of EPSPs, producing graded

depolarizations

Refractory period Yes No

Effect of drugs ACh effects inhibited by tetrodotoxin,

not by curare

ACh effects inhibited by curare, not by

tetrodotoxin

Drug Origin Effects

Botulinum toxin Produced by Clostridium botulinum (bacteria) Inhibits release of acetylcholine (ACh)

Curare Resin from a South American tree Prevents interaction of ACh with its nicotinic receptor proteins

a-Bungarotoxin Venom of Bungarus snakes Binds to ACh receptor proteins and prevents ACh from binding

Saxitoxin Red tide (Gonyaulax) algae Blocks voltage-gated Na^1 channels

Tetrodotoxin Pufferfish Blocks voltage-gated Na^1 channels

Nerve gas Artificial Inhibits acetylcholinesterase in postsynaptic membrane

Neostigmine Nigerian bean Inhibits acetylcholinesterase in postsynaptic membrane

Strychnine Seeds of an Asian tree Prevents IPSPs in spinal cord that inhibit contraction of antagonistic

muscles

Table 7.5 | Drugs That Affect the Neural Control of Skeletal Muscles