Human Physiology, 14th edition (2016)

The Nervous System 195

Glycine is a neurotransmitter in the spinal cord, brain stem,

and retina, whereas GABA is more widespread in the CNS.

In the spinal cord, GABA and glycine have important roles in

both sensory and motor transmission. However, glycine is par-

ticularly important in the spinal control of skeletal movements

(chapter 12; see figs. 12.29 and 12.30). Flexion of an arm, for

example, involves stimulation of the flexor muscles by motor

neurons in the spinal cord. The motor neurons that innervate

the antagonistic extensor muscles are inhibited by IPSPs pro-

duced by glycine released from other neurons. The importance

of the inhibitory actions of glycine is revealed by the deadly

effects of strychnine, a poison that causes spastic paralysis by

specifically blocking the glycine receptor proteins. Animals

poisoned with strychnine die from asphyxiation because they

are unable to relax the diaphragm.

GABA is the most prevalent neurotransmitter in the

brain; in fact, as many as one-third of all the neurons in the

brain use GABA as a neurotransmitter. Like glycine, GABA

is inhibitory—it hyperpolarizes the postsynaptic membrane

by opening Cl^2 channels. Also, the effects of GABA, like

those of glycine, are involved in motor control. For example,

large neurons called Purkinje cells mediate the motor func-

tions of the cerebellum by producing IPSPs in their post-

synaptic neurons. A deficiency of GABA-releasing neurons

is responsible for uncontrolled movements in people with

Huntington’s disease. Huntington’s disease is a neurodegen-

erative disorder caused by a defect in the huntingtin gene

(chapter 3, section 3.4).

exit of K^1 ) through NMDA channels in the dendrites of the
postsynaptic neuron.

Inhibitory Neurotransmitters

There are two inhibitory neurotransmitters in the CNS: GABA
( gamma-aminobutyric acid ), a derivative of glutamic acid,
and glycine. The glycine and GABA receptors are ligand-gated
ion channels that, like the nicotinic ACh receptor, open when
the receptor binds to its neurotransmitter ligand. When GABA
and glycine bind to their respective receptors, they open chan-
nels for Cl^2 that hyperpolarize the postsynaptic membrane and
produce an IPSP ( fig. 7.32 ).
Because active transport carriers keep the concentration of
Cl^2 lower inside than outside of mature neurons, Cl^2 will dif-
fuse into the postsynaptic neuron. This is true as long as the post-
synaptic membrane potential is less negative (more depolarized)
than the chloride equilibrium potential (chapter 6, section 6.4).
This may not be the case at rest, because the chloride equilib-
rium potential may be close to the resting membrane potential.
However, if an excitatory neurotransmitter partially depolarizes
the membrane, the movement of Cl^2 through its open chan-
nels is promoted. When this occurs, the hyperpolarizing effects
of Cl^2 entering the cell make it more difficult for the postsyn-
aptic neuron to reach the threshold depolarization required to
stimulate action potentials. Thus, the opening of Cl^2 channels
by an inhibitory neurotransmitter renders excitatory input less
effective.

Figure 7.32 GABA receptors contain a chloride channel. When GABA (gamma-aminobutyric acid) binds to its receptor, a
chloride ion (Cl^2 ) channel opens through the receptor. This permits the inward diffusion of Cl^2 , resulting in hyperpolarization, or
an IPSP.

1. Channel closed
   until receptor binds
   to GABA


2. Channel closed
   until receptor binds
   to GABA
   3. Diffusion of Cl–^
   into cell causes
   hyperpolarization (IPSP)
   2. GABA receptor
   binds to GABA, Cl–
   channel opens

GABA

GABA

Channel receptors

closed

Plasma

membrane

Chloride ion (Cl–)