CHAPTER 17
The Autonomic Nervous System 265communicans
and are distributed to autonomic effectors in
the areas supplied by these spinal nerves (Figure 17–2). These
postganglionic sympathetic nerves terminate mainly on
smooth muscle (eg, blood vessels, hair follicles, airways) and
on sweat glands in the limbs. Other postganglionic fibers
leave the chain ganglia to enter the thoracic cavity to termi-
nate in visceral organs. Postganglionic fibers from preverte-
bral ganglia also terminate in visceral targets.
PARASYMPATHETIC DIVISION
The parasympathetic nervous system is sometimes called the
craniosacral division
of the ANS because of the location of its
preganglionic neurons (Figure 17–3). The parasympathetic
nerves supply the visceral structures in the head via the oculo-
motor, facial, and glossopharyngeal nerves, and those in the
thorax and upper abdomen via the vagus nerves. The sacral
outflow supplies the pelvic viscera via branches of the second
to fourth sacral spinal nerves. Parasympathetic preganglionic
fibers synapse on ganglia cells clustered within the walls of vis-
ceral organs; thus these parasympathetic postganglionic fibers
are very short.
CHEMICAL TRANSMISSION AT
AUTONOMIC JUNCTIONS
ACETYLCHOLINE & NOREPINEPHRINE
The first evidence for chemical neurotransmission was provid-
ed by a simple yet dramatic study of heart rate control by the
parasympathetic nervous system performed by Otto Loewi in
1920 (Clinical Box 17–2). Transmission at the synaptic junc-
tions between pre- and postganglionic neurons and between the
postganglionic neurons and the autonomic effectors is chemi-
cally mediated. The principal transmitter agents involved are
acetylcholine
and
norepinephrine
(Figures 17–1 and 17–4).CLINICAL BOX 17–2
Pharmacological Control of Heart Rate
Using drugs to control heart rate and other physiological pro-
cesses is a very common therapy. It holds its roots in an obser-
vation made by Otto Loewi in 1920 that served as the founda-
tion for chemical transmission of nerve impulses. He provided
the first decisive evidence that a chemical messenger was re-
leased by cardiac nerves to affect heart rate. The experimental
design came to him in a dream on Easter Sunday of that year.
He awoke from the dream, jotted down notes, but the next
morning they were indecipherable. The next night, the dream
recurred and he went to his laboratory at 3:00
AM
to conduct a
simple experiment on a frog heart. He isolated the hearts from
two frogs, one with and one without its innervation. Both
hearts were attached to cannulas filled with Ringer solution.
The vagus nerve of the first heart was stimulated, and then the
Ringer solution from that heart was transferred to the nonin-
nervated heart. The rate of its contractions slowed as if its
vagus nerve had been stimulated. Loewi also showed that
when the sympathetic nerve of the first heart was stimulated
and its effluent was passed to the second heart, the rate of
contractions of the “donor” heart increased as if its sympa-
thetic fibers had been stimulated. These results proved that
nerve terminals release chemicals which cause the well-
known modifications of cardiac function that occur in re-
sponse to stimulation of its nerve supply. Loewi called the
chemical release by the vagus nerve
Vagusstoff.
Not long after,
it was identified chemically to be acetylcholine.FIGURE 17–4
Chemical coding of sympathetic preganglionic and postganglionic neurons.
CNS, central nervous system; PNS, periph-
eral nervous system.
(Reproduced with permission from Haines DE [editor]:
Fundamental Neuroscience for Basic and Clinical Applications,
3rd ed. Elsevier, 2006.)