3. AUTONOMIC NERVOUS SYSTEMS
111
ported ( Zchtli yomyaon, Carlson, 1906). The heart of Lampetra does
not contain adrenergic nerve fibers demonstrable by fluorescence histochemistry (see Falck et al., 1966), and catecholamines are variously
stated to cause a slight depression (Otorii, 1953) or an acceleration and
augmentation (Augustinsson et aZ., 1956; Falck ct aZ., 1966) of the
cardiac beat. It would therefore seem that the vagal innervation is
cholinergic, since acetylcholine accelerates the heartbeat, at the same
time depressing the force of contractions. Similar actions are exerted
by other choline csters, including succinylcholine, and nicotine, but not
by muscarine; the response to acetylcholine is inhibited by the nicotinic
blocking drugs hexnmcthonium and tubocurarine but is unaffected by
atropine (Otorii, 1953; Augustinsson et al., 1956; Falck et al., 1966). The
cholinergic receptors are therefore of the nicotinic type. Because of this,
Augustinsson ct al. (1956) suggested that acetylcholine was acting on
ganglion cells in the heart. It seems a simpler view that the lamprey
heart muscle has a closer affinity to the skeletal muscle than to the cardiac
muscle of higher vertebrates (Itina, 1959) and that acetylcholine is
acting directly on nicotinic receptors in the heart muscle itself. In this
case, one would expect treatment with curare to prevent vagal transmission to the heart, but Zwaardemaker (1924) observed cardiac
responses to medulla oblongata stimulation in lampreys immobilized
with curare. Perhaps the cardiac cholinergic receptors are relatively resistant to blockade by curare. The vagus does not appear to innervate
the heart in larval lampreys (Carlson, 1904, 1906).
Stimulation of either vagal trunk in Myxine causes a contraction of the
strongly muscular gallbladder ( Fange and Johnels, 1958). This pathway involves a ganglionic synapse in the hepatic plexus since topical
application of nicotine to the plexus abolishes the responses. The terminal neurons are probably cholinergic, for acetylcholine causes a
contraction of the gallbladder, whereas epinephrine appears to relax it.
The vagal innervation of the intestine is poorly understood. The muscularis of the gut wall is poorly developed, but it seems that all regions
of the intestine are contracted by acetylcholine and relaxed by catecholamines (Fange, 1918; von Euler and Bstlund, 1957; Johnels and
Ostlund, 1958). In addition, the isolated intestine is rcported to undergo
peristaltic movements (Olcott, 1931; Johnels and Bstlund, 1958). It is
therefore clear that the gut musculature is functional. However,
Fange (1948) and Fiinge and Johnels (1958) could not detect
any intestinal response to vagal stimulation in Myxine. Previously, Patterson and Fair (1933) had found that stimulation of the vagus in
Bdellostoina caused a very slight relaxation of the gut, but their records
were obtained in situ, and in view of the thinness of the gut wall the
111
ported ( Zchtli yomyaon, Carlson, 1906). The heart of Lampetra does
not contain adrenergic nerve fibers demonstrable by fluorescence histochemistry (see Falck et al., 1966), and catecholamines are variously
stated to cause a slight depression (Otorii, 1953) or an acceleration and
augmentation (Augustinsson et aZ., 1956; Falck ct aZ., 1966) of the
cardiac beat. It would therefore seem that the vagal innervation is
cholinergic, since acetylcholine accelerates the heartbeat, at the same
time depressing the force of contractions. Similar actions are exerted
by other choline csters, including succinylcholine, and nicotine, but not
by muscarine; the response to acetylcholine is inhibited by the nicotinic
blocking drugs hexnmcthonium and tubocurarine but is unaffected by
atropine (Otorii, 1953; Augustinsson et al., 1956; Falck et al., 1966). The
cholinergic receptors are therefore of the nicotinic type. Because of this,
Augustinsson ct al. (1956) suggested that acetylcholine was acting on
ganglion cells in the heart. It seems a simpler view that the lamprey
heart muscle has a closer affinity to the skeletal muscle than to the cardiac
muscle of higher vertebrates (Itina, 1959) and that acetylcholine is
acting directly on nicotinic receptors in the heart muscle itself. In this
case, one would expect treatment with curare to prevent vagal transmission to the heart, but Zwaardemaker (1924) observed cardiac
responses to medulla oblongata stimulation in lampreys immobilized
with curare. Perhaps the cardiac cholinergic receptors are relatively resistant to blockade by curare. The vagus does not appear to innervate
the heart in larval lampreys (Carlson, 1904, 1906).
Stimulation of either vagal trunk in Myxine causes a contraction of the
strongly muscular gallbladder ( Fange and Johnels, 1958). This pathway involves a ganglionic synapse in the hepatic plexus since topical
application of nicotine to the plexus abolishes the responses. The terminal neurons are probably cholinergic, for acetylcholine causes a
contraction of the gallbladder, whereas epinephrine appears to relax it.
The vagal innervation of the intestine is poorly understood. The muscularis of the gut wall is poorly developed, but it seems that all regions
of the intestine are contracted by acetylcholine and relaxed by catecholamines (Fange, 1918; von Euler and Bstlund, 1957; Johnels and
Ostlund, 1958). In addition, the isolated intestine is rcported to undergo
peristaltic movements (Olcott, 1931; Johnels and Bstlund, 1958). It is
therefore clear that the gut musculature is functional. However,
Fange (1948) and Fiinge and Johnels (1958) could not detect
any intestinal response to vagal stimulation in Myxine. Previously, Patterson and Fair (1933) had found that stimulation of the vagus in
Bdellostoina caused a very slight relaxation of the gut, but their records
were obtained in situ, and in view of the thinness of the gut wall the