3. AUTONOMIC NERVOUS SYSTEMS
121
mentally deflated swim bladders were no longer refilled. This observation shows that the vagi contain nerve fibers which are in some way
responsible for secretion into the swim bladder. However, Fange (1953)
was unable to show any filling responses to vagal stimulation. In fact,
the only clear response to vagal stimulation that he observed was an increase in the relative area of resorptive epithelium exposed to the enclosed gases brought about in a number of ways by contraction of the
muscularis mucosae, and a vasodilation in the resorptive epithelium,
This response would favor emptying of the swim bladder, and it probably masked completely those effects of vagal stimulation favoring filling. Fange showed that these “emptying” responses of the muscularis
mucosae and of the vasculature were probably mediated by adrenergic
nerves which, he suggested, contracted the muscularis mucosae of the
secretory portion but relaxed that of the resorptive portion of the
swim bladder and dilated the blood vessels in the resorptive region. In
view of their adrenergic nature, Fange postulated that these fibers were
sympathetic in origin, joining the vagus intracranially. In the absence of
conflicting evidence, this is still the safest interpretation. Fange’s
pharmacological arguments that the nerves are adrenergic have received
support from studies using the histochemical technique for demonstrating tissue monoamines. F a h l h et al. ( 1965), using this technique,
have shown that there is an adrenergic (norepinephrine) innervation of
blood vessels throughout the swim bladder and of the. muscularis mucosae
only in the secretory region in cod and trout; F a h l h (1965) found that
the muscularis of only the postulated resorptive region in Argentina was
adrenergically innervated. Many or all of these adrenergic neurons have
their cell bodies in or near the swim bladder (Fahlbn et al., 1965), a fact
which would explain why vagotomy does not alter catecholamine levels
in this organ (von Euler and Fange, 1961).
It is highly likely that the vagal nerve fibers which cause secretion
are cholinergic, for Fange (1953) has shown that atropine treatment,
like vagotomy, inhibits gas secretion into a deflated swim bladder. The
problem is which structure or structures are being affected by the
Fig. 4. Effects of vagal stimulation on the gut of Tinca. During stimulation of the
vagus (white bars below traces), the striated muscle contracts. The smooth muscle
contraction occurs only after a latent period of about 20 sec in ( a ) (10-sec period
of stimulation), 30 sec in ( b ) (20-sec period of stimulation), and 40 sec in ( c )
(stimulated for 50 sec). The increase in latency with increasing durations of stimulation indicates an inhibitory effect of vagal stimulation and suggests that the smooth
muscle contractions may be “rebound in nature. Time markers, 1 min. From
R. Mahn ( 1898), Untersuchungen iiber das physiologische Verhalten des Schleiendarms, Arch. Ges. Physiol. 72, 273-304. Springer, Berlin.
121
mentally deflated swim bladders were no longer refilled. This observation shows that the vagi contain nerve fibers which are in some way
responsible for secretion into the swim bladder. However, Fange (1953)
was unable to show any filling responses to vagal stimulation. In fact,
the only clear response to vagal stimulation that he observed was an increase in the relative area of resorptive epithelium exposed to the enclosed gases brought about in a number of ways by contraction of the
muscularis mucosae, and a vasodilation in the resorptive epithelium,
This response would favor emptying of the swim bladder, and it probably masked completely those effects of vagal stimulation favoring filling. Fange showed that these “emptying” responses of the muscularis
mucosae and of the vasculature were probably mediated by adrenergic
nerves which, he suggested, contracted the muscularis mucosae of the
secretory portion but relaxed that of the resorptive portion of the
swim bladder and dilated the blood vessels in the resorptive region. In
view of their adrenergic nature, Fange postulated that these fibers were
sympathetic in origin, joining the vagus intracranially. In the absence of
conflicting evidence, this is still the safest interpretation. Fange’s
pharmacological arguments that the nerves are adrenergic have received
support from studies using the histochemical technique for demonstrating tissue monoamines. F a h l h et al. ( 1965), using this technique,
have shown that there is an adrenergic (norepinephrine) innervation of
blood vessels throughout the swim bladder and of the. muscularis mucosae
only in the secretory region in cod and trout; F a h l h (1965) found that
the muscularis of only the postulated resorptive region in Argentina was
adrenergically innervated. Many or all of these adrenergic neurons have
their cell bodies in or near the swim bladder (Fahlbn et al., 1965), a fact
which would explain why vagotomy does not alter catecholamine levels
in this organ (von Euler and Fange, 1961).
It is highly likely that the vagal nerve fibers which cause secretion
are cholinergic, for Fange (1953) has shown that atropine treatment,
like vagotomy, inhibits gas secretion into a deflated swim bladder. The
problem is which structure or structures are being affected by the
Fig. 4. Effects of vagal stimulation on the gut of Tinca. During stimulation of the
vagus (white bars below traces), the striated muscle contracts. The smooth muscle
contraction occurs only after a latent period of about 20 sec in ( a ) (10-sec period
of stimulation), 30 sec in ( b ) (20-sec period of stimulation), and 40 sec in ( c )
(stimulated for 50 sec). The increase in latency with increasing durations of stimulation indicates an inhibitory effect of vagal stimulation and suggests that the smooth
muscle contractions may be “rebound in nature. Time markers, 1 min. From
R. Mahn ( 1898), Untersuchungen iiber das physiologische Verhalten des Schleiendarms, Arch. Ges. Physiol. 72, 273-304. Springer, Berlin.