1 04
IVAN (monHonY
FkJi’Py ( 1963) critickd lh~cq’s yq)roech on the grounds that he had
homopnizcd wholc ti,nimds ;md not the ncrvous tissue. Florey removed
the gaiiglion from G. inteetit/,aZis and made extracts of it. He reported
concentrations of ucetylaholine in the order of 20 to 120 pglg wet weight
of ganglion and concluded that such high concentrations must indicate
a. preponderance of cholinergic nerves. This is supported by his finding
that the muscles contract in the presence of acetylcholine, although
the effect ie not potentiated by cserine. However, he did find that
cholincsterase activity in the muscles is low and suggested that this
might explain the rather slow rate of relaxation of ascidian muscles
following contraction. However, there does not seem to be any good
evidence to confirni that muscle relaxation is slow. The re-expansion of
a whole ascidian after retraction is slow, but this is due, at least in part,
to the weakness of the opposing muscle system.
In a later paper Florey (1967) describes some additional careful
experiments in support of the presence of cholinergic nerves. He made
isolated musde prepurations and found that they responded to acetylcholine by contraction and were sensitive to concentrations of the drug
down to
to lO-’g/ml. This reaction was blocked by atropine,
d-tubocnrarine and other known cholinergic blocking agents. In
another experiment Florey stimulated a muficle preparation and found
that it releaRed quantities of acetylcholine equivalent to 10l2 molecules per impulse. The released acetylchoIine was assayed by means of
a molluscan heart preparation (Fig. 28). In a separate experiment
Florey stimulated electrically a muscle prcparation which had been
pinned in the middle to the bottom of a w i ~ x dish. The preparation
responded to repetitive stimulation by slow contractions, but this
response was totally abolished in the presence of d-tubocurare. Thus the
same agent which blocks the action of applied acetylcholine also blocks
neuromuscular transmission and further substantiates the conclusion
that, C . intestinalis poseesscs cholinergic nerves.
Florey’s experiments are very convincing, but nevertheless in the
light of Bacq’s experiments and the findings of Scudder and Karczmar
there still remains an element of uncertainty concerning the presence of
cholinergic nerves in ascidians. (See also p. 52 for a discussion of
acetylcholine in cardiac regulation.)
Passing referencc may be made here to the presence in ascidians of
5-hydroxytryptamine, another possible neuro-transmitter. Welsh and
Moorehead (1960) found very low levels of 5-hydroxytryptamine in the
cerebral ganglia of Chelyoeoma sp. but not in Molgula manhatteneis.*
* Wokh and Moorehead named their aacidian (’helyoaomu produclurcr. No Huch Hpocies
appears to e x k t and it IN tlpparently a mia-.rpolling of c‘. producturn Rtimpnon.
IVAN (monHonY
FkJi’Py ( 1963) critickd lh~cq’s yq)roech on the grounds that he had
homopnizcd wholc ti,nimds ;md not the ncrvous tissue. Florey removed
the gaiiglion from G. inteetit/,aZis and made extracts of it. He reported
concentrations of ucetylaholine in the order of 20 to 120 pglg wet weight
of ganglion and concluded that such high concentrations must indicate
a. preponderance of cholinergic nerves. This is supported by his finding
that the muscles contract in the presence of acetylcholine, although
the effect ie not potentiated by cserine. However, he did find that
cholincsterase activity in the muscles is low and suggested that this
might explain the rather slow rate of relaxation of ascidian muscles
following contraction. However, there does not seem to be any good
evidence to confirni that muscle relaxation is slow. The re-expansion of
a whole ascidian after retraction is slow, but this is due, at least in part,
to the weakness of the opposing muscle system.
In a later paper Florey (1967) describes some additional careful
experiments in support of the presence of cholinergic nerves. He made
isolated musde prepurations and found that they responded to acetylcholine by contraction and were sensitive to concentrations of the drug
down to
to lO-’g/ml. This reaction was blocked by atropine,
d-tubocnrarine and other known cholinergic blocking agents. In
another experiment Florey stimulated a muficle preparation and found
that it releaRed quantities of acetylcholine equivalent to 10l2 molecules per impulse. The released acetylchoIine was assayed by means of
a molluscan heart preparation (Fig. 28). In a separate experiment
Florey stimulated electrically a muscle prcparation which had been
pinned in the middle to the bottom of a w i ~ x dish. The preparation
responded to repetitive stimulation by slow contractions, but this
response was totally abolished in the presence of d-tubocurare. Thus the
same agent which blocks the action of applied acetylcholine also blocks
neuromuscular transmission and further substantiates the conclusion
that, C . intestinalis poseesscs cholinergic nerves.
Florey’s experiments are very convincing, but nevertheless in the
light of Bacq’s experiments and the findings of Scudder and Karczmar
there still remains an element of uncertainty concerning the presence of
cholinergic nerves in ascidians. (See also p. 52 for a discussion of
acetylcholine in cardiac regulation.)
Passing referencc may be made here to the presence in ascidians of
5-hydroxytryptamine, another possible neuro-transmitter. Welsh and
Moorehead (1960) found very low levels of 5-hydroxytryptamine in the
cerebral ganglia of Chelyoeoma sp. but not in Molgula manhatteneis.*
* Wokh and Moorehead named their aacidian (’helyoaomu produclurcr. No Huch Hpocies
appears to e x k t and it IN tlpparently a mia-.rpolling of c‘. producturn Rtimpnon.