324
FINDLAY E. RUSSELL
that retching and vomiting occurred in unanesthetized cats and not in
anesthetized ones was also interpreted to indicate that the toxin had a
direct effect on the central nervous system. These interpretations
must certainly be questioned, but it is not wholly unlikely that the
toxin does have a direct effect on the brain. Li (1963) suggested that
the cause of death following a lethal dose of the poison is respiratory
arrest from the action on the brain stem respiratory centers. Again,
this may in part be so, although the arguments put forth by Li are not
wholly convincing.
hitravenous or close intra-arterial injections of 4-10 pg/kg body
weight of the poison caused a block in skeletal muscle’s response to
30-per-second motor nerve excitation. The toxin also depressed the
response of the muscle to direct stimulation, although the depression
developed more gradually. The order of recovery was: return of
muscle response to direct stimulation, return of response to repetitive
nerve stimulation, and finally, return of response to slow stimulation
of the nerve. Further studies indicated that paralysis occurs in the
hind limbs at a time when the diaphragm is affected only partially,
and the forelimbs not a t all (Murtha and colleagues, 1958). These
findings illustrated the ascending type of paralysis noted previously by
Japanese workers.
Tetrodotoxin appears to have no effect on the resting potential
(Russell et al., 1961), although, as suggested by Kao and Fuhrman
(1963) in their excellent report on tarichatozin, the normal increase
in sodium and potassium conductances associated with activity is
probably markedly reduced. Since tetrodotoxin and tarichatoxin are
identical substances, some of the findings reported by Kao and Fuhrman
on the latter toxin are included here. The poison has no effect on
oxidative metabolism, on extrusion of sodium from the nerve, or on
the cholinesterase system. It has little effect on the postsynaptic cells
in the autonomic ganglion. These workers feel that all of the systemic
effects (of tarichatoxin) might be explained by its particular action on
the preganglionic cholinergic and somatic motor nerves. The postganglionic adrenergic nerves are probably affected more slowly and to a
lesser degree. They suggest a block in the preganglionic cholinergic
and somatic motor nerves might interfere with impulses regulating
vasomotor tone, and thus cause the hypotension, although as previously
noted there is some evidence that the toxin might have a direct effect
on the heart (and this writer suspects that some part of the hypotensive
crisis might be due to changes in the pulmonary circulation). They
further suggest that the deleterious effects on neural stimulation would
lead to the changes in the skeletal muscles. Tachycardia might occur
FINDLAY E. RUSSELL
that retching and vomiting occurred in unanesthetized cats and not in
anesthetized ones was also interpreted to indicate that the toxin had a
direct effect on the central nervous system. These interpretations
must certainly be questioned, but it is not wholly unlikely that the
toxin does have a direct effect on the brain. Li (1963) suggested that
the cause of death following a lethal dose of the poison is respiratory
arrest from the action on the brain stem respiratory centers. Again,
this may in part be so, although the arguments put forth by Li are not
wholly convincing.
hitravenous or close intra-arterial injections of 4-10 pg/kg body
weight of the poison caused a block in skeletal muscle’s response to
30-per-second motor nerve excitation. The toxin also depressed the
response of the muscle to direct stimulation, although the depression
developed more gradually. The order of recovery was: return of
muscle response to direct stimulation, return of response to repetitive
nerve stimulation, and finally, return of response to slow stimulation
of the nerve. Further studies indicated that paralysis occurs in the
hind limbs at a time when the diaphragm is affected only partially,
and the forelimbs not a t all (Murtha and colleagues, 1958). These
findings illustrated the ascending type of paralysis noted previously by
Japanese workers.
Tetrodotoxin appears to have no effect on the resting potential
(Russell et al., 1961), although, as suggested by Kao and Fuhrman
(1963) in their excellent report on tarichatozin, the normal increase
in sodium and potassium conductances associated with activity is
probably markedly reduced. Since tetrodotoxin and tarichatoxin are
identical substances, some of the findings reported by Kao and Fuhrman
on the latter toxin are included here. The poison has no effect on
oxidative metabolism, on extrusion of sodium from the nerve, or on
the cholinesterase system. It has little effect on the postsynaptic cells
in the autonomic ganglion. These workers feel that all of the systemic
effects (of tarichatoxin) might be explained by its particular action on
the preganglionic cholinergic and somatic motor nerves. The postganglionic adrenergic nerves are probably affected more slowly and to a
lesser degree. They suggest a block in the preganglionic cholinergic
and somatic motor nerves might interfere with impulses regulating
vasomotor tone, and thus cause the hypotension, although as previously
noted there is some evidence that the toxin might have a direct effect
on the heart (and this writer suspects that some part of the hypotensive
crisis might be due to changes in the pulmonary circulation). They
further suggest that the deleterious effects on neural stimulation would
lead to the changes in the skeletal muscles. Tachycardia might occur