sis, prevents the development of the most typical symptoms of phenol intoxi- 

 cation in fish. A further pharmacological analysis of phenol effects on 

 fish was carried out using curariform preparations (succinilcholine, 

 phlaxedil, paramyon) possessing pronounced blocking action on neuromuscular 

 conductivity in the myoneural synapse. The experiments indicated that 

 phenol does not exert a direct stimulating effect on the muscles of the 

 fish body, and that the r\er\/e impulses arising from the central nervous 

 system are the basis for motor reaction of fish under the influence of 

 phenol. This is indicated by the inhibition of motor reaction in phenol- 

 exposed fish by means of a pharmacological disturbance in the neuromuscular 

 nerve impulse transmission within the region of the myoneural synapse. In 

 this respect succinilcholine, from the group of preparations producing 

 stable depolarization of the terminal motor plate, was the most effective. 

 K. Kuba's (22) electrophysiological work completely confirmed the results 

 of our experiments. He also concluded that the myoneural synapse was one 

 of the points in which phenol action plays a dominant role. 



We obtained new evidence indicating the dominant role of the central 

 nervous system in the reaction of fish to phenol stimulation, and in parti- 

 cular, of stimulation of the brain in fishes with several spinal cords 

 (operative disconnection) and on an isolated head preparation (4, 3). The 

 brain proved to be prominent in the development of more characteristic com- 

 ponents of the reaction of fish to the toxic effect of organic toxins. 

 Motor activity occurred at the beginning and spasms later. 



After the complete removal of the brain, not one of these reactions 

 developed. The spinal cord is the most important link in the reflex arch, 

 the conductor of the impulses which are caused by phenol stimulation, from 

 various branches of the brain to peripheral neuromuscular systems in fish 

 (3). 



Naturally, the question of the specific phenol effect on the central 

 nervous system in fish was been raised. A partial answer to this question 

 was found during experiments with anticholinesterase preparations (phospha- 

 col, neostigmine, physostigmine) . The preliminary injection of these pre- 

 parations into test crucians fully inhibited the external symptom-complex 

 of phenol intoxication in fish. Experiments with anticholinesterase pre- 

 parations led to the conclusion that the dynamics of an acetylcholine meta- 

 bolism and, first of all, of a system of acetylcholine-cholinesterase in 

 cholinergic synapses of the central nervous system and neuromuscular 

 synapses, plays a dominant role in the development of the complex of re- 

 actions caused by phenol (4). Confirmation of this point of view came from 

 biochemical data on changes in the muscular cholinesterase activity under 

 the influence of phenol (5), as well as from electrophysiological data. 

 According to the latter, phenol increases the amplitude of the stimulating 

 synaptic potential and causes the appearance of tiny potentials on the 

 terminal plate, i.e., it facilitates neuromuscular transmission. It is 

 fascinating to explain the biphase course of phenol intoxication in fish, 

 namely, the intitial highest motor stimulation with subsequent spasms and 

 paralysis, in light of the dynamics of change in the acetylcholine concen- 

 tration in cholinergic structures of the central nervous system and in 



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