PMC:2812702 / 13495-16171 JSONTXT

{"project":"MyTest","denotations":[{"id":"19837460-17147132-27808540","span":{"begin":1312,"end":1314},"obj":"17147132"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"The potential-poison theory\nBoth Ehrlich and Langley had conceptualised the ‘receptor’ through analogy with chemical binding of substances, and their theories were viewed as ‘chemical’ in nature. This, however, meant that their theories got caught up in the controversy over whether pharmacological substances acted primarily through their chemical or their physical properties. The great competitor to the receptor concepts of Ehrlich and Langley was the so-called ‘potential-poison’ theory of the German pharmacologist Walther Straub (1874–1944).\nStraub had developed it during a research stay at the Stazione Zoologica in Naples at the start of the new century. There, he studied the antagonism between atropine and the poison of the fly agaric, muscarine, on the heart of the sea snail (Aplysia) and the torpedo fish. In essence, he argued that a poison acted as long as there was a concentration difference or ‘potential’ between the outside and the inside of the cell. The effect was due to a deformation or other physical disturbance of the cell membrane when the poison molecules penetrated it. Like Langley, Straub was quick to generalize, suggesting that his physical theory of drug action applied also to other alkaloids, such as pilocarpine, physostigmine and nicotine, and to the hormone adrenalin [17]. Straub's theory found significant supporters in Britain, in particular Henry Dale (1875–1968) and George Barger (1878–1939) of the Wellcome Physiological Research Laboratories and Arthur Cushny (1866–1926), who held the chair in pharmacology at University College London [18].\nStraub offered a direct challenge to Ehrlich's theory of so-called chemoreceptors. At the annual assembly of German naturalists and doctors in 1912, Straub pointed out that there were many pharmacologically active substances (such as nitrous oxide, carbonic acids and kali salts) whose constitution made it very unlikely that they were capable of reacting chemically within the organism. There might be receptors for certain poisons, he conceded, but to build a whole theory of chemoreceptors on this was impermissible [19].\nMoreover, it seems that Straub did not fully accept Langley's work as a contribution to the field of pharmacology. As late as 1938, Straub addressed the International Congress of Physiologists in Zurich with the following statement:… I may perhaps remind you that there are two types of pharmacologist: those who study the living organism with a chemical substance, for example Claude Bernard with curare or Langley with nicotine, and such who use a living organism to study a chemical substance; the former practise physiology, the latter pharmacology[20]!"}

{"project":"2_test","denotations":[{"id":"19837460-17147132-27808540","span":{"begin":1312,"end":1314},"obj":"17147132"}],"text":"The potential-poison theory\nBoth Ehrlich and Langley had conceptualised the ‘receptor’ through analogy with chemical binding of substances, and their theories were viewed as ‘chemical’ in nature. This, however, meant that their theories got caught up in the controversy over whether pharmacological substances acted primarily through their chemical or their physical properties. The great competitor to the receptor concepts of Ehrlich and Langley was the so-called ‘potential-poison’ theory of the German pharmacologist Walther Straub (1874–1944).\nStraub had developed it during a research stay at the Stazione Zoologica in Naples at the start of the new century. There, he studied the antagonism between atropine and the poison of the fly agaric, muscarine, on the heart of the sea snail (Aplysia) and the torpedo fish. In essence, he argued that a poison acted as long as there was a concentration difference or ‘potential’ between the outside and the inside of the cell. The effect was due to a deformation or other physical disturbance of the cell membrane when the poison molecules penetrated it. Like Langley, Straub was quick to generalize, suggesting that his physical theory of drug action applied also to other alkaloids, such as pilocarpine, physostigmine and nicotine, and to the hormone adrenalin [17]. Straub's theory found significant supporters in Britain, in particular Henry Dale (1875–1968) and George Barger (1878–1939) of the Wellcome Physiological Research Laboratories and Arthur Cushny (1866–1926), who held the chair in pharmacology at University College London [18].\nStraub offered a direct challenge to Ehrlich's theory of so-called chemoreceptors. At the annual assembly of German naturalists and doctors in 1912, Straub pointed out that there were many pharmacologically active substances (such as nitrous oxide, carbonic acids and kali salts) whose constitution made it very unlikely that they were capable of reacting chemically within the organism. There might be receptors for certain poisons, he conceded, but to build a whole theory of chemoreceptors on this was impermissible [19].\nMoreover, it seems that Straub did not fully accept Langley's work as a contribution to the field of pharmacology. As late as 1938, Straub addressed the International Congress of Physiologists in Zurich with the following statement:… I may perhaps remind you that there are two types of pharmacologist: those who study the living organism with a chemical substance, for example Claude Bernard with curare or Langley with nicotine, and such who use a living organism to study a chemical substance; the former practise physiology, the latter pharmacology[20]!"}