Henry Hallett Dale Biography (1875-1968)

Nationality
English
Gender
Male
Occupation
physiologist

Henry Hallett Dale was a British physiologist who devoted his scientific career to the study of how chemicals in the body regulate physiological functions. In 1936 Dale and German pharmacologist Otto Loewi were jointly awarded theNobel Prize in physiology or medicine for research demonstrating that nerve cells communicate with one another primarily by the exchange of chemical transmitters. In addition to his scientific work, Dale was a prominent figure in science and medicine in England at critical junctures in that nation's history. He was knighted in 1932.

Born June 9, 1875, in London, Henry Hallett Dale was the second son of sevenchildren born to Charles Dale, a London businessman, and his wife, Frances Hallett Dale. After graduating from Tollington Park College, London, and the Leys School, Cambridge, Dale entered Trinity College at Cambridge University in1894. His academic skills gained him first honors in the natural sciences and the Coutts-Trotter studentship at Trinity College.

Dale left Cambridge in 1900 to finish his clinical work in medicine at St. Bartholomew's Hospital in London. He received his bachelor's degree in 1903, and his medical doctorate in 1909. During this time, he also was awarded the George Henry Lewes studentship, which allowed him to pursue further physiological research. Later, Dale also received the Sharpey studentship in physiologyat University College, London. Dale used these opportunities for research from 1902 to 1904, studying with Ernest Henry Starling and William Maddock Bayliss at University College. Starling and Bayliss identified secretin--a substance secreted by the small intestine--as the first hormone, and Dale collaborated with the pair in further studies on the impact of secretin on cells in thepancreas. Dale's work with Starling and Bayliss instilled in him the idea that physiological functions could be affected by such chemicals as hormones. It was also in this laboratory that Dale first met Otto Loewi, who at the timewas visiting University College from Germany. Dale and Loewi would go on tobecome lifelong friends, collaborators, and co-recipients of the 1936 Nobel Prize.

In 1904 Dale spent three months working in the laboratory of the chemist PaulEhrlich in Germany. Members of Ehrlich's laboratory were studying the relationship between the chemical structure of biological molecules and their effect on immunological responses, research that would garner for Ehrlich the 1908Nobel Prize in physiology or medicine. As did the experience at Starling's laboratory in London, Ehrlich's research introduced Dale to the potential impact that chemicals can have on mediating biological and physiological processes.

After Dale returned to Starling's London laboratory, he was recommended to chemical manufacturer Henry Wellcome for a position with London's Wellcome Physiological Research Laboratories, a commercial laboratory. Established in the1890s to produce an antitoxin for diphtheria, the laboratories, by the firstdecade of the 1900s, had begun to promote and pursue basic scientific research.

Once Dale had settled at Wellcome, the company suggested that he consider examining the therapeutic properties of ergot, a fungus being used by obstetricians to induce and promote labor. For the next decade, Dale devoted his research efforts to studying the properties of the drug, leading to the accidentaldiscovery of the phenomenon of adrenaline (or epinephrine) reversal, in whichthe normally excitatory effects of these drugs are neutralized.

Dale's research on the effects of ergot also introduced him to ongoing efforts to study the central nervous system. Dale showed, with the chemist George Barger, that epinephrine is one chemical in a class of such chemicals that has"sympathomimetic" properties.

Dale's accomplishments drew the attention of Henry Wellcome, and Dale was promoted in 1906 to the directorship of the Wellcome Laboratories. Dale began studies of the chemicals that operate in the posterior pituitary lobe of the brain.

Dale resigned from the Wellcome Laboratories in 1914, and joined the scientific staff of the Medical Research Committee; after 1920 this group came to beknown as the Medical Research Council. During World War I Dale joined the wareffort by engaging in physiological studies of shock, dysentery, gangrene, and the effects of inadequate diet.

After the war, the Medical Research Council evolved to become the National Institute for Medical Research, and Dale served as the organization's first director from 1928 until 1942. His research efforts during the 1920s continued the work he began during the war--studying how histamine contributes to the swelling of tissue after traumatic shock. Dale demonstrated that histamine leads to the loss of plasma fluid into the tissues and produces swelling. This could lead to more serious problems, including decreased blood circulation, shock, and death.

Dale's study of histamine also contributed to his subsequent work on the nervous system. Histamine, like the"neurotransmitter acetylcholine, dilates vascular tissue in the human body.

In 1927 Dale collaborated with H. W. Dudley to isolate acetylcholine from thespleen of an ox and a horse. Having isolated the crucial compound, Dale sought to understand how and where acetylcholine plays its role in vasodilatation, or the widening of the cavities of blood vessels. Over the next decade, Dale worked with colleagues at the National Institute for Medical Research and concluded that acetylcholine serves as a neurotransmitter and that this is thechemical mediator involved in the transmission of nerve impulses. Dale's findings disproved the proposition of John Carew Eccles and other neurophysiologists who maintained that nerve cells communicate with one another via an electrical mechanism. Dale demonstrated that a chemical process and not an electrical one was the underlying mechanism for nerve transmission. A similar conclusion had been reached by Otto Loewi: As early as 1921 Loewi suggestedthat a chemical mediator was responsible for the conduction of nerve impulses; it would be Dale who would identify the mediator.

For their work, Dale and Loewi were jointly awarded the 1936 Nobel Prize in physiology or medicine. During the 1930s, Dale continued collaborative research with G. L. Brown, W. Feldberg, J. H. Gaddum, and M. Vogt at the National Institute for Medical Research. Their efforts produced more evidence that acetylcholine is a neurotransmitter involved in nerve impulses.

During World War II, Dale served as chair of the Scientific Advisory Committee to the War Cabinet. Having been elected a fellow of the Royal Society in 1914, he served as secretary from 1925 to 1935, and as president from 1940 to 1945. His many other public affiliations included serving as president of various organizations, such as the Royal Institution of Great Britain during themid-1940s, the British Association for the Advancement of Science in 1947, the Royal Society of Medicine from 1948 to 1950, and the British Council duringthe 1950s.

Other distinctions bestowed upon Dale include receiving the Copley Medal fromthe Royal Society in 1937 and being knighted with the Grand Cross Order of the British Empire in 1943. He also garnered the Order of Merit in 1944. Since1959 the Society for Endocrinology has awarded the Dale Medal for the kind of excellence in research exemplified by Dale; and since 1961 the Wellcome Trust he chaired from 1938 until 1960 has endowed the Henry Dale professorship with the Royal Society.

In later years Dale worked with Thorvald Madsen of Copenhagen directing an international campaign to standardize drugs and vaccines. The 1925 conference of the Health Organization of the League of Nations adopted such standards forinsulin and pituitary products largely because of Dale's efforts. He repeated these efforts to see into law the Therapeutic Substances Act in England. His other political activities included promoting both the peaceful use of nuclear energy and the value of scientific research. He died on July 23, 1968, after a brief illness.

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