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HUGH R. BUTT, M.D.

Arch Neurol Psychiatry 1937;37(1):142-153.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The first intimation of the chemical mediation of nerve impulses was given by Elliott¹ (1905). He observed that the structures innervated by sympathetic nerves responded in a characteristic manner to epinephrine long after these nerves had been cut and had undergone degeneration. If a structure, smooth muscle, for example, contracted in response to sympathetic impulses it contracted in response to epinephrine, and if sympathetic impulses caused relaxation, the response to epinephrine also was relaxation. It was obvious that epinephrine did not affect any part of the peripheral nerves, for they had undergone degeneration. On the basis of these observations Elliott suggested that the sympathtetic nerve impulse arriving at a smooth muscle cell might liberate epinephrine in the cell and that this epinephrine acts as a chemical mediator in the process of stimulation. This would explain the manner in which epinephrine from the adrenal gland mimics the action of sympathetic . . . [Full Text PDF of this Article]

Author Affiliations
Fellow in Medicine, the Mayo Clinic ROCHESTER, MINN.

Footnotes
Review prepared while in the Department of Neurology of the Mayo Clinic and presented at the neurologic seminary, Dec. 19, 1935.