Release of Catecholamines

  • Ross J. Baldessarini
Part of the Handbook of Psychopharmacology book series (HBKPS, volume 3)


The cornerstone of the neurohumoral theory of synaptic transmission (Elliott, 1905; Dixon, 1907) is the ability of nerves to release an active neurotransmitter on stimulation. The experiments of Loewi demonstrated the release of Vagusstoff (later shown to be acetylcholine) or a sympathin (later shown to be epinephrine) on stimulation of frog cardiac nerves and the effect of these substances to slow or accelerate, respectively, a second isolated heart (e.g., Loewi, 1921). These experiments were later applied to the mammalian heart by Rylant (1927), and made more specifically pertinent to sympathetic nerves by Cannon and his colleagues (Cannon and Uridil, 1921; Cannon and Rosenblueth, 1937). These classical experiments in neuropharmacology were essentially the application of sensitive and quite specific bioassays to demonstrate the release of active hormone on stimulation of a peripheral nerve. The identity of neural “sympathin” in mammalian sympathetic neurons (norepinephrine) as the desmethylated congener of the catecholamine originally extracted from the adrenal gland (e.g., Abel, 1899) (epinephrine) was suspected in the 1920s and 1930s (e.g., Bacq, 1934), but depended on the application of suitable quantitative biochemical and bioassay methods for its definitive demonstration, notably by von Euler (1946).


Tyrosine Hydroxylase Adrenal Medulla Adrenergic Nerve Adrenergic Neuron Nicotinic Agonist 
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Copyright information

© Plenum Press, New York 1975

Authors and Affiliations

  • Ross J. Baldessarini
    • 1
  1. 1.Psychiatric Research Laboratories, Department of PsychiatryHarvard Medical School, Massachusetts General HospitalBostonUSA

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