Antidromic Vasodilation and Plasma Extravasation
Fig. 1. Schematic illustrations defining the dendritic domains in three very different systems: the substantia nigra (SN) dopaminergic neurons, the olfactory bulb (OB) and primary sensory neurons (PSN) of the spinal cord dorsal root ganglia. These neurons dendritically release monoamines (Dopamine: DA), amino acids (GABA) and neuropeptides (e.g. substance P: SP) respectively . The scheme represents the dendritic and axonal territories following the classical criteria discussed in the chapter. The main function of the dendritically-released substances are indicated below each cell type. A historical account of the evidence supporting dendritic release of transmitters in each neuronal prototype is found in the main text. IGZ indicates impulse generating zone at the origin of the axonal process. Olfactory bulb GABAergic granule cell neurons are considered "axonless".
The basic concepts concerning neurons, their connections, synapses and transmitters were solidly established by the late sixties and early seventies. They are still fundamentally correct and have inspired decades of excellent neurochemical, electrophysiological, neuropharmacological and anatomical studies. The resulting studies have provided us with a reliable framework to understand how the nervous system operates. However, even in the early days of the neuronal theories, there were observations which did not tightly fit with the emerging neuronal principles. A glaring example is that of the sensory axonal reflex. At the beginning of the XX century, Bayliss (1901) and Langley (1923) demonstrated that peripheral terminals (dendrites) of sensory nerves were responsible for the "antidromically"- induced vasodilation. In other words, the dendritic sensory branch which should carry impulses "somatopetally" on occasion carried impulses "somatofugally", against the law of conduction, i.e. antidromically. Later, Lewis and Marvin (1926) proposed that a histamine-like compound released by sensory peripheral branches is responsible for the reported antidromic vasodilation. These unorthodox ideas provoked the imagination of Sir Henry Dale who left us essential principles in physiology and pharmacology. He reasoned that the sensory transmitter which produced antidromic vasodilation in the periphery should be the same transmitter that is released orthodromically at the central ends of the same sensory neurons (Dale, 1935). In other words, he was telling us that if we want to search for sensory neurotransmitters it would be easier to do it in the periphery as opposed to in the CNS where the mesh work of synapses and transmitters would make the task most difficult. This statement was liberally borrowed by many neuroscientists and became the famous "Dale's principle", interpreted wrongly as the "one neuron-one transmitter hypothesis". Dale's reasoning was instead that the same neuron should contain the same transmitters in all its processes which would imply, in modern terms, that dendrites should also contain the same neurotransmitter as axonal terminal processes. The Dale hypothesis ("Dale's principle") does not discuss how many transmitters could be involved.
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