Neurohumoral Transmission

NEUROHUMORAL TRANSMISSION

Neurohumoral transmission implies that nerves transmit their message across synapses and neuroeffector junctions by the release of humoral (chemical) messengers.

Junctional transmission was thought to be electrical (it does occur in some lower animals and probably in certain areas of mammalian brain) but observations at the turn of last century prompted Elliott (1905) to suggest that sympathetic nerves functioned by the release of an adrenaline like substance, and Dixon (1907) to propose that vagus released a muscarine like chemical. Otto Loewi (1921) provided direct proof of humoral transmission by perfusing two frog hearts in series. Stimulation of vagus nerve of the first heart caused arrest of both. Thus, a chemical must have been released by vagal stimulation in the first heart which passed in the perfusate and arrested the second heart. This vagusstoff was found in 1926 to be acetylcholine, which earlier Dale (1914) had characterised as ‘para-sympathomimetic’. The sympathetic transmitter was eventually shown to be noradrenaline in 1946 by Von Euler. Many humoral transmitters (dopamine, 5HT, GABA, purines, peptides, etc.) are now known.

To be considered as a post-junctionally acting neurohumoral transmitter a substance must fulfill the following criteria:

§  It should be present in the presynaptic neurone (usually along with enzymes synthesizing it).

§It should be released in the medium following nerve stimulation.

§Its application should produce responses identical to those produced by nerve stimulation.

§Its effects should be antagonized or potentiated by other substances which similarly alter effects of nerve stimulation.