The nervous release and the action of substances which affect intestinal muscle through neither adrenoreceptors nor cholinoreceptors

Abstract

Mammalian gastrointestinal muscle is supplied by non-adrenergic, intrinsic inhibitory neurons. The substantial evidence which exists to suggest that adenosine triphosphate is the transmitter released from these nerves is discussed briefly. It is shown that the intrinsic inhibitory neurons compose the efferent link in a cascade of descending reflexes extending from the oesophagus to the anal sphincter. Gastrointestinal muscle is also supplied by non-cholinergic excitatory nerves. The pharmacology of transmission from a group of such nerves to the smooth muscle of the guinea-pig proximal colon is described and evidence is presented to suggest that 5-hydroxytryptamine (5-HT) may be the transmitter substance. The contraction is blocked by phentolamine and methysergide which both antagonize the contractile action of 5-HT. When the muscle is desensitized by continued exposure to 5-HT, the noncholinergic contraction can no longer be elicited.

Effects of Enkephalins and Morphine on Spontaneous Electrical Activity and on Junction Potentials Elicited by Parasympathetic Nerve Stimulation in Cat and Rabbit Colon

“…Thus it seems that both the action of opiates on i.j.ps and the initiation of intense spike activity are independent phenomena. Therefore, the spiking activity produced by opiates could be due to excitation of intramural non-cholinergic excitatory neurones (see Ambache & Freeman, 1968;Furness & Costa, 1973;Fasth, Hulten & Nordgren, 1980).…”

Morphology and serotonergic innervation of physiologically identified cells of the guinea pig's myenteric plexus

“…In addition, enteric serotonergic neurons specifically and avidly take up 5-HT, providing an adequate inactivating mechanism for the amine as a transmitter (Gershon and Altman, 1971;Robinson and Gershon, 1971;Gershon et al, 1976;Gershon and Jonakait, 1979). On a gross level, 5-HT also mimics many of the authentic neurally mediated responses of the gut (Brownlee and Johnson, 1963;Bulbring and Gershon, 1967;Furness and Costa, 1973;Costa and Furness, 1979a;Jule, 1980); however, considerable controversy has arisen over whether these gross effects can be traced to physiological actions of 5-HT (see Costa and Furness, 1979b;Gershon, 1982) and over whether nerve-activated, slow excitatory postsynaptic potentials (EPSPs) in enteric neurons are mediated by 5-HT Johnson et al, 1981). Neurons of the myenteric plexus have been categorized as type I or S, type II or AH (Holman et al, 1972;Nishi and North, 1973;Hirst et al, 1974) and, more recently, types III (non-spiking) and IV (delayed spiking; Wood, 1983).…”

GABAA‐receptor‐mediated inhibition of the delayed increase in intragastric pressure to stimulation of vagal afferent fibres in cats

“…There are two types of inhibitory nerves in the guinea-pig intestine: noradrenergic (Furness & Costa, 1974) and intrinsic enteric inhibitory nerves (Furness & Costa, 1973). In this preparation, GABA stimulates intrinsic enteric inhibitory nerves but not terminals of inhibitory noradrenergic nerves.…”