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Effects of annetocin, an oxytocin-related peptide isolated from the earthwormEisenia foetida, and some putative neurotransmitters on gut motility of the earthworm

✍ Scribed by Ukena, K. ;Oumi, T. ;Matsushima, O. ;Ikeda, T. ;Fujita, T. ;Minakata, H. ;Nomoto, K.


Publisher
John Wiley and Sons
Year
1995
Tongue
English
Weight
847 KB
Volume
272
Category
Article
ISSN
0022-104X

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✦ Synopsis


Abstract

Annetocin, an oxytocin‐related peptide recently isolated from the lumbricid earthworm Eisenia foetida, and putative transmitter substances were examined for their effects on rhythmic, spontaneous contractions of isolated gut preparations of the earthworm. Significant, dose‐dependent effects of the following substances were observed: acetylcholine (ACh), gamma‐aminobutyric acid (GABA), and dopamine were excitatory, while serotonin (5‐HT) and octopamine were inhibitory. Annetocin, oxytocin, and vasotocin stimulated spontaneous contraction of the earthworm gut, annetocin being approximately 10‐fold more potent than oxytocin or vasotocin. However, arginine‐vasopressin (Arg‐vasopressin), lysine‐vasopressin (Lys‐vasopressin), tocinoic acid (N‐terminal hexapeptide fragment of oxytocin), and MSH release‐inhibiting factor (MIF; C‐terminal tripeptide fragment of oxytocin) did not show any effect on the earthworm gut motility. On the other hand, oxytocin, vasotocin, Arg‐vasopressin, Lys‐vasopressin, and tocinoic acid caused spontaneous contractions of isolated rat uterine preparations, where the potency was in this order, while annetocin and MIF exerted no oxytocic activity on the uterus. Dose‐response relationship of the effects of annetocin and its related peptides on the annelid and mammalian systems shows that amino acid residue at the third position of these peptides is important for exertion of excitatory action on the smooth muscle systems. The results in the present study suggest that receptors for annetocin and for GABA on the earthworm gut, unlike those for ACh, desensitize during continuous exposure to these substances. © 1995 Wiley‐Liss, Inc.