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Ishihara Test 24 Plates Pdf Download

in the current study, we set out to identify the type of receptors linked to the stimulation of nt secretion from intestinal n cells, in addition to the identity of the secretagogues released from ldcs and the way they stimulate nt secretion. ach, an important neurotransmitter, has been shown to stimulate nt secretion from some endocrine cells ( 33, 50, 57 ). in addition, the possible receptor mediated by ach is suggested to be the muscarinic (m) receptor in the bon n cells ( 57 ). in our present study, ach by itself stimulated nt secretion in a concentration-dependent manner. this ach effect was blocked by the muscarinic receptor antagonist atropine. thus, ach evoked nt release via activation of a cholinergic receptor. nt secretion is also stimulated by some other substances, such as α-msh ( 25, 28, 54 ), which is a strong stimulator of nt synthesis. in the present study, we excluded the possibility that α-msh stimulated nt secretion by itself. this is because, in the presence of α-msh, ach still evoked nt release, albeit with a much lower potency than in the absence of α-msh. in addition, when the effect of α-msh was blocked by an antagonist, mtii, nt secretion in response to ach was completely abolished. these results show that an unidentified nt-secretagogue, which is probably α-msh, mediates the effect of ach on nt secretion. this conclusion is supported by two lines of evidence. firstly, when the effect of ach was blocked by the antagonist, mtii, nt secretion in response to ach was completely abolished. this ach effect was blocked by the antagonist, atropine, which is required for stimulation by ach in bon cells. secondly, the nt-secretory response to ach stimulation in the bon endocrine cell line was abolished by chronic eb treatment, which specifically targets mitochondrial function. this effect is reversible through removal of eb, the secretory effect of ach was restored.

ishihara test 24 plates pdf download


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