Bartfai T, Bertorelli R, Consolo S, Diaz-Arnesto L, Fisone G, Hökfelt T, Iverfeldt K, Palazzi E, Ogren S O
Department of Biochemistry, Arrhenius Laboratory, University of Stockholm, Sweden.
J Physiol (Paris). 1988;83(3):126-32.
Autoinhibition of acetylcholine release by the coexisting peptide galanin in the septal afferents to the hippocampus of the rat was examined in tissue slices from the hippocampus. Galanin inhibits the evoked release of the coexisting neurotransmitter, acetylcholine, in the ventral hippocampus, providing an example of autoinhibition of release of a neurotransmitter by one of the coexisting neurotransmitters. The galanin mediated inhibition of the acetylcholine release is a complement to the well known strong cholinergic autoinhibition. The effects of the coexisting galanin and acetylcholine on several second messenger systems were also examined: acetylcholine acting at muscarinic receptors depresses cyclic adenosine 3',5'-monophosphate and stimulates elevation of cyclic guanosine 3',5'-monophosphate levels, whereas neither cyclic adenosine 3',5'-monophosphate nor cyclic guanosine 3',5'-monophosphate levels were affected by galanin (1 microM). Galanin however inhibited partly the muscarinic stimulation of phosphoinositide breakdown, suggesting that inositol phosphate(s) or diacylglycerol may act as second messenger(s) of the galanin action in the hippocampus. The effects of chronic changes in firing rate on the coexisting neurotransmitters in the rat ventral spinal cord containing serotonin, thyrotropin releasing hormone, substance P and substance K were examined. The tissue levels of the coexisting transmitters were studied in rats chronically treated with imipramine (14 days; 2 x 10 mumoles/kg/day) and zimelidine (14 days; 2 x 10 mumoles/kg/day). Upon treatment with zimelidine the tissue levels of the serotonin metabolite 5-hydroxyindoleacetic acid fall by 32% while thyrotropin releasing hormone levels seem to increase 35% and substance P/substance K levels also increase 48 and 72% respectively. Imipramine treatment resulted in similar although less pronounced changes.(ABSTRACT TRUNCATED AT 250 WORDS)
在大鼠海马的组织切片中，研究了共存肽甘丙肽对海马隔传入纤维中乙酰胆碱释放的自身抑制作用。甘丙肽抑制腹侧海马中共存神经递质乙酰胆碱的诱发释放，这为一种共存神经递质对另一种神经递质释放的自身抑制提供了一个例子。甘丙肽介导的乙酰胆碱释放抑制是对众所周知的强烈胆碱能自身抑制的一种补充。还研究了共存的甘丙肽和乙酰胆碱对几种第二信使系统的影响：作用于毒蕈碱受体的乙酰胆碱会降低环磷酸腺苷水平，并刺激环磷酸鸟苷水平升高，而甘丙肽（1微摩尔）对环磷酸腺苷和环磷酸鸟苷水平均无影响。然而，甘丙肽部分抑制了毒蕈碱对磷酸肌醇分解的刺激作用，这表明肌醇磷酸或二酰基甘油可能作为甘丙肽在海马中作用的第二信使。研究了放电率的长期变化对大鼠腹侧脊髓中含5-羟色胺、促甲状腺激素释放激素、P物质和K物质的共存神经递质的影响。在长期用丙咪嗪（14天；2×10微摩尔/千克/天）和齐美利定（14天；2×10微摩尔/千克/天）治疗的大鼠中，研究了共存递质的组织水平。用齐美利定治疗后，5-羟色胺代谢物5-羟吲哚乙酸的组织水平下降32%，而促甲状腺激素释放激素水平似乎升高35%，P物质/K物质水平也分别升高48%和72%。丙咪嗪治疗导致了类似但不太明显的变化。（摘要截短于250字）
