Epelbaum J
Prog Neurobiol. 1986;27(1):63-100. doi: 10.1016/0301-0082(86)90012-2.
Since its discovery, at the beginning of 1973, somatostatin's multiple actions, in relation to its wide anatomical distribution have been widely documented. Its biochemical pathways have been elucidated with the discovery of other molecular forms as well as the mechanisms of its neuronal release. However, no definite proof is available concerning a neurotransmitter role for any peptide of the somatostatin family other than somatostatin-14. The precise determination of the roles of somatostatin in brain are still hampered by the poor pharmacology of the peptide. New tools are badly needed and in particular a true antagonist at the receptor site. The mechanisms of action of somatostatin are now well under way at least in the pituitary model. More information should come from this model and be applied to brain cells in vitro. The greatest challenge of somatostatin brain function lies in its role in the pathophysiology of neurological diseases such as Alzheimer's dementia and Huntington's disease. Nature has been using somatostatin-related molecules since inhibitory control was first needed in cell functions. Time will tell us if somatostatin is really an old peptide involved in senile dementia.
自1973年初被发现以来，生长抑素的多种作用与其广泛的解剖分布相关，已得到广泛记录。随着其他分子形式的发现及其神经元释放机制的阐明，其生化途径也已被揭示。然而，除了生长抑素-14之外，关于生长抑素家族中任何肽的神经递质作用尚无确凿证据。生长抑素在大脑中的作用的确切确定仍因该肽较差的药理学特性而受阻。迫切需要新的工具，尤其是受体位点的真正拮抗剂。至少在垂体模型中，生长抑素的作用机制目前正在深入研究。更多信息应来自该模型并应用于体外脑细胞。生长抑素脑功能的最大挑战在于其在神经疾病如阿尔茨海默病性痴呆和亨廷顿病的病理生理学中的作用。自从细胞功能首次需要抑制控制以来，自然界一直在使用与生长抑素相关的分子。时间将告诉我们生长抑素是否真的是一种与老年痴呆有关的古老肽。
