Wang H L, Bogen C, Reisine T, Dichter M
Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia 19104.
Proc Natl Acad Sci U S A. 1989 Dec;86(23):9616-20. doi: 10.1073/pnas.86.23.9616.
The prosomatostatin-derived peptides somatostatin-14 (Som-14) and somatostatin-28 (Som-28) are believed to act as neurotransmitters in the central nervous system. To examine possible mechanisms by which these peptides induce their physiological actions in brain, the effects of Som-14 and Som-28 on voltage-dependent K+ currents in rat cerebral cortical neurons in culture were examined by using whole-cell patch-clamp techniques. Som-14 increased a delayed rectifier K+ current (IK) in the cortical neurons, while Som-28 reduced IK in the neurons, both in a concentration-dependent manner. Som-14 and Som-28 could induce opposite changes in IK in the same neurons. Elevating intracellular cAMP in the cortical neurons did not modify the effects of Som-14 or Som-28 on IK, indicating that the peptides can regulate this ionic current through cAMP-independent mechanisms. Pretreatment of the neocortical cells with pertussis toxin, which inactivates inhibitory GTP-binding proteins, abolished both Som-14 and Som-28 modulation of IK, indicating that Som-14 and Som-28 receptors are coupled to IK via GTP-binding proteins. These studies show that Som-14 and Som-28 can induce opposite biological effects, suggesting that Som-14 and Som-28, acting through distinct receptors, may function as different neurotransmitters or neuromodulators.
源自前促生长素抑制素的肽类,即生长抑素-14(Som-14)和生长抑素-28(Som-28),被认为在中枢神经系统中充当神经递质。为了研究这些肽类在大脑中诱导其生理作用的可能机制,利用全细胞膜片钳技术检测了Som-14和Som-28对培养的大鼠大脑皮质神经元中电压依赖性钾电流的影响。Som-14增加了皮质神经元中的延迟整流钾电流(IK),而Som-28则降低了神经元中的IK,两者均呈浓度依赖性。Som-14和Som-28可在同一神经元中诱导IK产生相反的变化。提高皮质神经元内的细胞内cAMP水平并未改变Som-14或Som-28对IK的影响,这表明这些肽类可通过不依赖cAMP的机制调节这种离子电流。用百日咳毒素预处理新皮质细胞可使抑制性GTP结合蛋白失活,从而消除Som-14和Som-28对IK的调节作用,这表明Som-14和Som-28受体通过GTP结合蛋白与IK偶联。这些研究表明,Som-14和Som-28可诱导相反的生物学效应,提示Som-14和Som-28通过不同的受体发挥作用,可能作为不同的神经递质或神经调质发挥功能。