Meyer D K, Conzelmann U, Schultheiss K
Department of Pharmacology, University of Freiburg, F.R.G.
Neuroscience. 1989;28(1):61-8. doi: 10.1016/0306-4522(89)90232-7.
Slices (300 microns) of rat caudatoputamen were incubated in Krebs-Henseleit medium and loaded with [3H]glutamine, part of which was converted to [3H]GABA. This conversion takes place only in GABA-neurons most of which probably contribute to the striatonigral pathway. After a 24 min equilibration period, release of radioactivity was stimulated with veratridine (3.1-4 mumol/l) or K+ (15-25 mmol/l) in the absence or presence of somatostatin-14. From the radioactivity released [3H]GABA was separated by cationic exchange chromatography and measured. Somatostatin-14 affected the release of [3H]GABA in a manner which depended on its concentration as well as on the extent of stimulus-evoked release. Somatostatin-14 (1 nmol/l) enhanced the moderate release (2-4% of tissue content) elicited by veratridine (3.1 mumol/l) or K+ (20 mmol/l), but had no effect on the more pronounced release (5-8% of tissue content) elicited by veratridine (4 mumol/l) or K+ (25 mmol/l). Somatostatin-14 (10 nmol/l) had no effect on the moderate release of [3H]GABA, but diminished the pronounced one. Further experiments provided evidence that the somatostatin-14-induced enhancement was not brought about by a direct action on GABA-neurons but was probably indirect, i.e. mediated by other striatal neurons. In contrast, the diminution of the release of [3H]GABA caused by somatostatin-14 may be due to its direct action on releasing neurons. Two antisera against somatostatin lowered the pronounced release indicating that endogenous somatostatin may also enhance the release of [3H]GABA. In addition, endogenous somatostatin seems also to be able to diminish the release under certain experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
将大鼠尾状壳核切片（300微米）置于Krebs - Henseleit培养基中，并加载[3H]谷氨酰胺，其中一部分会转化为[3H]GABA。这种转化仅发生在GABA能神经元中，其中大部分可能参与纹状体黑质通路。在24分钟的平衡期后，在不存在或存在生长抑素-14的情况下，用藜芦定（3.1 - 4微摩尔/升）或K +（15 - 25毫摩尔/升）刺激放射性物质的释放。从释放的放射性物质中，通过阳离子交换色谱法分离并测量[3H]GABA。生长抑素-14以一种取决于其浓度以及刺激诱发释放程度的方式影响[3H]GABA的释放。生长抑素-14（1纳摩尔/升）增强了由藜芦定（3.1微摩尔/升）或K +（20毫摩尔/升）引起的适度释放（组织含量的2 - 4%），但对由藜芦定（4微摩尔/升）或K +（25毫摩尔/升）引起的更明显释放（组织含量的5 - 8%）没有影响。生长抑素-14（10纳摩尔/升）对[3H]GABA的适度释放没有影响，但减少了明显的释放。进一步的实验提供了证据，表明生长抑素-14诱导的增强不是通过对GABA能神经元的直接作用引起的，而是可能是间接的，即由其他纹状体神经元介导。相反，生长抑素-14引起的[3H]GABA释放减少可能是由于其对释放神经元的直接作用。两种抗生长抑素抗血清降低了明显的释放，表明内源性生长抑素也可能增强[3H]GABA的释放。此外，内源性生长抑素似乎在某些实验条件下也能够减少释放。（摘要截短于250字）
