Sved A F
Department of Behavioral Neuroscience, University of Pittsburgh, PA 15260.
Brain Res. 1990 Apr 2;512(2):253-8. doi: 10.1016/0006-8993(90)90634-N.
Epinephrine levels in the intermediolateral cell group in the rat spinal cord are very low, although there is a dense projection to this region from cells containing all the enzymes required for epinephrine biosynthesis. One explanation for this finding is that epinephrine in the nerve terminals is degraded as soon as it is synthesized, so that no epinephrine is actually stored in synaptic vesicles. To test this hypothesis, epinephrine levels were measured in spinal cord of rats pretreated with an inhibitor of monoamine oxidase, the major enzyme involved in epinephrine degradation. Selected other tissues (i.e. brainstem, hypothalamus, adrenal gland, superior cervical ganglion) were examined for comparison. Pargyline treatment (75 mg/kg i.p., 4 h prior to sacrifice) increased catecholamine levels in spinal cord, hypothalamus, and brainstem. However, the percent increase in epinephrine in the spinal cord and brainstem was much larger than that for dopamine and norepinephrine in the 3 central nervous system regions studied, as well as larger than that for epinephrine in the hypothalamus. These results suggest that phenylethanolamine N-methyltransferase (PNMT)-containing terminals in the rat spinal cord can synthesize epinephrine, but that little if any epinephrine is stored in synaptic vesicles due to the rapid metabolism of cytoplasmic catecholamines by monoamine oxidase. In contrast, pargyline pretreatment had no effect on catechol levels in the adrenal gland, suggesting that little metabolism of catecholamines takes place in those epinephrine-synthesizing cells. Furthermore, since pargyline pretreatment increased norepinephrine levels but decreased dopamine levels in the superior cervical ganglion, it is suggested that most of the dopamine in that sympathetic ganglion is present as a precursor to norepinephrine in noradrenergic postganglionic sympathetic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
大鼠脊髓中间外侧细胞群中的肾上腺素水平非常低，尽管从含有肾上腺素生物合成所需所有酶的细胞到该区域有密集的投射。这一发现的一种解释是，神经末梢中的肾上腺素一旦合成就会被降解，因此实际上没有肾上腺素储存在突触小泡中。为了验证这一假设，在预先用单胺氧化酶抑制剂处理的大鼠脊髓中测量了肾上腺素水平，单胺氧化酶是参与肾上腺素降解的主要酶。选取其他组织（即脑干、下丘脑、肾上腺、颈上神经节）进行比较。帕吉林处理（腹腔注射75mg/kg，处死前4小时）可提高脊髓、下丘脑和脑干中的儿茶酚胺水平。然而，脊髓和脑干中肾上腺素的增加百分比远大于所研究的3个中枢神经系统区域中多巴胺和去甲肾上腺素的增加百分比，也大于下丘脑中肾上腺素的增加百分比。这些结果表明，大鼠脊髓中含苯乙醇胺N-甲基转移酶（PNMT）的神经末梢能够合成肾上腺素，但由于单胺氧化酶对细胞质儿茶酚胺的快速代谢，几乎没有肾上腺素储存在突触小泡中。相比之下，帕吉林预处理对肾上腺中的儿茶酚水平没有影响，这表明在那些合成肾上腺素的细胞中儿茶酚胺的代谢很少。此外，由于帕吉林预处理增加了颈上神经节中的去甲肾上腺素水平但降低了多巴胺水平，因此表明该交感神经节中的大多数多巴胺以去甲肾上腺素能节后交感神经元中去甲肾上腺素前体的形式存在。（摘要截短至250字）
