Folan J C, Heym C
Department of Anatomy, University College Dublin, Ireland.
J Chem Neuroanat. 1989 Mar-Apr;2(2):107-18.
The distribution pattern of opioid-immunoreactive nerve cell bodies and varicose fibres in the rat superior cervical ganglion after chronic administration of the tricyclic antidepressant imipramine, various receptor blockades (muscarinic antagonist, atropine sulphate; opiate antagonist, naloxone; kappa-antagonist, MR2266BS), and denervation was investigated immunohistochemically using a biotin-streptavidin-peroxydase complex method. Antisera to four peptides derived from two different precursors of the opioid family were used. In control superior cervical ganglia sparsely scattered nerve fibres and no neuronal cell bodies were immunoreactive when antisera to dynorphin A (1-17) or alpha-neo-endorphin (cleavage products of prodynorphin) were applied. A moderate number of nerve fibres and neuronal perikarya were immunoreactive to antisera directed against met-enkephalin-arg-phe (cleavage product of proenkephalin) and leu-enkephalin (cleavage product of prodynorphin and proenkephalin); non-identical cell bodies contained met-enkephalin-arg-phe- or leu-enkephalin-immunoreactivity. After drug treatment specific changes in the immunoreactivity of the investigated peptides in the superior cervical ganglion were demonstrated. (a) Treatment with imipramine resulted in an increase of nerve fibres demonstrating immunoreactivity to antisera against dynorphin A and alpha-neoendorphin. In contrast, no alteration in the numbers of nerve fibers but a numerical increase of postganglionic cell bodies immunoreactive to either met-enkephalin-arg-phe or leu-enkephalin antisera was demonstrated. Moreover, some perikarya exhibited immunoreactivity to both these opioids. (b) Receptor blockade with the muscarinic antagonist atropine sulphate or the general opiate antagonist naloxone had no effect on the number and distribution of dynorphin A or alpha-neoendorphin immunoreactive fibres, whereas both met-enkephalin-arg-phe and leu-enkephalin-immunoreactive fibres and postganglionic perikarya were increased in number. (c) After the kappa antagonist (MR2266BS), an increase of fibres with prodynorphin-derived opioid immunoreactivity as well as those with met-enkephalin-arg-phe- or leu-enkephalin-immunolabelling was visible and the met-enkephalin-arg-phe and leu-enkephalin-immunoreactive cell bodies were increased in number. The preganglionic origin of the investigated fibres with prodynorphin cleavage products was concluded from the complete disappearance of such fibres after preganglionic denervation. Denervation also resulted in an increase of met-enkephalin-arg-phe- and leu-enkephalin-immunoreactive perikarya. Small intensely fluorescent (SIF) cells, which in controls were nonrea
采用生物素-链霉亲和素-过氧化物酶复合物法，通过免疫组织化学方法研究了慢性给予三环类抗抑郁药丙咪嗪、各种受体阻断剂（毒蕈碱拮抗剂硫酸阿托品；阿片类拮抗剂纳洛酮；κ-拮抗剂MR2266BS）以及去神经支配后，大鼠颈上神经节中阿片样物质免疫反应性神经细胞体和曲张纤维的分布模式。使用了针对阿片类家族两种不同前体衍生的四种肽的抗血清。在对照颈上神经节中，当应用强啡肽A（1-17）或α-新内啡肽（前强啡肽的裂解产物）的抗血清时，稀疏分布的神经纤维且无神经元细胞体具有免疫反应性。中等数量的神经纤维和神经元胞体对针对甲硫氨酸脑啡肽-精氨酸-苯丙氨酸（前脑啡肽的裂解产物）和亮氨酸脑啡肽（前强啡肽和前脑啡肽的裂解产物）的抗血清具有免疫反应性；不同的细胞体含有甲硫氨酸脑啡肽-精氨酸-苯丙氨酸或亮氨酸脑啡肽免疫反应性。药物治疗后，颈上神经节中所研究肽的免疫反应性出现了特定变化。（a）丙咪嗪治疗导致对强啡肽A和α-新内啡肽抗血清呈免疫反应性的神经纤维增加。相比之下，神经纤维数量没有改变，但对甲硫氨酸脑啡肽-精氨酸-苯丙氨酸或亮氨酸脑啡肽抗血清呈免疫反应性的节后细胞体数量增加。此外，一些胞体对这两种阿片样物质均具有免疫反应性。（b）用毒蕈碱拮抗剂硫酸阿托品或一般阿片类拮抗剂纳洛酮进行受体阻断，对强啡肽A或α-新内啡肽免疫反应性纤维的数量和分布没有影响，而甲硫氨酸脑啡肽-精氨酸-苯丙氨酸和亮氨酸脑啡肽免疫反应性纤维以及节后胞体的数量均增加。（c）κ-拮抗剂（MR2266BS）处理后，可见具有前强啡肽衍生的阿片样物质免疫反应性的纤维以及具有甲硫氨酸脑啡肽-精氨酸-苯丙氨酸或亮氨酸脑啡肽免疫标记的纤维增加，且甲硫氨酸脑啡肽-精氨酸-苯丙氨酸和亮氨酸脑啡肽免疫反应性细胞体数量增加。从节前去神经支配后此类纤维的完全消失可推断出具有前强啡肽裂解产物的所研究纤维的节前起源。去神经支配还导致甲硫氨酸脑啡肽-精氨酸-苯丙氨酸和亮氨酸脑啡肽免疫反应性胞体增加。小而强荧光（SIF）细胞，在对照中不……
