Immunohistochemical evidence for different opioid systems in the rat superior cervical ganglion as revealed by imipramine treatment and receptor blockade.
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
Folan
J C
JC
Department of Anatomy, University College Dublin, Ireland.
Heym
C
C
D000595:Amino Acid Sequence; D000818:Animals; D001285:Atropine / Q000494:pharmacology*; D001575:Benzomorphans / Q000494:pharmacology; D003714:Denervation; D004399:Dynorphins / Q000032:analysis; D004723:Endorphins / Q000032:analysis*; D004743:Enkephalin, Leucine / Q000032:analysis; D004744:Enkephalin, Methionine / Q000031:analogs & derivatives / Q000032:analysis; D005728:Ganglia, Sympathetic / Q000032:analysis* / Q000187:drug effects; D007099:Imipramine / Q000494:pharmacology*; D007150:Immunohistochemistry; D008297:Male; D008969:Molecular Sequence Data; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology*; D009474:Neurons / Q000032:analysis; D011498:Protein Precursors / Q000032:analysis; D051381:Rats; D011919:Rats, Inbred Strains
D001575:Benzomorphans; D004723:Endorphins; D009292:Narcotic Antagonists; D011498:Protein Precursors; D009270:Naloxone; C027247:MR 2266; D004744:Enkephalin, Methionine; D004743:Enkephalin, Leucine; C025681:alpha-neoendorphin; C027511:enkephalin-Met, Arg(6)-Phe(7)-; D004399:Dynorphins; D001285:Atropine; D007099:Imipramine