Increased dopamine-beta-hydroxylase-like immunoreactivity in non-noradrenergic axons supplying the guinea-pig uterine artery after 6-hydroxydopamine treatment.
We have reinvestigated the immunohistochemistry of autonomic axons supplying the guinea-pig uterine artery to determine whether non-noradrenergic paracervical ganglion neurons projecting to the artery contain immunoreactivity to dopamine-beta-hydroxylase (DBH) or somatostatin (SOM) in addition to neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP). In untreated arteries no VIP axons had immunoreactivity to tyrosine hydroxylase (TH), although 9% had immunoreactivity to DBH. Somatostatin immunoreactivity was detected in 25% of non-noradrenergic axons containing NPY and VIP. After in vivo treatment with 6-hydroxydopamine (6-OHDA), noradrenergic axons containing immunoreactivity to NPY, DBH and TH were absent from the adventitia-medial junction. However, 65-70% of the non-noradrenergic axons with NPY and VIP showed DBH immunoreactivity after 6-OHDA. These axons did not show catecholamine fluorescence after incubation with pargyline together with noradrenaline, dopamine or L-DOPA. The number of axons with SOM immunoreactivity increased by 44% after 6-OHDA treatment, but only 24% of SOM axons had DBH immunoreactivity. Surgical destruction of the non-noradrenergic autonomic axons in 6-OHDA-treated animals led to the loss of all DBH immunoreactivity. These results demonstrate that DBH immunoreactivity can be detected in a small proportion of non-noradrenergic axons supplying uterine arteries from untreated animals. After chemical sympathectomy with 6-OHDA, the levels of DBH immunoreactivity in axons of non-noradrenergic neurons increased, and more axons with DBH immunoreactivity were detected. DBH immunoreactivity seemed to increase preferentially in axons with NPY and VIP, but not SOM. The number of NPY, VIP axons containing SOM also increased after 6-OHDA. These findings demonstrate that peripheral neurons containing several different potential neurotransmitters can change their levels of neuropeptides and transmitter-synthesizing enzymes in response to local environmental changes.
D000818:Animals; D001158:Arteries / Q000294:innervation*; D001369:Axons / Q000187:drug effects / Q000201:enzymology*; D004299:Dopamine beta-Hydroxylase / Q000276:immunology / Q000378:metabolism*; D005260:Female; D005455:Fluorescent Antibody Technique; D005725:Ganglia, Autonomic / Q000166:cytology / Q000201:enzymology; D006168:Guinea Pigs; D006892:Hydroxydopamines / Q000494:pharmacology*; D009478:Neuropeptide Y / Q000032:analysis; D016627:Oxidopamine; D013004:Somatostatin / Q000032:analysis; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D014599:Uterus / Q000098:blood supply*; D014660:Vasoactive Intestinal Peptide / Q000032:analysis
D006892:Hydroxydopamines; D009478:Neuropeptide Y; D014660:Vasoactive Intestinal Peptide; D013004:Somatostatin; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase; D004299:Dopamine beta-Hydroxylase