Melatonin attenuates neuronal NADPH-d/NOS expression in the hypoglossal nucleus of adult rats following peripheral nerve injury.
Oxidative stress and massive production of nitric oxide (NO) have been implicated in the neuropathogenesis following peripheral nerve injury. This study was aimed to ascertain whether melatonin would exert its neuroprotective effect on the lesioned hypoglossal neurons after peripheral axotomy, since it is known to reduce the oxidative damage in a variety of experimental neuropathologies in which NO is involved. Right-sided hypoglossal nerve transection was performed in adult rats following which the animals were given two different doses of melatonin administered intraperitoneally for 3, 7, 14, 21 and 30 successive days. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry were carried out to detect the neuronal NADPH-d/NOS expression in the hypoglossal nucleus (HN). At various time intervals following axotomy, the neurons in the affected HN were induced to express NADPH-d/NOS reactivity on the lesioned side peaking at 14 days. However, the enzyme expression was markedly depressed by melatonin treatment in a dose-dependent manner in terms of frequency of labelled neurons and staining intensity. It is suggested that the suppressive effect of melatonin on NADPH-d/NOS expression may be attributed to its antioxidant properties. Hence, in consideration of therapeutic strategies for reducing the oxidative stress following peripheral nerve injury, melatonin may prove to be beneficial.
Department of Anatomy, College of Medicine, National Taiwan University, 100, Taipei, Taiwan.
H M
HM
Chang
E A
EA
Ling
J H
JH
Lue
C Y
CY
Wen
J Y
JY
Shieh
D000818:Animals; D019771:Axotomy / Q000009:adverse effects*; D002452:Cell Count; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D007002:Hypoglossal Nerve / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008550:Melatonin / Q000378:metabolism / Q000494:pharmacology*; D009046:Motor Neurons / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D009252:NADPH Dehydrogenase / Q000187:drug effects* / Q000378:metabolism; D009410:Nerve Degeneration / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D018696:Neuroprotective Agents / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D059348:Peripheral Nerve Injuries; D010525:Peripheral Nerves / Q000187:drug effects* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D018696:Neuroprotective Agents; D019001:Nitric Oxide Synthase; D009252:NADPH Dehydrogenase; D008550:Melatonin