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.