Vlr. Rao et al., Traumatic injury to rat brain upregulates neuronal nitric oxide synthase expression and L-[H-3]nitroarginine binding, J NEUROTRAU, 16(10), 1999, pp. 865-877
Overstimulation of N-methyl-D-aspartate (NMDA) receptors is felt to precipi
tate the neuronal damage following traumatic brain injury (TBI). NMDA recep
tor-mediated, glutamate-induced excitotoxicity is thought to be mediated vi
a nitric oxide (NO) formed by neuronal nitric oxide synthase (nNOS), The pr
esent study examined the mRNA and protein levels of nNOS in the ipsilateral
and contralateral cortex of rats as a function of time (5 minutes to 1 wee
k) after controlled cortical impact (CCI) brain injury, Sham-operated rats
served as controls. TBI resulted in a significant increase in the levels of
nNOS mRNA (1.5- to 2.8-fold, p <.05) between 2 and 4 hours after the injur
y, There was also a significant increase in the levels of nNOS protein (by
55% to 90%,p <.05) and binding densities of the nNOS-specific ligand L-[H-3
]nitroarginine (L-[H-3]NOARG) (by 35% to 59%,p <.05) between 2 and 12 hours
after the injury, Increased nNOS expression and function may contribute to
the concomitant excitotoxic neuronal death after TBI.