Responses of nitric oxide synthase expression in the gracile nucleus to sciatic nerve injury in young and aged rats

Ma, Sheng-Xing; Cornford, Marcia E.; Vahabnezhad, Iaheh; Wei, Shimin; Li, Xiyan

doi:10.1016/s0006-8993(99)02379-3

Cited by 31 publications

(31 citation statements)

References 27 publications

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“…These results are similar to previous studies that showed the upregulation of NOS-LI neurons in the lumbar DRG [4,5,13] and GN [6] after sciatic nerve injury. The increase in the mean number of NOS-LI neurons in the CN at 2 and 4 weeks after MNT was similar to that in GN at 2 weeks after sciatic nerve injury [6]. However, the percentage of NOS-LI neurons in C6 DRG (11.5 ± 0.02%) in this study was much less than that in lumbar DRG (41.2 ± 3.9%) at 4 weeks after nerve injury [5].…”

Section: Discussionsupporting

confidence: 92%

“…The inputs are integrated into cuneothalamic projection neurons (CTNs) and/or interneurons, and further transmitted to the contralateral thalamus through the medial lemniscus [1][2][3]. Peripheral nerve injury leads to a modification of the number of nitric oxide (NO)-synthesizing neurons, which were identified histochemically by the occurrence of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) activity or immunocytochemically with an antibody for neuronal nitric oxide synthase (nNOS), in the DRG, spinal cord, and gracile nucleus (GN) [4][5][6][7][8]. Indeed, NADPH-d positive and/or nNOS-like immunoreactive (nNOS-LI) neurons have been reported to be present in the CN [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

“…Peripheral injury of sciatic nerve has been shown to result in a rise in the number of nNOS-LI neurons in rat lumbar DRGs, but not in monkey [4,5,13]; the nNOS-LI fibers and neurons increased in the spinal cord laminae III-IV and GN but reduced in laminae I-II [6,7,13]. These differences may be due to different regions and species.…”

Section: Introductionmentioning

confidence: 99%

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Nitric Oxide Implicates c-Fos Expression in the Cuneate Nucleus Following Electrical Stimulation of the Transected Median Nerve

et al. 2011

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In this study, we investigated whether nitric oxide (NO) modulated injury-induced neuropeptide Y (NPY) releasing and c-Fos expression in the cuneate nucleus (CN) after median nerve transection (MNT). We first examined the temporal changes of neuronal nitric oxide synthase (nNOS) expression in the dorsal root ganglion (DRG) and CN after MNT. Following MNT, the amounts of nNOS-like immunoreactive (nNOS-LI) neurons in the DRG and CN significantly increased as compared with those of the sham-operated rats. Furthermore, 4 weeks after MNT, the increases of nNOS-LI neurons in the DRG and CN were attenuated by pre-emptive lidocaine treatment in a dose-dependent manner. Finally, 4 weeks after MNT, pre-stimulation administration of L-NAME (N (ω)-Nitro-L: -arginine methyl ester) or 7-NI (7-nitroindazole) suppressed the amount of NPY release from the stimulated terminals and thus attenuated c-Fos expression in the CN. Our data implied that NO would modulate neuronal activity in the DRG and CN both after MNT.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Nitric Oxide Implicates c-Fos Expression in the Cuneate Nucleus Following Electrical Stimulation of the Transected Median Nerve

et al. 2011

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“…units: nNOS, 1900660 vs. 10906100; nitrotyrosine, 780610 vs. 310610). In fact dietary acetyl L-carnitine of aged mice caused these levels to be statistically indistinguishable from corresponding values found for the untreated younger group (nNOS, Cortex may thus differ from other brain regions with respect to age-induced nNOS elevation, since nNOS has been measured as unchanged by age in the rat hypothalamus [12,46] and in the rat gracile nucleus [26]. Nitrosative stress has been implicated in both aging and in the pathogenesis of several neurodegenerative diseases [10].…”

Section: 5 Measurement Of Locomotor Activity 7 Statistical Analysesmentioning

confidence: 99%

Reversal of biochemical and behavioral parameters of brain aging by melatonin and acetyl l-carnitine

Sharman

Vaziri

et al. 2002

Brain Research

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“…NADPHd and NOS protein are inducible in term of de novo synthesis in traumatically injured neurons (Wu, 2000). After peripheral axotomy, NOS protein and NOS mRNA increase in some neuronal populations (Verge et al, 1992;Vizzard et al, 1995); moreover, NOS is up-regulated in axotomized motoneurons (Yu, 1994;Yu, 1997;Mü ller and Stoll, 1998;Ma et al, 2000).…”

Section: Nos Induction After Axotomymentioning

confidence: 99%

Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection

et al. 2002

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When vestibular damage occurs, nitric oxide synthase (NOS) expression in rat cerebellar flocculus is affected. Since compensation for postural symptoms occurs and Purkinje cells play an important role in movement coordination and motor learning, we analyzed in situ the induction of NOS in the Purkinje cell population of the cerebellum (corpus cerebelli) of frog after unilateral transection of the eighth statoacoustic nerve to gain insight into the role of NO in neural plasticity after injury. Three days after neurectomy, the early effects induced NADPH diaphorase reactivity in most of the Purkinje cells on the ipsilateral side, while on the contralateral side the highest labeling was observed at 15 days. This finding can give information on the dynamics of vestibular compensation, in which NOS involvement was investigated. At 30 days, NADPH diaphorase reactivity was present in a large number of Purkinje cells of the whole cerebellum, while at 60 days a down-regulation for NADPH diaphorase reactivity was evident. A similar trend was observed for NOS-immunoreactivity, which was still present at 60 days in a high percentage of Purkinje cells, mainly on the ipsilateral side. On the basis of cell density evaluations, it was proposed that the early induction of NOS after neurectomy was linked to the degeneration of a part of the Purkinje neurons, while the permanence of NOS labeling might be due to a neuroprotective role of NO in the restoration phase of the vestibular compensation process. Anat Rec 268: 73-83, 2002.

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Responses of nitric oxide synthase expression in the gracile nucleus to sciatic nerve injury in young and aged rats

Cited by 31 publications

References 27 publications

Nitric Oxide Implicates c-Fos Expression in the Cuneate Nucleus Following Electrical Stimulation of the Transected Median Nerve

Nitric Oxide Implicates c-Fos Expression in the Cuneate Nucleus Following Electrical Stimulation of the Transected Median Nerve

Reversal of biochemical and behavioral parameters of brain aging by melatonin and acetyl l-carnitine

Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection

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