A nitric oxide synthase inhibitor decreases 6-hydroxydopamine effects on tyrosine hydroxylase and neuronal nitric oxide synthase in the rat nigrostriatal pathway

Gomes, Margarete Zanardo; Raisman‐Vozari, Rita; Bel, Elaine Aparecida Del

doi:10.1016/j.brainres.2008.01.088

Cited by 53 publications

(37 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…44) In addition, high levels of neuronal and inducible NOSs (nNOS and iNOS) were observed in the SN of PD patients and parkinsonism model. 45,46) These reports suggest that iNOS may play a role in the pathogenesis of PD which is related to CNS inflammation.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Pyo

Jeong

Yeo

et al. 2013

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

The anti-inflammatory and neuroprotective effects of trans-cinnamaldehyde (TCA) were investigated on the inflammatory cells and the dopaminergic degeneration in mice. TCA inhibited the up-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the lipopolysaccharide (LPS)-induced inflammatory BV2 microglial cells. To investigate the TCA efficacy on the 6-hydroxydopamine (6-OHDA)-induced dopaminergic degeneration in mice, an intracerebroventricular injection of 6-OHDA was given to the mice, and TCA (30 mg/kg) was intraperitoneally administered. At 7 d after the 6-OHDA injection, 6-OHDA led to a severe loss of tyrosine hydroxylase (TH)-positive dopaminergic neurons in the striatum and substantia nigra (SN). On the other hand, TCA dramatically maintained the number of TH-positive dopaminergic neurons in the striatum and SN regions of the 6-OHDA-treated mice, which indicates that TCA is able to inhibit the 6-OHDA-induced reduction of TH expression in the dopaminergic neurons in the striatum and SN regions. TCA also inhibited the induction of iNOS and COX-2 in the 6-OHDA model, similarly as shown in the LPS-induced inflammatory BV2 microglial cells. These results indicate that TCA has a neuroprotective effect on dopaminergic neurons and that this effect may be associated with the inhibition of inflammatory responses. These findings suggest that TCA may be a therapeutic candidate for the prevention of inflammationmediated neurodegenerative diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Pyo

Jeong

Yeo

et al. 2013

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…The role of oxidative stress in the pathogenesis of MPTP/MPP + -induced DAergic degeneration, has been suggested [56,58,61,[139][140][141]147]. Numerous studies have proposed that nNOS inhibitors, including 7-NI, may reduce DAergic neuronal degeneration, both in vitro and in vivo through antioxidative mechanisms [148][149][150]. The neuroprotective effect of 7-NI against MPP + -induced DA striatal depletion is probably due to a block in the rise of the toxic NO 3¯ produced by the combination of NO and ˙OH induced by MPP + , as shown in previous studies [142,151].…”

Section: Involvement Of No In Neurodegeneration Of Daergic Nigrostriamentioning

confidence: 99%

Nitric Oxide Modulation of the Basal Ganglia Circuitry: Therapeutic Implication for Parkinson's Disease and Other Motor Disorders

Pierucci

Galati

Valentino

et al. 2011

CNSNDDT

View full text Add to dashboard Cite

Several recent studies have emphasized a crucial role for the nitrergic system in movement control and the pathophysiology of the basal ganglia (BG). These observations are supported by anatomical evidence demonstrating the presence of nitric oxide synthase (NOS) in all the basal ganglia nuclei. In fact, nitrergic terminals have been reported to make synaptic contacts with both substantia nigra dopamine-containing neurons and their terminal areas such as the striatum, the globus pallidus and the subthalamus. These brain areas contain a high expression of nitric oxide (NO)-producing neurons, with the striatum having the greatest number, together with important NO afferent input. In this paper, the distribution of NO in the BG nuclei will be described. Furthermore, evidence demonstrating the nitrergic control of BG activity will be reviewed. The new avenues that the increasing knowledge of NO in motor control has opened for exploring the pathophysiology and pharmacology of Parkinson's disease and other movement disorders will be discussed. For example, inhibition of striatal NO/guanosine monophosphate signal pathway by phosphodiesterases seems to be effective in levodopa-induced dyskinesia. However, the results of experimental studies have to be interpreted with caution given the complexities of nitrergic signalling and the limitations of animal models. Nevertheless, the NO system represents a promising pharmacological intervention for treating Parkinson's disease and related disorders.

show abstract

“…Immunohistochemistry was performed using a standard peroxidase-based method (28). Randomly sampled sections were incubated with a tyrosine hydroxylase (TH) antibody (1:2000, Pel Freez, USA) overnight at 4°C followed by a biotinylated secondary antibody (Vectastain ABC kit, Vector Laboratories, USA) and HRP-conjugated streptavidin (Vectastain ABC kit, Vector Laboratories).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Lack of tolerance for the anti-dyskinetic effects of 7-nitroindazole, a neuronal nitric oxide synthase inhibitor, in rats

Novaretti

Padovan-Neto

Tumas

et al. 2010

Braz J Med Biol Res

View full text Add to dashboard Cite

A nitric oxide synthase inhibitor decreases 6-hydroxydopamine effects on tyrosine hydroxylase and neuronal nitric oxide synthase in the rat nigrostriatal pathway

Cited by 53 publications

References 72 publications

Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Nitric Oxide Modulation of the Basal Ganglia Circuitry: Therapeutic Implication for Parkinson's Disease and Other Motor Disorders

Lack of tolerance for the anti-dyskinetic effects of 7-nitroindazole, a neuronal nitric oxide synthase inhibitor, in rats

Contact Info

Product

Resources

About