DETA/NONOate, a nitric oxide donor, produces antidepressant effects by promoting hippocampal neurogenesis

Yao, Hua; Huang, Xinyan; Zhou, Li; Zhou, Qi‐Gang; Hu, Yao; Luo, Chunxia; Li, Fēi; Zhu, Dong‐Ya

doi:10.1007/s00213-008-1200-1

Cited by 33 publications

(21 citation statements)

References 62 publications

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“…In this same line of evidence, treatment with antidepressives causes a decrease in NO production in cerebral cortex and hippocampus [24]. On the other hand, administration of a NO donor reversed chronic mild stress-induced behavioral despair and impairment in hippocampal neurogenesis in mice [19,23].…”

Section: Introductionmentioning

confidence: 94%

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Maternal Depression Model: Long-Lasting Effects on the Mother Following Separation from Pups

et al. 2011

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This study was carried out to ascertain the effects of maternal separation (3 h per day) of mothers from their pups in the neonatal period in rats, which has been suggested to induce a depressive-like state, would have long lasting effects on different parameters including hippocampal Na(+), K(+)-ATPase activity, NO production, free radical production and antioxidant enzymes activities in dams. Fourty-eight Wistar rats were divided into 3 groups: control, brief separation (10 min) and long separation (3 h). The neonatal interventions were done on postpartum days 1-10. At 35 days post-partum the dams were killed and the hippocampal Na(+), K(+)-ATPase activity were measured, as well as the activity of the antioxidant enzymes catalase, glutathione peroxidase, superoxide dismutase, free radicals production, and the production of nitric oxide. Hippocampal Na(+), K(+)-ATPase activity was decreased in the brief separated group and in dams subjected to 3 h separation from their pups. A reduction in nitric oxide levels in the hippocampus in dams of the long separated group was also observed. It is concluded that the withdrawal of pups from their mothers make the mothers more susceptible to the development of neurochemical alterations that could be related to depressive features.

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Section: Introductionmentioning

confidence: 94%

“…Recent studies, both in humans [18] and in animal models [19][20][21][22][23], suggest an involvement of endogenous hippocampal nitric oxide (NO) in the neurobiology of stress and depression. Intra-hippocampal administration of nitric oxide synthase (NOS) inhibitors induce antidepressant-like effects in rodents [20,21].…”

Section: Introductionmentioning

confidence: 99%

Maternal Depression Model: Long-Lasting Effects on the Mother Following Separation from Pups

et al. 2011

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“…Conversely, L-NNA, depending on its dose is able to cause an antidepressant-like effect, which can be reversed by l-arginine, administered at a dose that produces no effect in the FST (da Silva et al 2000). Interestingly, exogenous administration of l-arginine (250-500 mg/kg), at same doses that produce anti-immobility effect, increased neuronal NO signal (Heinzen and Pollack 2002) and DETA/NONOate, a NO donor, produces antiimmobility effect associated with enhancement of NO x levels and hippocampal neurogenesis (Hua et al 2008). Accordingly, a low dose of L-NAME (100 mg/kg, ip) decreased the immobility time in the FST, whereas high doses (175-300 mg/kg, ip) did not produce any anti-immobility effect in the FST (Harkin et al 1999).…”

Section: Discussionmentioning

confidence: 90%

The modulation of NMDA receptors and l-arginine/nitric oxide pathway is implicated in the anti-immobility effect of creatine in the tail suspension test

et al. 2015

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The modulation of N-methyl-D-aspartate receptor (NMDAR) and L-arginine/nitric oxide (NO) pathway is a therapeutic strategy for treating depression and neurologic disorders that involves excitotoxicity. Literature data have reported that creatine exhibits antidepressant and neuroprotective effects, but the implication of NMDAR and L-arginine/nitric oxide (NO) pathway in these effects is not established. This study evaluated the influence of pharmacological agents that modulate NMDAR/L-arginine-NO pathway in the anti-immobility effect of creatine in the tail suspension test (TST) in mice. The NOx levels and cellular viability in hippocampal and cerebrocortical slices of creatine-treated mice were also evaluated. The anti-immobility effect of creatine (10 mg/kg, po) in the TST was abolished by NMDA (0.1 pmol/mouse, icv), D-serine (30 µg/mouse, icv, glycine-site NMDAR agonist), arcaine (1 mg/kg, ip, polyamine site NMDAR antagonist), L-arginine (750 mg/kg, ip, NO precursor), SNAP (25 μg/mouse, icv, NO donor), L-NAME (175 mg/kg, ip, non-selective NOS inhibitor) or 7-nitroindazole (50 mg/kg, ip, neuronal NOS inhibitor), but not by DNQX (2.5 µg/mouse, icv, AMPA receptor antagonist). The combined administration of sub-effective doses of creatine (0.01 mg/kg, po) and NMDAR antagonists MK-801 (0.001 mg/kg, po) or ketamine (0.1 mg/kg, ip) reduced immobility time in the TST. Creatine (10 mg/kg, po) increased cellular viability in hippocampal and cerebrocortical slices and enhanced hippocampal and cerebrocortical NO x levels, an effect potentiated by L-arginine or SNAP and abolished by 7-nitroindazole or L-NAME. In conclusion, the anti-immobility effect of creatine in the TST involves NMDAR inhibition and enhancement of NO levels accompanied by an increase in neural viability.

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“…Likewise, the prior administration of 7-nitroindazole and the iNOS inhibitor aminoguanidine significantly reduced the number of BrdU ϩ cells in the dentate gyrus after pentylenetrazol-induced seizures in the adult rat brain (55), supporting a role for NO in brain repair after brain injury or seizures. DETA/NONOate has also been shown to produce antidepressant effects by promoting hippocampal neurogenesis in young adult mice (56). The explanation for these paradoxical effects of NO lie in the existence and differential effects of the NOS isoforms and/or the FIGURE 6.…”

Section: Discussionmentioning

confidence: 99%

Intracellular Nitric Oxide Mediates Neuroproliferative Effect of Neuropeptide Y on Postnatal Hippocampal Precursor Cells

Cheung

Newland

Zaben

et al. 2012

Journal of Biological Chemistry

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Background: Neuropeptide Y and nitric oxide are key regulators of adult hippocampal neurogenesis. Results: Pharmacological inhibition of intracellular NO signaling pathways abolished neuropeptide Y-mediated neuroproliferation. Conclusion: An intracellular NO-cGMP-PKG and ERK pathway mediates the neuropeptide Y neuroproliferative effect. Significance: This work unites two significant modulators of hippocampal neurogenesis and provides a mechanism for the independent extra-and intracellular regulation of postnatal neural precursors by NO.

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DETA/NONOate, a nitric oxide donor, produces antidepressant effects by promoting hippocampal neurogenesis

Abstract: Our findings suggest that exogenous NO benefits chronic stress-induced depression by stimulating hippocampal neurogenesis and may represent a novel approach for the treatment of depressive disorders.

Cited by 33 publications

References 62 publications

Maternal Depression Model: Long-Lasting Effects on the Mother Following Separation from Pups

Maternal Depression Model: Long-Lasting Effects on the Mother Following Separation from Pups

The modulation of NMDA receptors and l-arginine/nitric oxide pathway is implicated in the anti-immobility effect of creatine in the tail suspension test

Intracellular Nitric Oxide Mediates Neuroproliferative Effect of Neuropeptide Y on Postnatal Hippocampal Precursor Cells

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