Nitric oxide-induced cGMP synthesis in the cholinergic system during the development and aging of the rat brain

Domek-Łopacińska, K.; Waarenburg, Marjo P. H. van de; Ittersum, Marjanne Markerink‐van; Steinbusch, Harry W.M.; Vente, Jan de

doi:10.1016/j.devbrainres.2005.06.003

Cited by 15 publications

(4 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, incubation of mature and senescent brain slices with the highly selective PDE2 inhibitor, Bay 60-7550, resulted in similar increase in cGMP immunoreactivity [19]. On the other hand, there is evidence that the ability of cholinergic neurons in the basal forebrain and inter-neurons in the striatum to synthesize cGMP via the NO-dependent pathway was decreased during aging [22]. Study by Ibarra et al [29] showed that, in the human cortex and striatum, sGC expression decreased with age.…”

Section: Guanylyl Cyclase and Cgmp Synthesismentioning

confidence: 80%

Cyclic GMP and Nitric Oxide Synthase in Aging and Alzheimer's Disease

2010

View full text Add to dashboard Cite

Cyclic guanosine monophosphate (cGMP) is an important secondary messenger synthesized by the guanylyl cyclases which are found in the soluble (sGC) and particular isoforms. In the central nervous system, the nitric oxide (NO)-sensitive sGC isoform is the major enzyme responsible for cGMP synthesis. Phosphodiesterases (PDEs) are enzymes for hydrolysis of cGMP in the brain, and they are mainly isoforms 2, 5, and 9. The NO/cGMP signaling pathway has been shown to play an important role in the process underlying learning and memory. Aging is associated with an increase in PDE expression and activity and a decrease in cGMP concentration. In addition, aging is also associated with an enhancement of neuronal NO synthase, a lowering of endothelial, and no alteration in inducible activity. The observed changes in NMDA receptor density along with the Ca(2+)/NO/cGMP pathway underscore the lower synaptic plasticity and cognitive performance during aging. This notion is in agreement with last data indicating that inhibitors of PDE2 and PDE9 improve learning and memory in older rats. In this review, we focus on recent studies supporting the role of Ca(2+)/NO/cGMP pathway in aging and Alzheimer's disease.

show abstract

Section: Guanylyl Cyclase and Cgmp Synthesismentioning

confidence: 80%

Cyclic GMP and Nitric Oxide Synthase in Aging and Alzheimer's Disease

2010

View full text Add to dashboard Cite

show abstract

“…Although there are no data on NO‐responsive cGMP‐producing structures in the human brain, it has been demonstrated in the rat forebrain that the cholinergic innervation responds to an NO donor with increased cGMP synthesis (de Vente et al. , 2000, 2001; Domek‐Lopacinska et al. , 2005b).…”

Section: Discussionmentioning

confidence: 99%

Expression of the cGMP‐specific phosphodiesterases 2 and 9 in normal and Alzheimer's disease human brains

Reyes-Irisarri

Ittersum

Mengod

et al. 2007

Eur J of Neuroscience

101

View full text Add to dashboard Cite

We studied the mRNA expression of cGMP‐hydrolysing phosphodiesterases (PDEs) in selected brain areas of normal elderly people and patients with Alzheimer's disease. Using radioactive in‐situ hybridization histochemistry we found a widespread distribution of the mRNA for PDE2 and PDE9, whereas no specific hybridization signal was observed for PDE5. We observed PDE2 and PDE9 mRNA in all cortical areas studied (insular cortex, entorhinal cortex and visual cortex), although to a different extent. PDE2 mRNA was high in the claustrum, whereas PDE9 mRNA was moderate. PDE2 and PDE9 mRNAs was present in the putamen. No cGMP‐hydrolysing PDE expression was observed in the globus pallidus. PDE2 and PDE9 mRNA was observed in all subareas of the hippocampus; however, there were significant differences in the amount of expression. In the Purkinje and cerebellar granule cells only PDE9 expression was observed. PDE2 and PDE9 mRNA expression was not significantly different in Alzheimer's disease brains.

show abstract

“…Aging is associated with considerable reduction in the number of striatal neurons containing NO synthase [ 21 , 22 ] suggesting a significant decrease in NO production and corresponding alterations in NO-dependent processes. In fact, the data on age-related changes in the striatal NO synthase (NOS) activity and in NO-cGMP-protein kinase G (PKG) signaling are controversial [ 23 – 25 ]. The aim of the present study was to investigate age-related alterations in the expression of genes involved in NO signaling and to explore the manifestation of several forms of NO-dependent plasticity in the dorsal striatum of mice at four different ages.…”

Section: Introductionmentioning

confidence: 99%

Age-Related Alterations in the Expression of Genes and Synaptic Plasticity Associated with Nitric Oxide Signaling in the Mouse Dorsal Striatum

2015

View full text Add to dashboard Cite

Age-related alterations in the expression of genes and corticostriatal synaptic plasticity were studied in the dorsal striatum of mice of four age groups from young (2-3 months old) to old (18–24 months of age) animals. A significant decrease in transcripts encoding neuronal nitric oxide (NO) synthase and receptors involved in its activation (NR1 subunit of the glutamate NMDA receptor and D1 dopamine receptor) was found in the striatum of old mice using gene array and real-time RT-PCR analysis. The old striatum showed also a significantly higher number of GFAP-expressing astrocytes and an increased expression of astroglial, inflammatory, and oxidative stress markers. Field potential recordings from striatal slices revealed age-related alterations in the magnitude and dynamics of electrically induced long-term depression (LTD) and significant enhancement of electrically induced long-term potentiation in the middle-aged striatum (6-7 and 12-13 months of age). Corticostriatal NO-dependent LTD induced by pharmacological activation of group I metabotropic glutamate receptors underwent significant reduction with aging and could be restored by inhibition of cGMP hydrolysis indicating that its age-related deficit is caused by an altered NO-cGMP signaling cascade. It is suggested that age-related alterations in corticostriatal synaptic plasticity may result from functional alterations in receptor-activated signaling cascades associated with increasing neuroinflammation and a prooxidant state.

show abstract

Nitric oxide-induced cGMP synthesis in the cholinergic system during the development and aging of the rat brain

Cited by 15 publications

References 50 publications

Cyclic GMP and Nitric Oxide Synthase in Aging and Alzheimer's Disease

Cyclic GMP and Nitric Oxide Synthase in Aging and Alzheimer's Disease

Expression of the cGMP‐specific phosphodiesterases 2 and 9 in normal and Alzheimer's disease human brains

Age-Related Alterations in the Expression of Genes and Synaptic Plasticity Associated with Nitric Oxide Signaling in the Mouse Dorsal Striatum

Contact Info

Product

Resources

About