Changes in the expression of extracellular regulated kinase (ERK 1/2) in the R6/2 mouse model of Huntington's disease after phosphodiesterase IV inhibition

Fusco, Francesca R.; Anzilotti, Serenella; Giampà, Carmela; Dato, Clemente; Laurenti, Daunia; Leuti, Alessandro; D’Amato, Luca Colucci; Perrone, Lorena; Bernardi, Giorgio; Melone, Mariarosa Anna Beatrice

doi:10.1016/j.nbd.2012.01.011

Cited by 23 publications

(19 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3). These results are consistent with our previous observations of reduced levels of pERK in the R6/2 mouse model after treatment with other neuroprotective agents [33] The results were confirmed by western blotting (Fig. 3 K).…”

Section: Resultssupporting

confidence: 93%

“…In a previous paper, we observed that projection neurons as well as parvalbuminergic interneurons, which are most vulnerable to HD de- generation, contain pERK levels that tend to increase with age (in the wild-type animals) and with the progression of the disease (in the R6/2 mice). Such increase was reversed by PDE inhibition [33].…”

Section: Discussionmentioning

confidence: 95%

“…The question whether systemic BDNF is capable to cross the blood-brain barrier (BBB) has been the subject of several studies [33], [48]. In particular, many authors deny the existence of BDNF transport into brain [49], [48].…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Systemic Delivery of Recombinant Brain Derived Neurotrophic Factor (BDNF) in the R6/2 Mouse Model of Huntington’s Disease

et al. 2013

Self Cite

View full text Add to dashboard Cite

Loss of huntingtin-mediated BDNF gene transcription has been shown to occur in HD and thus contribute to the degeneration of the striatum. Several studies have indicated that an increase in BDNF levels is associated with neuroprotection and amelioration of neurological signs in animal models of HD. In a recent study, an increase in BDNF mRNA and protein levels was recorded in mice administered recombinant BDNF peripherally. Chronic, indwelling osmotic mini-pumps containing either recombinant BDNF or saline were surgically placed in R6/2 or wild-type mice from 4 weeks of age until euthanasia. Neurological evaluation (paw clasping, rotarod performance, locomotor activity in an open field) was performed. After transcardial perfusion, histological and immunohistochemical studies were performed. We found that BDNF- treated R6/2 mice survived longer and displayed less severe signs of neurological dysfunction than the vehicle treated ones. Primary outcome measures such as brain volume, striatal atrophy, size and morphology of striatal neurons, neuronal intranuclear inclusions and microglial reaction confirmed a neuroprotective effect of the compound. BDNF was effective in increasing significantly the levels of activated CREB and of BDNF the striatal spiny neurons. Moreover, systemically administered BDNF increased the synthesis of BDNF as demonstrated by RT-PCR, and this might account for the beneficial effects observed in this model.

show abstract

Section: Resultssupporting

confidence: 93%

Section: Discussionmentioning

confidence: 95%

See 1 more Smart Citation

Systemic Delivery of Recombinant Brain Derived Neurotrophic Factor (BDNF) in the R6/2 Mouse Model of Huntington’s Disease

et al. 2013

Self Cite

View full text Add to dashboard Cite

show abstract

“…Conversely, the subsets of neurons that are more resistant to HD degeneration, namely somatostatin-NOS-NPY and cholinergic interneurons, showed decreased p-Erk with disease progression in the R6/2 mice [89]. This appears to indicate that Erk activity may be directly involved in HD progression and can define differences in striatal neuronal susceptibility.…”

Section: Discussionmentioning

confidence: 90%

“…Also, insulin was shown to inhibit Erk1/2 phosphorylation in a PI-3K-dependent manner in Neuro2a cells [88]. In R6/2 HD mice, Fusco and collaborators [89] investigated Erk activation among different subsets of striatal neurons. They verified that the most susceptible striatal neurons to degeneration in HD, striatal medium spiny projection neurons and parvalbuminergic interneurons, exhibited increased p-Erk levels with disease progression.…”

Section: Discussionmentioning

confidence: 99%

Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells

Ribeiro

Rosenstock

Oliveira

et al. 2014

Free Radical Biology and Medicine

117

View full text Add to dashboard Cite

Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington's disease knock-in striatal cells, Free Radical Biology and Medicine, http://dx.doi.org/10.1016/j. freeradbiomed.2014.06.023 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

show abstract

Emerging Role for PDE4 in Neuropsychiatric Disorders: Translating Advances from Genetic Studies Into Relevant Therapeutic Strategies

Zoubovsky

Sawa

Brandon

2014

Cyclic‐Nucleotide Phosphodiesterases in the Central Nervous System

View full text Add to dashboard Cite

Changes in the expression of extracellular regulated kinase (ERK 1/2) in the R6/2 mouse model of Huntington's disease after phosphodiesterase IV inhibition

Cited by 23 publications

References 72 publications

Systemic Delivery of Recombinant Brain Derived Neurotrophic Factor (BDNF) in the R6/2 Mouse Model of Huntington’s Disease

Systemic Delivery of Recombinant Brain Derived Neurotrophic Factor (BDNF) in the R6/2 Mouse Model of Huntington’s Disease

Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells

Emerging Role for PDE4 in Neuropsychiatric Disorders: Translating Advances from Genetic Studies Into Relevant Therapeutic Strategies

Contact Info

Product

Resources

About