Regular ArticleAge-Dependent Differences in Survival of Striatal Somatostatin–NPY–NADPH–Diaphorase-Containing Interneurons versus Striatal Projection Neurons after Intrastriatal Injection of Quinolinic Acid in Rats☆
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Cited by (42)
Neuropeptide Y (NPY) as a therapeutic target for neurodegenerative diseases
2016, Neurobiology of DiseaseCitation Excerpt :However, with RIA analysis, other authors did not observed changes in striatal NPY levels (Beal et al., 1986a), which suggests that the spared NPY interneurons can be in an hyperactive state to compensate for the neuronal loss. Even though this model is widely used, some methodological particularities can influence these results such as the rats' age and quinolinic acid injection speed (Figueredo-Cardenas et al., 1994; Figueredo-Cardenas et al., 1997). The MJD striatal lentiviral-based mouse model consists in the stereotaxic injection into the mouse striatum of lentiviral vectors encoding for mutant ataxin-3 in one hemisphere, and for wild-type ataxin-3, as an internal control, in the other hemisphere (Goncalves et al., 2013; Simoes et al., 2012).
Phosphodiesterase 10A (PDE10A) localization in the R6/2 mouse model of Huntington's disease
2013, Neurobiology of DiseaseCitation Excerpt :Moreover, PDE10A expression does not change with TP10 treatment in HD animals. In recent years, many studies have investigated the mechanisms by which certain neurons are more vulnerable, and certain neurons more resistant, to HD degeneration (Chen et al., 1998; Figueredo-Cardenas et al., 1997; Fusco et al., 1999; Sun et al., 2002a,b). In a previous study, our group showed that striatal cholinergic interneurons contain higher amounts of BDNF, which is essential for striatal survival and is greatly decreased in HD, compared to the more vulnerable medium spiny neurons (Fusco et al., 2001).
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
2012, Neurobiology of DiseaseCitation Excerpt :Indeed, we observed that projection neurons as well as parvalbuminergic interneurons, which are most vulnerable to HD degeneration, 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). Conversely, the subsets of neurons that are more resistant to HD degeneration, such as the somatostatin-NOS-NPY (Figueredo-Cardenas et al., 1997) and the cholinergic interneurons (Meade et al., 2000) showed that pERK decreased with age (in the wild-type) and progression of the disease (in the R6/2). Studies focusing on the intrinsic characteristics of the different striatal neurons in models of HD have tried to shed light on what makes certain neurons more vulnerable, and certain neurons more resistant, to HD degeneration (Chen et al., 1998; Figueredo-Cardenas et al., 1997; Fusco et al., 1999; Sun et al., 2002a,b).
Protective effect of melatonin on 3-NP induced striatal interneuron injury in rats
2011, Neurochemistry InternationalCitation Excerpt :These models simultaneously induce motor deficits and striatal pathological changes similar to HD. In QA and 3-NP models, a clear demarcation of the site of striatal damage is visible, with a lesion core of extensive destruction surrounded by the transition zone with lesser damage (Huang et al., 1995; Figueredo-Cardenas et al., 1997). A similar region of lesser neuronal loss called the penumbra also surrounds the site of severe damage in ischemic cerebral damage.
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