Chronic quinolinic acid lesions in rats closely resemble Huntington's disease

Beal, M. Flint; Ferrante, RJ; Swartz, KJ; Kowall, N. W.

doi:10.1523/jneurosci.11-06-01649.1991

Cited by 474 publications

(245 citation statements)

References 45 publications

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“…NOS-positive neurons are presumed to belong to a parvalbumin-negative subpopulation of type 2A neurons, as shown in Table 1. They have been shown both in vitro as well as in vivo to be susceptible to AMPA-induced excitotoxicity (Beal et al, 1991;Weiss et al, 1994), which supports our proposal.…”

Section: Expression Of Cabps and Vulnerability To Excitatory Amino Acsupporting

confidence: 90%

Combinations of AMPA Receptor Subunit Expression in Individual Cortical Neurons Correlate with Expression of Specific Calcium-Binding Proteins

1997

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The functional properties of AMPA-type glutamate receptors are determined by their subunit composition. We detected the expression of the AMPA receptor subunits (GluR1-GluR4) in neurons in the somatosensory cortex of adult rats by combining nonradioactive in situ hybridization using digoxigenin-labeled RNA probes of GluR1 and GluR2 with immunocytochemistry using specific antibodies against GluR1, GluR2/3, and GluR4. On the basis of differential expression of the GluR1 and GluR2 subunits, we classified the cortical neurons into four categories. To correlate the differential expression of AMPA receptor subunits in each neuron with that of two calcium-binding proteins, parvalbumin and calbindin-D28k, we used a triple-labeling method. The majority of cortical neurons (ϳ2/3) showed expression of GluR2 and undetectable expression of GluR1. GluR1-/GluR2-expressing neurons and GluR1-expressing/GluR2-undetectable neurons comprised ϳ1/10 each. Regarding the morphology, most GluR1-undetectable/GluR2-expressing neurons were pyramidal cells in layers II/III, V, and VI, whereas most GluR1-expressing/GluR2-undetectable neurons were nonpyramidal cells in layers II-VI. The GluR1-/GluR2-expressing neurons were either pyramidal or nonpyramidal. The majority of GluR1-/GluR2-expressing nonpyramidal cells was intensely stained with monoclonal antibody against calbindin-D28k, and one-half of the GluR1-undetectable/GluR2-expressing pyramidal neurons in layer II/III were lightly stained with this antibody. Most of GluR1-expressing/GluR2-undetectable neurons possessed parvalbumin immunoreactivity. These results indicate that neurons in the rat somatosensory cortex express differential combinations of GluR subunits, which correlate with the specific expression of the calcium-binding proteins.

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Section: Expression Of Cabps and Vulnerability To Excitatory Amino Acsupporting

confidence: 90%

Combinations of AMPA Receptor Subunit Expression in Individual Cortical Neurons Correlate with Expression of Specific Calcium-Binding Proteins

1997

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“…HPLC analysis of ATP content was performed essentially as described (37,38). HPLC analysis of catecholamine levels was performed as described (39,40). For sample preparation, adult male fly heads were dissected out and homogenized in 0.1 M perchloric acid (generally 50 l per four or five heads) by using a motorized hand-held tissue grinder.…”

Section: Methodsmentioning

confidence: 99%

Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin

Yang

Gehrke²,

Imai³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

731

724

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Mutations in Pink1, a gene encoding a Ser͞Thr kinase with a mitochondrial-targeting signal, are associated with Parkinson's disease (PD), the most common movement disorder characterized by selective loss of dopaminergic neurons. The mechanism by which loss of Pink1 leads to neurodegeneration is not understood. Here we show that inhibition of Drosophila Pink1 (dPink1) function results in energy depletion, shortened lifespan, and degeneration of select indirect flight muscles and dopaminergic neurons. The muscle pathology was preceded by mitochondrial enlargement and disintegration. These phenotypes could be rescued by the wild type but not the pathogenic C-terminal deleted form of human Pink1 (hPink1). The muscle and dopaminergic phenotypes associated with dPink1 inactivation show similarity to that seen in parkin mutant flies and could be suppressed by the overexpression of Parkin but not DJ-1. Consistent with the genetic rescue results, we find that, in dPink1 RNA interference (RNAi) animals, the level of Parkin protein is significantly reduced. Together, these results implicate Pink1 and Parkin in a common pathway that regulates mitochondrial physiology and cell survival in Drosophila.mitochondria ͉ Parkinson's disease ͉ Pten-induced kinase 1 ͉ indirect flight muscle P arkinson's disease (PD) is the most common movement disorder characterized pathologically by the deficiency of brain dopamine content and the selective degeneration of dopaminergic neurons in the substantia nigra. The most common forms of PD are sporadic with no known cause. Nevertheless, postmortem studies have identified common features associated with sporadic PD, such as mitochondrial complex I dysfunction, oxidative stress, and aggregation of abnormal proteins (1, 2).Although initial studies on the etiology of PD have focused on environmental factors, recent genetic studies have firmly established the contribution of inheritable factors in PD pathogenesis (2, 3). At least ten distinct loci have been associated with rare familial forms of PD (FPD). It is anticipated that understanding the molecular lesions associated with these FPD genes will shed light on the pathogenesis of the more common forms of the disease. Dominant mutations in ␣-Synuclein (␣-Syn) and LRRK2͞dardarin and recessive mutations in parkin, DJ-1, and Pink1 have been associated with FPD (4-10). Of these five genes, ␣-Syn, parkin, and DJ-1 have been most intensively studied. Studies using in vivo animal models and in vitro cell culture have linked mutations of these genes to impairments of mitochondrial structure and function and oxidative stress response, reinforcing the general involvement of mitochondrial dysfunction and oxidative stress in PD pathogenesis (11-21). Consistent with this notion, these proteins have been shown to be present in mitochondria or interact with mitochondrial proteins (8,(22)(23)(24), suggesting that they may directly regulate mitochondria function.A further link between mitochondria and PD was supported by the fact that Pink1 encodes a predicted Se...

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“…GABAergic interneuron precursor cells which are produced from medial ganglionic eminence (MGE) which is transient embryonic structure developed in the brain [89], transplantation of these precursor cells in hippocampus of mice 88 ,57 showed development into mature functioning cells which integrated into the hippocampus & improve learning & memory [90,91]. This shows that MGE have the characteristics for stem cell therapy including high ability for migration differentiation & circuit modulation [92].…”

Section: Neural Progenitor Cells (Gabaergic Interneuron Precursor Celmentioning

confidence: 99%

Stem Cells for Neuro-regeneration: State of the Art

Wagih¹,

Elhawary²,

Ellessy³

et al. 2015

BIO

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Neuroregeneration (NR) is a long-sought medical dream which has intrigued vast research in the past decades. A traditional physiologic dogma that central nervous system does not regenerate has been strongly challenged in the recent years since the advent of the stem cell era. Stem cell research in the regenerative field passes through three main stages. The first stage is the in-vitro experiments which studies the exact molecular and cellular mechanisms underlying stem cell-mediated NR. The second stage is the application of these data in experimental animal settings to provide "proof of concept" of stem cell therapy in animal models. The final step is the translation of these data in pilot clinical trials. In this review, we will try to gather the different data of stem cell-mediated NR from various experimental and clinical researches.

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Chronic quinolinic acid lesions in rats closely resemble Huntington's disease

Cited by 474 publications

References 45 publications

Combinations of AMPA Receptor Subunit Expression in Individual Cortical Neurons Correlate with Expression of Specific Calcium-Binding Proteins

Combinations of AMPA Receptor Subunit Expression in Individual Cortical Neurons Correlate with Expression of Specific Calcium-Binding Proteins

Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin

Stem Cells for Neuro-regeneration: State of the Art

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