Development of GABAergic neurons from the ventricular zone in the superior colliculus of the mouse

Tsunekawa, Naoko; Yanagawa, Yuchio; Obata, Kunihiko

doi:10.1016/j.neures.2004.11.011

Cited by 32 publications

(36 citation statements)

References 28 publications

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“…As glutamatergic and GABAergic transmissions have antagonistic effects, increases in GABAergic activity in an ischemic setting can compensate for the excess glutamatergic signaling, leading to decreased cell death; conversely, decreased GABAergic signaling in this setting promotes cell death (28,29). The findings in this study were also consistent with our previous observations of increased neuronal death and decreased Bcl-2 levels in the SNr following an ischemic event (20). In addition, our data show that post-ischemia ATV treatment increases GAD 65/67 immunoreactivity, which may suggest a potential mechanism for the observed neuroprotective effects by enhancing GABAergic transmission, which is consistent with other studies demonstrating that inducing certain inhibitory conditions can be used to control cell death following ischemia (28,(30)(31)(32)(33).…”

Section: Discussionsupporting

confidence: 92%

“…It is important to stress that changes in dopamine production and release during ischemia are potentially harmful to cells. However, ATV treatment was able to restore basal dopamine levels, suggesting a specific function in dopamine synthesis, which is supported by the neurological responses and behavioral recovery (20,36). On the other hand, we also recorded increased TH immunostaining in the GpM of sham animals treated with ATV, but these changes were not accompanied by neurological or behavioral defects.…”

Section: Discussionsupporting

confidence: 56%

“…GAD65 plays an important role in the local control of GABA synthesis at synapses, whereas GAD67 is responsible for maintaining GABA at baseline levels for use as both a neurotransmitter and a metabolite (20). GAD 65/67 immunoreactivity was significantly decreased within the GpL by 78 hours post-injury (P≤0.05) (figure 3a-C,b), a phenomenon that could be rescued with ATV treatment (P≤0.05) (figure 3a-D,b) to levels similar to those observed in the controls ( figure 3a-A-B,b).…”

Section: Atv Rescues the Loss Of Gad 65/67 Immunoreactivity In The Gpmentioning

confidence: 99%

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La atorvastatina protege las neuronas GABAérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas

et al. 2014

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Author contributions:Angélica María Sabogal: conducted the experiments, collected and discussed results, and prepared the manuscript. César Augusto Arango: consulted on cerebral ischemia procedures and nigrostriatal physiology; discussed results and reviewed the manuscript. Gloria Patricia Cardona: managed and supervised experiments; reviewed scientific merit; performed input protein analysis; reviewed, revised and approved the manuscript; submitted the manuscript. Ángel Enrique Céspedes: approved the project; managed and supervised the study; analyzed and interpreted the results, discussions and conclusions; reviewed and approved the manuscript. Introduction: Cerebral ischemia is the third leading cause of death and the primary cause of permanent disability worldwide. Atorvastatin is a promising drug with neuroprotective effects that may be useful for the treatment of stroke. However, the effects of atorvastatin on specific neuronal populations within the nigrostriatal system following cerebral ischemia are unknown. Objective: To evaluate the effects of atorvastatin on dopaminergic and GABAergic neuronal populations in exofocal brain regions in a model of transient occlusion of the middle cerebral artery. Materials and methods: Twenty-eight male eight-week-old Wistar rats were used in this study. Both sham and ischemic rats were treated with atorvastatin (10 mg/kg) or carboxymethylcellulose (placebo) by gavage at 6, 24, 48 and 72 hours post-reperfusion. We analyzed the immunoreactivity of glutamic acid decarboxylase and tyrosine hydroxylase in the globus pallidus, caudate putamen and substantia nigra. Results: We observed neurological damage and cell loss in the caudate putamen following ischemia. We also found an increase in tyrosine hydroxylase immunoreactivity in the medial globus pallidus and substantia nigra reticulata, as well as a decrease in glutamic acid decarboxylase immunoreactivity in the lateral globus pallidus in ischemic animals treated with a placebo. However, atorvastatin treatment was able to reverse these effects, significantly decreasing tyrosine hydroxylase levels in the medial globus pallidus and substantia nigra reticulata and significantly increasing glutamic acid decarboxylase levels in the lateral globus pallidus. Conclusion: Our data suggest that post-ischemia treatment with atorvastatin can have neuroprotective effects in exofocal regions far from the ischemic core by modulating the GABAergic and dopaminergic neuronal populations in the nigrostriatal system, which could be useful for preventing neurological disorders. Atorvastatin protectsKey words: GABAergic neurons, dopaminergic neurons, brain ischemia; models, animal; rats. doi: http://dx.doi.org/10.7705/biomedica.v34i2.1851La atorvastatina protege las neuronas gabérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas Introducción. La isquemia cerebral es la tercera causa de muerte y la primera de discapacidad permanente en el mundo. La atorvastatina es un fárm...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 56%

Section: Atv Rescues the Loss Of Gad 65/67 Immunoreactivity In The Gpmentioning

confidence: 99%

See 1 more Smart Citation

La atorvastatina protege las neuronas GABAérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas

et al. 2014

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“…GAD67 and GAD65 genes are expressed in spatially restricted domains of the embryonic CNS (Katarova et al, 2000;Brox et al, 2003;Tsunekawa et al, 2005;Tanaka et al, 2006). In the developing forebrain, these two GADs are coexpressed with the homeobox genes Dlx2 and Dlx5, which are sequentially induced and are upstream regulators of GAD (Liu et al, 1997;Eisenstat et al, 1999;Stuhmer et al, 2002a,b).…”

Section: Introductionmentioning

confidence: 99%

GAD isoforms exhibit distinct spatiotemporal expression patterns in the developing mouse lens: Correlation with Dlx2 and Dlx5

Kwakowsky

Schwirtlich

Zhang

et al. 2007

Developmental Dynamics

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Gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter of the adult nervous system and its biosynthetic enzyme glutamic acid decarboxylase (GAD) are abundantly expressed in the embryonic nervous system and are involved in the modulation of cell proliferation, migration, and differentiation. Here we describe for the first time the expression of GABA and embryonic and adult GAD isoforms in the developing mouse lens. We show that the GAD isoforms are sequentially induced with specific spatiotemporal profiles: GAD65 and embryonic GAD isoforms prevail in primary fibers, while GAD67 is the predominant GAD expressed in the postnatal secondary fibers. This pattern correlates well with the expression of Dlx2 and Dlx5, known as upstream regulators of GAD. GABA and GAD are most abundant at the tips of elongating fibers and are absent from organelle-free cells, suggesting their involvement is primarily in shaping of the cytoskeleton during fiber elongation stages. Developmental Dynamics 236: 3532-3544, 2007.

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“…These studies have shown that immature neurons expressing the gamma-aminobutyric acid (GABA) synthetic enzyme, glutamic acid decarboxylase, migrate considerable distances in the developing cerebral cortex, hippocampus, and superior colliculus (Tanaka et al, 2003;Tsunekawa et al, 2005;Britto et al, 2006;Manent et al, 2006). Neurons that synthesize gonadotropin-releasing hormone also migrate substantial distances from their place of birth in the nasal compartment to the basal forebrain (Tobet and Schwarting, 2006).…”

Section: Introductionmentioning

confidence: 99%

The migratory behavior of immature enteric neurons

Hao

Anderson

Kobayashi

et al. 2008

Developmental Neurobiology

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While they are migrating caudally along the developing gut, around 10%-20% of enteric neural crest-derived cells start to express pan-neuronal markers and tyrosine hydroxylase (TH). We used explants of gut from embryonic TH-green fluorescence protein (GFP) mice and time-lapse microscopy to examine whether these immature enteric neurons migrate and their mode of migration. In the gut of E10.5 and E11.5 TH-GFP mice, around 50% of immature enteric neurons (GFP + cells) migrated, with an average speed of around 15 lm/h. This is slower than the speed at which the population of enteric neural crest-derived cells advances along the developing gut, and hence neuronal differentiation seems to slow, but not necessarily halt, the caudal migration of enteric neural crest cells. Most migrating immature enteric neurons migrated caudally by extending a long-leading process followed by translocation of the cell body. This mode of migration is different from that of non-neuronal enteric neural crestderived cells and neural crest cells in other locations, but resembles that of migrating neurons in many regions of the developing central nervous system (CNS). In migrating immature enteric neurons, a swelling often preceded the movement of the nucleus in the direction of the leading process. However, the centrosomal marker, pericentrin, was not localized to either the leading process or swelling. This seems to be the first detailed report of neuronal migration in the developing mammalian peripheral nervous system. ' 2008 Wiley Periodicals, Inc. Develop Neurobiol 69: 22-35, 2009

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Development of GABAergic neurons from the ventricular zone in the superior colliculus of the mouse

Cited by 32 publications

References 28 publications

La atorvastatina protege las neuronas GABAérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas

La atorvastatina protege las neuronas GABAérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas

GAD isoforms exhibit distinct spatiotemporal expression patterns in the developing mouse lens: Correlation with Dlx2 and Dlx5

The migratory behavior of immature enteric neurons

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