The cellular neurobiology of neuronal development: The cerebellar granule cell

Burgoyne, Robert D.; Cambray-Deakin, M.A.

doi:10.1016/0165-0173(88)90006-9

Cited by 183 publications

(96 citation statements)

References 159 publications

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“…Bergmann glial fibers and Purkinje cell dendrites were not stained, whereas Purkinje cell bodies were intensely stained in developing mouse cerebellum (Suzuki, 2007;Kawahara, 2007), consistent with the previous findings (Cambray-Deakin and Burgoyne, 1987). During postnatal development the external granular layer becomes thinner, while the molecular layer becomes enlarged (Burgoyne and Cambray-Deakin, 1988). Along with this, intense staining was observed in the molecular layer from wild-type and Wld S mice.…”

Section: Evidence For Neuronal Distribution Of Acetyl Alpha-tubulin Asupporting

confidence: 88%

“…In the mouse brain, the expression of alpha-tubulin is high during early postnatal days, and subsequently decrease upon maturation (Burgoyne and Cambray-Deakin, 1988), whereas tubulin acetylation in vivo is known to occur concomitantly with maturation (Black and Keyser, 1987), indicative of its association with microtubule stability (Westermann and Weber, 2003). Immunohistochemistry using the monoclonal antibody specific for acetylated alpha-tubulin showed intense particulate staining in the molecular layer of postnatally developing and adult mouse cerebellum (Suzuki, 2007;Kawahara, 2007).…”

Section: Evidence For Neuronal Distribution Of Acetyl Alpha-tubulin Amentioning

confidence: 99%

“…Along with this, intense staining was observed in the molecular layer from wild-type and Wld S mice. The level of microtubule acetylation in Wld S cerebellum was increased at P14-21 (Suzuki, 2007;Kawahara, 2007), which corresponds to the stage when granule cells migrate into the internal granule layer (IGL) along extending parallel fiber axons, and form short dendrites (Burgoyne and Cambray-Deakin, 1988). These findings suggest that microtubule acetylation occurs in a manner that depends on developmental stages.…”

Section: Evidence For Neuronal Distribution Of Acetyl Alpha-tubulin Amentioning

confidence: 99%

See 2 more Smart Citations

SIRT2 (Sirtuin2) - An Emerging Regulator of Neuronal Degeneration

Koike¹,

Suzuki²,

Kawahata³

2012

Neurodegeneration

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Section: Evidence For Neuronal Distribution Of Acetyl Alpha-tubulin Asupporting

confidence: 88%

Section: Evidence For Neuronal Distribution Of Acetyl Alpha-tubulin Amentioning

confidence: 99%

Section: Evidence For Neuronal Distribution Of Acetyl Alpha-tubulin Amentioning

confidence: 99%

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SIRT2 (Sirtuin2) - An Emerging Regulator of Neuronal Degeneration

Koike¹,

Suzuki²,

Kawahata³

2012

Neurodegeneration

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“…Cerebellar granule neurons are generated in the external granule layer and migrate to the internal granule (Ryder & Cepko, 1994). During their postnatal migration, CGNs require excitatory inputs from the glutamatergic mossy fibers for proper differentiation and development; otherwise, they die by apoptosis (Burgoyne & Cambray-Deakin, 1988). This condition can be mimicked in vitro in primary cultures of CGNs.…”

Section: Introductionmentioning

confidence: 99%

Contribution of serine racemase/d‐serine pathway to neuronal apoptosis

et al. 2012

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SummaryRecent data indicate that age-related N-methyl-D-aspartate receptor (NMDAR) transmission impairment is correlated with the reduction in serine racemase (SR) expression and D-serine content. As apoptosis is associated with several diseases and conditions that generally occur with age, we investigated the modulation of SR ⁄ D-serine pathway during neuronal apoptosis and its impact on survival. We found that in cerebellar granule neurons (CGNs), undergoing apoptosis SR/D-serine pathway is crucially regulated. In the early phase of apoptosis, the expression of SR is reduced, both at the protein and RNA level through pathways, upstream of caspase activation, involving ubiquitin proteasome system (UPS) and c-Jun N-terminal kinases (JNKs). Forced expression of SR, together with treatment with NMDA and D-serine, blocks neuronal death, whereas pharmacological inhibition and Sh-RNA-mediated suppression of endogenous SR exacerbate neuronal death. In the late phase of apoptosis, the increased expression of SR contribute to the last, NMDAR-mediated, wave of cell death. These findings are relevant to our understanding of neuronal apoptosis and NMDAR activity regulation, raising further questions as to the role of SR/D-serine in those neuro-pathophysiological processes, such as aging and neurodegenerative diseases characterized by a convergence of apoptotic mechanisms and NMDAR dysfunction.

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“…The second aim was to identify any particular group of mGluRs that are responsible for the neuronal effects of ACPD, glutamate, or BMAA. A rat cerebellar granule cell model has been used, as these cultures have a largely homogenous cellular composition, and express NMDA, non-NMDA, and mGluRs (Burgoyne and Cambray-Deakin, 1988;Chuang et al, 1992;Aronica et al, 1993a). An abstract of this study has already appeared (Staton and Bristow, 1996).…”

mentioning

confidence: 99%

Role of Group III Metabotropic Glutamate Receptors in Excitotoxin‐Induced Cerebellar Granule Cell Death

Staton

Bristow

1998

Journal of Neurochemistry

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Abstract:The neuronal effects of the metabotropic glutamate receptor agonist (1 S,3R)-aminocyclopentane-1 ,3-dicarboxylic acid have been studied in cultured rat cerebellar granule cells, and compared with those of the endogenous excitotoxin glutamate, and the dietary excitotoxin /3-N-methylamino-L-alanine. Glutamate,~3-N-methylamino-L-alanine, and (1 S ,3R) -aminocyclopentane-1 ,3-dicarboxylic acid all caused concentration-dependent cerebellar granule cell death over a 24-h exposure period. The metabotropic antagonist (RS) -a-methyl-4-carboxyphenylglycine reduced glutamate-, /3-N-methylamino-L-alanine-, and (1 S ,3R)-aminocyclopentane-1 ,3-dicarboxylic acid-induced death by 50, 37, and 90%, respectively. (1 S ,3R) -Aminocyclopentane-1 ,3-dicarboxylic acid-induced death was unaffected by the group I antagonist (RS)-1 -aminoindan-1 ,5-dicarboxylic acid, increased by the group II antagonist ethylglutamic acid, and markedly decreased by the group Ill antagonist (RS) -amethylserine-O-phosphate. Neither (1 S ,3R) -aminocyclopentane-1 ,3-dicarboxylic acid nor the group I agonist (RS)-3,5-dihydroxyphenylglycine caused an increase in intracellular free calcium levels. The group Ill agonist L-(+)-2-amino-4-phosphonobutyric acid also induced concentration-dependent cerebellar granule cell death, and so it was suggested that the group Ill metabotropic glutamate receptors were responsible for (1 S,3R)-aminocyclopentane-1 ,3-dicarboxylic acid-induced death. Blocking these receptors with (RS) -a-methylserine-O-phosphate also prevented a proportion of glutamate-and /3-N-methylamino-L-alanineinduced death. Key Words: (1 S,3R)-Aminocyclopentane-1 ,3-dicarboxylic acid-/3-N-Methylamino-L-alanine-Rat cerebellar granule cells-Glutamate. J. Neurochem. 71, 1280Neurochem. 71, -1288Neurochem. 71, (1998.Glutamate is the principal excitatory neurotransmitter in the mammalian brain, where it activates both ionotropic glutamate receptors and metabotropic glutamate receptors (mGluRs). Tonotropic glutamate receptors are ligand-gated ion channels that comprise NMDA and a-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) kainate subtypes (Monaghan et al., 1989). Overactivation of ionotropic receptors results in neuronal death via excitotoxicity , and some of the intracellular events that lead to death can be influenced by mGluRs (Pin and Duvoisin, 1995).mGluRs are coupled to U proteins, and this family of glutamate receptors comprises eight subtypes, to date, that are divided into three groups, based on their second messenger coupling, sequence similarity, and ligand selectivities (Pin and Duvoisin, 1995). Group I includes mGluRi and mGluR5, which are coupled to polyphosphoinositide (PPI) hydrolysis. mGluRs from groups II (mGluR2 and mGluR3) and III (mGluR4, mGluR6, mGluR7, and mGluR8) are negatively coupled to adenylate cyclase activity. In addition, an mGluR receptor coupled to phospholipase D has been identified in the hippocampus (Pellegrini-Giampetro et al., 1996). This coupling to disparate transduction pathways may underlie th...

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The cellular neurobiology of neuronal development: The cerebellar granule cell

Cited by 183 publications

References 159 publications

SIRT2 (Sirtuin2) - An Emerging Regulator of Neuronal Degeneration

SIRT2 (Sirtuin2) - An Emerging Regulator of Neuronal Degeneration

Contribution of serine racemase/d‐serine pathway to neuronal apoptosis

Role of Group III Metabotropic Glutamate Receptors in Excitotoxin‐Induced Cerebellar Granule Cell Death

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