Transcriptional regulation through glutamate receptors: Involvement of tyrosine kinases

López-Bayghen, Esther; Aguirre, Adán; Ortega, Arturo

doi:10.1002/jnr.10807

Cited by 10 publications

(9 citation statements)

References 39 publications

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“…Glutamate uptake into neurons and glial cells is important for the termination of glutamatergic transmission. They are essential for the maintenance of low extracellular levels of glutamate [36]. We observed a reduced expression of GLAST in 6-OHDA infused rats.…”

Section: Discussionmentioning

confidence: 68%

Enhanced glutamate, IP3 and cAMP activity in the cerebral cortex of Unilateral 6-hydroxydopamine induced Parkinson's rats: Effect of 5-HT, GABA and bone marrow cell supplementation

et al. 2011

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Parkinson's disease is characterized by progressive cell death in the substantia nigra pars compacta, which leads to dopamine depletion in the striatum and indirectly to cortical dysfunction. Increased glutamatergic transmission in the basal ganglia is implicated in the pathophysiology of Parkinson's disease and glutamate receptor mediated excitotoxicity has been suggested to be one of the possible causes of the neuronal degeneration. In the present study, the effects of serotonin, gamma-aminobutyric acid and bone marrow cells infused intranigrally to substantia nigra individually and in combination on unilateral 6-hydroxydopamine induced Parkinson's rat model was analyzed. Scatchard analysis of total glutamate and NMDA receptor binding parameters showed a significant increase in Bmax (P < 0.001) in the cerebral cortex of 6-hydroxydopamine infused rat compared to control. Real Time PCR amplification of NMDA2B, mGluR5, bax, and ubiquitin carboxy-terminal hydrolase were up regulated in cerebral cortex of 6-hydroxydopamine infused rats compared to control. Gene expression studies of GLAST, ά-Synuclien and Cyclic AMP response element-binding protein showed a significant (P < 0.001) down regulation in 6-OHDA infused rats compared to control. Behavioural studies were carried out to confirm the biochemical and molecular studies. Serotonin and GABA along with bone marrow cells in combination showed reversal of glutamate receptors and behaviour abnormality shown in the Parkinson's rat model. The therapeutic significance in Parkinson's disease is of prominence.

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Section: Discussionmentioning

confidence: 68%

Enhanced glutamate, IP3 and cAMP activity in the cerebral cortex of Unilateral 6-hydroxydopamine induced Parkinson's rats: Effect of 5-HT, GABA and bone marrow cell supplementation

et al. 2011

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“…It is evident that other signaling cascades are involved in the glutamate effect as neither of the transfected isoforms are as effective as the exposure to the excitatory amino acid. In this regard, we have previously reported the involvement of tyrosine kinases cascades in the transcriptional regulation of the chkbp promoter through AMPA receptors (López‐Bayghen et al . 2003b).…”

Section: Discussionmentioning

confidence: 96%

Glutamate‐dependent transcriptional regulation of GLAST: role of PKC

López-Bayghen

Ortega

2004

Journal of Neurochemistry

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The Na + -dependent glutamate/aspartate transporter GLAST plays a major role in the removal of glutamate from the synaptic cleft. Short-term, as well as long-term changes in transporter activity are triggered by glutamate. An important locus of regulation is the density of transporter molecules present at the plasma membrane. A substrate-dependent change in the translocation rate of the transporter molecules accounts for the short-term effect, whereas the long-term modulation apparently involves transcriptional regulation. Using cultured chick cerebellar Bergmann glial cells, we report here that glutamate receptors activation mediate a substantial reduction in the transcriptional activity of the chglast promoter through the Ca 2+ /diacylglicerol-dependent protein kinase (PKC) signaling cascade. Overexpression of constitutive active PKC isoforms of mimic the glutamate effect. Accordingly, increased levels of c-Jun or c-Fos, but not Jun-B, Jun-D or Fos-B, lower the chglast promoter activity. Serial deletions and electrophorectic mobility shift assays were used to define a specific region within the 5¢ proximal region of the chglast promoter, associated with transcriptional repression. A putative glutamate response element could be defined in the proximal promoter stretch more likely between nts -40 and ) 78. These results demonstrate that GLAST is under glutamate-dependent transcriptional control through PKC, and support the notion of a pivotal role of this neurotransmitter in the regulation of its own removal from the synaptic cleft, thereby modulating, mainly in the long term, glutamatergic transmission.

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“…1994) suggesting that phosphorylation is a fundamental step in DNA binding. In BGC, AMPA receptors activate a broad range of Ser/Thr kinases such as PKB, PKC, MAPK, p90 Rsk (Lopez‐Bayghen et al. 2003b), that could possibly phosphorylate YY1 in response to Glu.…”

Section: Discussionmentioning

confidence: 99%

Glutamate‐dependent transcriptional regulation of GLAST/EAAT1: a role for YY1

Rosas¹,

Vargas²,

López-Bayghen³

et al. 2007

Journal of Neurochemistry

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Glutamate is the major excitatory transmitter in the vertebrate brain and its extracellular levels are tightly regulated to prevent excitotoxic effects. The Na + -dependent glutamate/aspartate transporter GLAST/EAAT1 is regulated in the short and in the long term by glutamate. A receptors-independent change in its membrane translocation rate, accounts for an acute modulation in GLAST/EAAT1 transport. In contrast, activation of the a-amino-3-hydroxy-5-methylisoxazole-4-propionate subtype of glutamate receptors represses the transcription of the chick glast gene. A glutamate responsive element has been mapped to the promoter region of this gene containing a bonafide binding site for the transcription factor Ying-Yang 1. Using cultured chick cerebellar Bergmann glia cells, glutamate elicited a time and dose-dependent increase in Ying-Yang 1 DNA binding consistent with the negative response generated in a reporter gene construct controlled for Ying-Yang 1. Over-expression of this transcription factor leads to a substantial reduction in GLAST/EAAT1 transporter uptake and an important decrease in mRNA levels, all associated with the transcriptional repression of the chick glast promoter activity. These results provide evidence for an involvement of Ying-Yang 1 in the transcriptional response to glutamate in glial cells and favor the notion of a relevant role of this factor in GLAST/EAAT1 transcriptional control.

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Transcriptional regulation through glutamate receptors: Involvement of tyrosine kinases

Cited by 10 publications

References 39 publications

Enhanced glutamate, IP3 and cAMP activity in the cerebral cortex of Unilateral 6-hydroxydopamine induced Parkinson's rats: Effect of 5-HT, GABA and bone marrow cell supplementation

Enhanced glutamate, IP3 and cAMP activity in the cerebral cortex of Unilateral 6-hydroxydopamine induced Parkinson's rats: Effect of 5-HT, GABA and bone marrow cell supplementation

Glutamate‐dependent transcriptional regulation of GLAST: role of PKC

Glutamate‐dependent transcriptional regulation of GLAST/EAAT1: a role for YY1

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