Temporospatial coupling of networked synaptic activation of AMPA-type glutamate receptor channels and calcium transients in cultured motoneurons

Jahn, Klaus; Großkreutz, Julian; Haastert, Kirsten; Ziegler, Elke; Schlesinger, Friedrich; Grothe, Claudia; Dengler, Reinhard; Bufler, J.

doi:10.1016/j.neuroscience.2006.07.034

Cited by 32 publications

(18 citation statements)

References 27 publications

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“…Motor neurons in general display a significantly higher occurrence of spontaneous Ca 2? transients than non-motor neurons suggestive of increased AMPAergic synaptic input (Jahn et al 2006). This correlates to the fact that motor neurons appear to have AMPA receptors with higher relative Ca 2?…”

Section: Discussionmentioning

confidence: 83%

Analysis of Neuroprotective Effects of Valproic Acid on Primary Motor Neurons in Monoculture or Co-cultures with Astrocytes or Schwann Cells

et al. 2009

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Chronic dysregulation of the intracellular Ca(2+) homeostasis (excitotoxicity) is thought to contribute to the development of motor neuron diseases. Valproic acid (VPA) is widely used as an antiepileptic drug and acts mainly by inhibition of sodium channels and by enhancing the level of the inhibitory neurotransmitter gamma-aminobutyric acid. Neuroprotective capacities of VPA are supposed to arise also from the inhibition of histone deacetylases. We investigated the viability of highly purified rat embryonic motor neurons cultured on glial feeder layers, composed of either astrocytes or Schwann cells, or in the absence of glia, monoculture in presence of VPA and/or kainate (KA) using immunocytochemistry and calcium imaging. A significant effect of the culture and co-culture conditions on the viability of motor neurons in our in vitro model of excitotoxicity was detected. The neuroprotective effect of VPA on primary embryonic motor neuron cultures was not proven. A functional interaction between VPA and KA occurred during the first 10 days in culture.

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Section: Discussionmentioning

confidence: 83%

Analysis of Neuroprotective Effects of Valproic Acid on Primary Motor Neurons in Monoculture or Co-cultures with Astrocytes or Schwann Cells

et al. 2009

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“…RyR oxidation in neurons was also shown to regulate brain function (Kakizawa et al, 2012). In motor neurons, RyRs can modulate glutamatergic stimulation (Jahn et al, 2006), and it is possible that RyRs are dysregulated in ALS causing abnormal cytosolic and mitochondrial calcium influx (Grosskreutz et al, 2010). However, while the RyR inhibitor dantrolene showed protective effects on SOD1 mutant motor neurons in culture, it did not extend survival of G93A mice (Staats et al, 2012).…”

Section: Oxidative Stress and Mitochondria-er Involvement In Alsmentioning

confidence: 99%

Mitochondria and endoplasmic reticulum crosstalk in amyotrophic lateral sclerosis

Manfredi

Kawamata

2016

Neurobiology of Disease

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Physical and functional interactions between mitochondria and the endoplasmic reticulum (ER) are crucial for cell life. These two organelles are intimately connected and collaborate to essential processes, such as calcium homeostasis and phospholipid biosynthesis. The connections between mitochondria and endoplasmic reticulum occur through structures named mitochondria associated membranes (MAMs), which contain lipid rafts and a large number of proteins, many of which serve multiple functions at different cellular sites. Growing evidence strongly suggest that alterations of ER-mitochondria interactions are involved in neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), a devastating and rapidly fatal motor neuron disease. Mutations in proteins that participate in ER-mitochondria interactions and MAM functions are increasingly being associated with genetic forms of ALS and other neurodegenerative diseases. This evidence strongly suggests that, rather than considering the two organelles separately, a better understanding of the disease process can derive from studying the alterations in the their crosstalk. In this review we discuss normal and pathological ER-mitochondria interactions and the evidence that link them to ALS.

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“…Blocking this ER-mediated Ca 2+ -entry affects neuronal activity and under conditions of chronic hyperexcitability, STIM proteins are upregulated (Steinbeck et al, 2011). Contributions to electrophysiological excitation-mediated Ca 2+ transients from ER Ca 2+ release have been documented in motoneurons (Scamps et al, 2004, Jahn et al, 2006. Supporting the possibility that neuronal excitability and neuronal protein processing and ER function could share common pathways, blocking L-type Ca 2+ channels has been reported to increase autophagy (Williams et al, 2008).…”

Section: Protein Degradation and Endoplasmic Reticulum Stressmentioning

confidence: 98%

Molecular and Electrical Abnormalities in the Mouse Model of Amyotrophic Lateral Sclerosis

Quinlan¹,

Elbasiouny²,

Heckman³

2012

Amyotrophic Lateral Sclerosis

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Temporospatial coupling of networked synaptic activation of AMPA-type glutamate receptor channels and calcium transients in cultured motoneurons

Cited by 32 publications

References 27 publications

Analysis of Neuroprotective Effects of Valproic Acid on Primary Motor Neurons in Monoculture or Co-cultures with Astrocytes or Schwann Cells

Analysis of Neuroprotective Effects of Valproic Acid on Primary Motor Neurons in Monoculture or Co-cultures with Astrocytes or Schwann Cells

Mitochondria and endoplasmic reticulum crosstalk in amyotrophic lateral sclerosis

Molecular and Electrical Abnormalities in the Mouse Model of Amyotrophic Lateral Sclerosis

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