ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Altered Ca2+ signaling and mitochondrial deficiencies in hippocampal neurons of trisomy 16 mice: a model of Down's syndrome.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 65 citations in OpenAlex.
- Charting the future: current and future directions in translational research for individuals with Down syndrome.Journal of neurodevelopmental disorders · 2025Review
- Knockdown of Myo-Inositol Transporter SMIT1 Normalizes Cholinergic and Glutamatergic Function in an Immortalized Cell Line Established from the Cerebral Cortex of a Trisomy 16 Fetal Mouse, an Animal Model of Human Trisomy 21 (Down Syndrome).Neurotoxicity research · 2017Article
- Altered voltage dependent calcium currents in a neuronal cell line derived from the cerebral cortex of a trisomy 16 fetal mouse, an animal model of Down syndrome.Neurotoxicity research · 2012Article
- Effects of long-term memantine on memory and neuropathology in Ts65Dn mice, a model for Down syndrome.Behavioural brain research · 2011Article
- Dysregulation of Ca2+ signaling in astrocytes from mice lacking amyloid precursor protein.American journal of physiology. Cell physiology · 2011Article
- H(2)O(2)-mediated modulation of cytosolic signaling and organelle function in rat hippocampus.Pflugers Archiv : European journal of physiology · 2009Article
- Live imaging of neuronal connections by magnetic resonance: Robust transport in the hippocampal-septal memory circuit in a mouse model of Down syndrome.NeuroImage · 2007Article
- [Corneal anomalies in murine trisomy 16].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2005Article
- Failure of brain-derived neurotrophic factor-dependent neuron survival in mouse trisomy 16.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Mitochondrial membrane potential and glutamate excitotoxicity in cultured cerebellar granule cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Apolipoprotein E isoforms increase intracellular Ca2+ differentially through a omega-agatoxin IVa-sensitive Ca2+-channel.Brain pathology (Zurich, Switzerland) · 1998Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been suggested that augmented nerve cell death in neurodegenerative diseases might result from an impairment of mitochondrial function. To test this hypothesis, we investigated age-dependent changes in neuronal survival and glutamate effects on Ca2+ homeostasis and mitochondrial energy metabolism in cultured hippocampal neurons from diploid and trisomy 16 (Ts16) mice, a model of Down's syndrome. Microfluorometric techniques were used to measure survival rate, [Ca2+]i level, mitochondrial membrane potential, and NAD(P)H autofluorescence. We found that Ts16 neurons die more than twice as fast as diploid neurons under otherwise identical culture conditions. Basal [Ca2+]i levels were elevated in Ts16 neurons. Moreover, in comparison to diploid neurons, Ts16 neurons showed a prolonged recovery of [Ca2+]i and mitochondrial membrane potential after brief glutamate application. Glutamate evoked an initial NAD(P)H decrease that was found to be extended in Ts16 neurons in comparison to diploid neurons. Furthermore, for all age groups tested, glutamate failed to cause a subsequent NAD(P)H overshoot in Ts16 cultures in contrast to diploid cultures. In the presence of cyclosporin A, an inhibitor of the mitochondrial membrane permeability transition, NAD(P)H increase was observed in both diploid and Ts16 neurons. The results support the hypothesis that Ca2+ impairs mitochondrial energy metabolism and may play a role in the pathogenesis of neurodegenerative changes in neurons from Ts16 mice.
Indexed as
Identifiers
9736644PMC6793219W1873261269What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.