Lactate induced excitotoxicity in hippocampal slice cultures

Xiang, Zhou; Yuan, Maoli; Hassen, Getaw Worku; Gampel, Mordechai; Bergold, Peter J.

doi:10.1016/j.expneurol.2003.10.015

Cited by 39 publications

(20 citation statements)

References 40 publications

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“…A parallel is the finding that aged animals are more impaired and exhibit larger infarcts following ischemia than younger animals (DiNapoli et al, 2008). In addition, HOTC prepared from older rats show more vulnerability to OGD than those prepared from younger animals Siqueira et al, 2004;Xiang et al, 2004). Finally, it is likely that the presence of intact synaptic pathways contributes to the differential selectivity and severity of responses produced by OGD in HOTC compared to dissociated cultures.…”

Section: Mixed Cultures Respond To Ogdmentioning

confidence: 80%

Primary culture of cellular subtypes from postnatal mouse for in vitro studies of oxygen glucose deprivation

Jones

Novak

Elliott

2011

Journal of Neuroscience Methods

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Section: Mixed Cultures Respond To Ogdmentioning

confidence: 80%

Primary culture of cellular subtypes from postnatal mouse for in vitro studies of oxygen glucose deprivation

Jones

Novak

Elliott

2011

Journal of Neuroscience Methods

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“…Moreover, experimental OGD elicited extensive increases in the release of GABA and aspartate, and lead to a time-dependent activation of caspase-3. In OHCs prepared exceptionally from 20-to 30-day-old rats and cultured for 1 week, lactic acidosis was identified as a contributor to excitotoxic CA1 and CA3 neuronal loss, the effect being at least partly mediated through the activation of both NMDA and AMPA receptors (10).…”

Section: Hippocampal Slice Cultures As a Model Of Ischemia-induced Nementioning

confidence: 99%

“…Cultures are usually prepared from 6-7-day-old (P6-7) rats, although both younger and older rats (from P4 up to P30) have been applied, and slices can be maintained in culture conditions from one week up to 1-2 months (6)(7)(8)(9)(10). When prepared from P6-7 rats, dentate granule cells are still proliferating, while the other main neuronal cell types, e.g.…”

mentioning

confidence: 99%

Organotypic Hippocampal Slice Cultures: A Model System to Study Basic Cellular and Molecular Mechanisms of Neuronal Cell Death, Neuroprotection, and Synaptic Plasticity

Holopainen

2005

Neurochem Res

100

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The hippocampus has become one of the most extensively studied areas of the mammalian brain, and its proper function is of utmost importance, particularly for learning and memory. The hippocampus is the most susceptible brain region for damage, and its impaired function has been documented in many human brain diseases, e.g. hypoxia, ischemia, and epilepsy regardless of the age of the affected patients. In addition to experimental in vivo models of these disorders, the investigation of basic anatomical, physiological, and molecular aspects requires an adequate experimental in vitro model, which should meet the requirements for well-preserved representation of various cell types, and functional information processing properties in the hippocampus. In this review, the characteristics of organotypic hippocampal slice cultures (OHCs) together with the main differences between the in vivo and in vitro preparations are first briefly outlined. Thereafter, the use of OHCs in studies focusing on neuron cell death and synaptic plasticity is discussed.

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“…Intracellular pH can go as low as 6.1-6.2, if hyperglycemia precedes ischemia [74], suggesting that nutritional status may be critical to the degree of closure of gap junction channels by ischemia. In hippocampal slices, neuronal loss at pH 6.4 is greater in the presence of lactate, which was attributed to a reduction in glutamate uptake [153]. Reduced coupling of astrocytes, here due to acidification, could contribute to reduced glutamate uptake.…”

Section: Pattern Of Connexin Expression In the Adult Mammalian Brainmentioning

confidence: 99%

Role of connexin-based gap junction channels and hemichannels in ischemia-induced cell death in nervous tissue

Contreras

Sánchez

Véliz

et al. 2004

Brain Research Reviews

220

185

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Gap junction channels and hemichannels formed of connexin subunits are found in most cell types in vertebrates. Gap junctions connect cells via channels not open to the extracellular space and permit the passage of ions and molecules of ~1 kDa. Single connexin hemichannels, which are connexin hexamers, are present in the surface membrane before docking with a hemichannel in an apposed membrane. Because of their high conductance and permeability in cell-cell channels, it had been thought that connexin hemichannels remained closed until docking to form a cell-cell channel. Now it is clear that at least some hemichannels can open to allow passage of molecules between the cytoplasm and extracellular space. Here we review evidence that gap junction channels may allow intercellular diffusion of necrotic or apoptotic signals, but may also allow diffusion of ions and substances from healthy to injured cells, thereby contributing to cell survival. Moreover, opening of gap junction hemichannels may exacerbate cell injury or mediate paracrine or autocrine signaling. In addition to the cell specific features of an ischemic insult, propagation of cell damage and death within affected tissues may be affected by expression and regulation of gap junction channels and hemichannels formed by connexins.

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Lactate induced excitotoxicity in hippocampal slice cultures

Cited by 39 publications

References 40 publications

Primary culture of cellular subtypes from postnatal mouse for in vitro studies of oxygen glucose deprivation

Primary culture of cellular subtypes from postnatal mouse for in vitro studies of oxygen glucose deprivation

Organotypic Hippocampal Slice Cultures: A Model System to Study Basic Cellular and Molecular Mechanisms of Neuronal Cell Death, Neuroprotection, and Synaptic Plasticity

Role of connexin-based gap junction channels and hemichannels in ischemia-induced cell death in nervous tissue

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