Cortical neurons containing calretinin are selectively resistant to calcium overload and excitotoxicity in vitro

Lukas, W; Jones, Kenneth A.

doi:10.1016/0306-4522(94)90233-x

Cited by 144 publications

(65 citation statements)

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“…Further, cells with still detectable CG-1 signal following exposure to BAPTA were more likely to express one of these CaBPs, suggesting cell survival may be linked to expression of these proteins, in general agreement with other studies (Hof et al, 1991;Mattson et al, 1991;Freund et al, 1992;Iacopino et al, 1992;Burke and Baimbridge, 1993;Lukas and Jones, 1994;Prendergast et al, 2001;Mulholland et al, 2003) (though see (Mockel and Fischer, 1994;Airaksinen et al, 1997;Klapstein et al, 1998;Bouilleret et al, 2000;Isaacs et al, 2000)). The data we describe here are consistent with our hypothesis that loss of calcium triggers apoptotic injury in the developing brain and is inversely related to expression of CB, CR, and PV (Lema Tome et al, 2006b).…”

Section: -Discussionsupporting

confidence: 91%

Loss of calcium and increased apoptosis within the same neuron

et al. 2007

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Loss of neuronal calcium is associated with later apoptotic injury but observing reduced calcium and increased apoptosis in the same cell would provide more definitive proof of this apparent correlation. Thus, following exposure to vehicle or the calcium chelator BAPTA (1-20 μM), primary cortical neurons were labeled with Calcium Green-1 which was then cross-linked with EDAC, prior to immunostaining for various proteins. We found that BAPTA-induced changes in calcium were highly correlated with changes in expression of activated caspase-3 as well as the calcium binding proteins calbindin, calretinin, and parvalbumin. Additionally, in brain slices from P7 neonatal rats, BAPTA induced significant loss of calcium in a brain region we have previously shown to express only moderate levels of calcium binding proteins as well as display robust apoptosis following calcium entry blockade. In contrast, BAPTA had little influence on calcium levels in a brain region we have previously shown to express robust calcium binding proteins as well as display far less apoptosis following calcium entry blockade. These data suggest that the ability of developing neurons to buffer changes in calcium may be critical to their long-term survival.

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Section: -Discussionsupporting

confidence: 91%

Loss of calcium and increased apoptosis within the same neuron

et al. 2007

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“…However, some CR-negative neurons were morphologically changed in a way which may suggest neuronal death. Thus, the cell density loss may probably be related to the appearance of excitotoxicity phenomenon, which was suggested by results of previous studies [27][28][29]. It has been established that the excitotoxicity caused by different factors leads to serious neuronal disorders and even death of nervous cells.…”

Section: Discussionmentioning

confidence: 84%

Effects of monosodium glutamate treatment on calretinin-immunoreactive neurons in hippocampus of postnatal rats

Rycerz

Krawczyk

Jaworska-Adamu

et al. 2015

Folia Histochem Cytobiol.

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Introduction. Calretinin (CR) is a protein, which is present in GABAergic neurons and belongs to the calciumbinding proteins family. It may reduce the excitotoxicity phenomenon through its Ca 2+ buffering properties. This phenomenon is due to the increase of calcium ions levels caused by the excess of glutamate -the main excitatory neurotransmitter. The aim of the study was to investigate alterations of calretinin-immunoreactivity in neurons of hippocampal CA1 region and dentate gyrus with hilus in 10 day-old rats treated with monosodium glutamate (MSG). Material and methods. Ten 7 day-old Wistar rats were used. The MSG-group consisted of 5 MSG-treated rats at a dose of 4 g/kg b.w. for 3 consecutive days and the second group consisted of 5 control animals. After euthanasia the brains containing hippocampus were dissected and embedded in paraffin blocks. The immunohistochemical peroxidase-antiperoxydase reaction was performed on tissue sections. The morphometric analyses of CR-immunopositive neurons: density, percentage ratio to the density of all cells and an assessment of digital immunostaining intensity were performed. Results. The distribution of the CR-immunoreactive neurons in the hippocampus was irregular. In the MSGgroup there were single cells, which were more intensely stained than in control animals. Some of cells contained processes of different length. The density of CR-immunopositive cells and their percentage ratio to the density of all cells did not change significantly after MSG treatment. However, there was a statistically significant increase in the staining intensity of CR-immunopositive cells. Conclusions. The obtained results indicate that CR-positive cells in P7-P10 rats are only slightly affected by MSG in CA1 region and dentate gyrus with hilus of the hippocampus.

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“…CaBP act as intracellular facilitators of calcium diffusion or as intracellular calcium buffering systems. Since an increase in intracellular calcium levels triggers molecular events related to neuronal degeneration, it has been suggested that CaBP protect against calcium overload, rendering neurons more resistant to various toxic insults and neurodegenerative diseases (Lukas and Jones, 1994;FigueredoCardenas et al, 1998;Tsuboi et al, 2000). However, the efficacy of reduced CaBPs as markers of neuronal death in the epileptic hippocampus has been challenged.…”

Section: Discussionmentioning

confidence: 99%