Diltiazem-induced Neuroprotection in Glutamate Excitotoxicity and Ischemic Insult of Retinal Neurons View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-01

AUTHORS

Géraldine Vallazza-Deschamps, Céline Fuchs, David Cia, Luc-Henri Tessier, José A. A. Sahel, Henri Dreyfus, Serge Picaud

ABSTRACT

Purpose: Cell death is often related to an abnormal increase in Ca2+ flux. In the retina, Ca2+ channels are mainly from the L-type that do not inactivate with time. Under excitotoxic and ischemic conditions, their continuous activation may therefore contribute significantly to the lethal Ca2+ influx. To assess this hypothesis, the Ca2+ channel blocker, diltiazem, was applied in excitotoxic and ischemic conditions. Methods: To induce excitotoxicity, retinal cell cultures from newborn rats were incubated with glutamate. The toxicity of glutamate was quantified by neuronal immunostaining with an antibody directed against the neuron specific enolase. Glutamate receptor function in vitro was assessed in pig retinal cell cultures by patch clamp recording. Retinal ischemia was induced by raising the intraocular pressure in adult rats. Retinal cell loss was quantified on retinal sections by measuring nuclear cell densities. Results: In retinal cell culture, glutamate application induced a major cell loss. This cell loss was attributed to glutamate excitotoxicity because glutamate receptor blockers like MK-801 and CNQX increased significantly neuronal survival. MK-801 and CNQX, which block NMDA and AMPA/Kainate receptors, respectively, had additive effects. Expression of AMPA/Kainate glutamate receptors in mixed adult retinal cell cultures was attested by patch clamp recording. In newborn rat retinal culture, glutamate excitotoxicity was significantly reduced by addition of the L-type Ca2+ channel blocker, diltiazem. In in vivo experiments, the increase in ocular pressure induced a decrease in cell number in the inner nuclear and ganglion cell layers. When animals received diltiazem injections, the ischemic treatment induced a less severe reduction in retinal cells; this neuroprotection was statistically significant in the ganglion cell layer. Conclusion: These results are consistent with previous studies suggesting that Ca2+ channel activation contributes to retinal cell death following either glutamate excitotoxicity or retinal ischemia. Under both conditions, the L-type Ca2+ channel blocker, diltiazem, can limit cell death. These results extend the potential application of diltiazem in retinal neuroprotection to retinal pathologies involving glutamate excitotoxicity and ischemia. More... »

PAGES

25-35

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10633-005-7341-1

DOI

http://dx.doi.org/10.1007/s10633-005-7341-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005513909

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16249955


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100 neuron specific enolase
101 neuronal immunostaining
102 neuronal survival
103 neurons
104 neuroprotection
105 newborn rat retinal culture
106 newborn rats
107 nuclear
108 nuclear cell densities
109 number
110 ocular pressure
111 patch clamp recordings
112 pathology
113 pig retinal cell cultures
114 potential applications
115 pressure
116 previous studies
117 rat retinal cultures
118 rats
119 receptor blockers
120 receptor function
121 receptors
122 recordings
123 reduction
124 results
125 retina
126 retinal cell cultures
127 retinal cell death
128 retinal cell loss
129 retinal cells
130 retinal cultures
131 retinal ischemia
132 retinal neurons
133 retinal neuroprotection
134 retinal pathology
135 retinal sections
136 sections
137 severe reduction
138 specific enolase
139 study
140 survival
141 time
142 toxicity
143 toxicity of glutamate
144 treatment
145 type Ca2
146 types
147 vitro
148 vivo experiments
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