NeuropharmacologyResearch PaperGlutamate-mediated calcium signaling: A potential target for lithium action
Section snippets
Preparation of primary culture of hippocampal neurons
Primary cultures of hippocampal neurons were prepared from 18-day-old Sprague–Dawley rat embryos, as described (Mao and Wang, 2003) with few modifications. All experiments were approved by the local committee on Ethics for Animal Experimentation, Stockholm, Sweden, in accordance to the Swedish national law on the ethical use of animal. All efforts were made to minimize the number of animals used and their suffering. Briefly, hippocampi were dissected and placed into cold Hanks' balance salt
Seven days of lithium treatment reduces glutamate-mediated Ca2+ response in hippocampal neurons
The effect of glutamate on [Ca2+]i was studied in primary cultures of rat hippocampal neurons. Neurons were identified according to their characteristic morphological features under the microscope and by their capacity to respond to NMDA. The majority of neurons had a pyramidal soma with two or more primary dendrites. The neurons accounted for the majority of cells on the coverslip under the above-described culturing conditions. When cells were exposed to glutamate (1 μM), an almost immediate
Discussion
It has been postulated for many years that perturbation in calcium signaling is one mechanism by which lithium can exert its action in mood disorders and other neuropsychiatric diseases (Wasserman et al 2004, Perova et al 2007, Bauer et al 2003). Nevertheless, there are relatively few studies that have examined the effect of lithium on calcium signaling pathways in neurons. Here we show that seven days' exposure of neurons to lithium is associated with multiple perturbations in calcium
Acknowledgments
This work was supported by grants from the Swedish Research Council, the Märtha and Gunnar V. Philipson Foundation and the Persson Family Foundation.
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