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. Author manuscript; available in PMC: 2013 Aug 19.
Published in final edited form as: J Neuroimmune Pharmacol. 2011 Dec 10;7(2):388–400. doi: 10.1007/s11481-011-9325-0

Figure 8.

Figure 8

Summary of the mean ± sem calcium changes (Fluorescence Increase) in response to fMCM or fMCM+LM11A-31. A. After a brief delay, fMCM (solid circles, n=119 neurons) induced a rise in calcium with no recovery over the first 6 min. A gradual destabilization of calcium developed over the next 60 min giving rise to high intracellular calcium. Co-stimulation with LM11A-31 did not change the acute calcium rise but largely prevented the destabilization (n=114 neurons). Neurons treated with aCSF (n=101 neurons) showed stable calcium levels throughout illustrating the integrity of the neurons in the absence of stimulation. B. Astrocytes (n=60) in the same cultures as A showed small increases in intracellular calcium (note change in scale versus A) but minimal long-term destabilization. The addition of LM11A-31 (n=58) suppressed the calcium changes to near background (aCSF) levels. C. Example of the typical calcium profile of most astrocytes showing negligible acute and small long-term changes relative to aCSF controls. D. Example of calcium responses seen in a subset of astrocytes which showed pulses of calcium during the delayed phase. This activity was not synchronized between astrocytes and occurred after the appearance of calcium elevations in the neurons.