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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Anesthesiology. 2012 May;116(5):1013–1024. doi: 10.1097/ALN.0b013e31825153ea

Figure 1. Gabapentin reduces catecholamine secretion but not calcium entry evoked by cholinergic stimulation.

Figure 1

(A) Chromaffin cells were seeded on 24-well plates and treated with 1mM gabapentin (GBP) or vehicle (control) for 18–24 h. The amount of catecholamines released under basal conditions (in the absence of secretagogue) or during a 5-min stimulation with carbachol (100 μM) was determined using high performance liquid chromatography (HPLC) and expressed as a percentage of total cellular content (mean ± SEM). Gabapentin significantly reduced carbachol-evoked secretion (** p = 0.00023) but not basal release (p = 0.15). (B) Gabapentin treatment (GBP) did not alter the total cellular content of norepinephrine (p = 0.43) or epinephrine (p = 0.16) compared to control cells (mean ± SEM). (C) Secretion evoked by carbachol in gabapentin treated cells (GBP) was normalized to controls (CTL). Gabapentin reduced both epinephrine (epi) (p = 0.0007) and norepinephrine (norepi) (p = 0.0001) secretion to a similar extent (mean ± SEM). (D) Same layout as in panel C except using a 5-min stimulation with 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) (30 μM), a selective nicotinic receptor agonist. Gabapentin significantly reduced both epinephrine (epi) (p = 0.042) and norepinephrine (norepi) (p = 0.026) secretion. (E) Representative experiment showing the [Ca2+]i increase evoked by a 5-min application of 100μM carbachol in FURA-2 loaded chromaffin cells (n = 8 cells, mean ± SEM - for clarity error bars are only shown for a few data points). (F) Pooled data from multiple experiments like that shown in panel E. The peak increase in [Ca2+]i evoked by carbachol was not significantly altered in gabapentin treated cells compared to control cells (mean ± SEM; p = 0.10).