Dear Editor,

Imidazolines compounds elicit diverse effects on cell growth and death. At least, three subtypes of imidazoline receptors I1Rs have been described: I1R, I2R and I3R.1, 2, 3 Some imidazoline ligands are potent inhibitors of vascular smooth muscle cell proliferation through the activation of I2R.2 Other imidazoline compounds inhibited the growth of clonal pancreatic β-cells by an unknown mechanism.4 In contrast, independent of imidazoline receptors, some imidazoline compounds protect cerebellar granule cells against glutamate-induced neurotoxicity.5 At present, no effect dependent on I1R stimulation on survival or cell death is described. However, a recent study has demonstrated a neuroprotective effect of several imidazoline, having affinity for I1R, on cytotoxicity induced by naphthazarin in astrocystes.6 But, this neuroprotection does not depend on I1R stimulation. Our laboratory is interested in I1 imidazoline receptor. I1Rs are involved in the central regulation of blood pressure and cardiovascular function.7 Some cell lines, such as PC12 cells, express the I1R localized on plasma membranes.1 In these cells, several transduction pathways associated with the receptors have been described: imidazolines, such as benazoline, increase the diacylglycerol level in the cells through the activation of a phosphatidylcholine-specific phospholipase C (PC-PLC) and decrease concentration-dependently the forskolin-stimulated cAMP level in insensitive-pertussis toxin manner.1 These two transduction pathways are largely involved in the signalling of cell growth, cell transformation and cell death. The present work addressed the issue of the implication of I1R in death or growth of PC12 cells.

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