Cultured postnatal rat septohippocampal neurons change intracellular calcium in response to ethanol and nerve growth factor

Ethanol exposure affects cellular mechanisms involved in the regulation of calcium (Ca2+) homeostasis. Neurotrophins, such as nerve growth factor (NGF), stabilize intracellular Ca2+(Ca2+]i) during a variety of neurotoxic insults. In this study, changes in Ca2+]i during treatment with ethanol and NGF were measured at the cell body of neurons using the Ca2+ indicator indo-1. Cultured postnatal day-of-birth (P0) septohippocampal (SH) neurons that were labeled with 1,1'-dioctadecyl-3,3,3',3'-tetramethyl-indocarbocyanine perchlorate (DiI), increased Ca2+]i in response to ethanol. This response was dose-related. P0 SH neurons treated with NGF had lower Ca2+]i than neurons withdrawn from NGF, implying that NGF may modulate Ca2+ homeostasis in these neurons. NGF also prevented the dose-related increase in Ca2+]i in ethanol-treated SH neurons. The SH neurons increased Ca2+]i when they were stimulated with 30 mM potassium chloride (KCl). Ethanol inhibited the potassium-stimulated change in Ca2+]i but the combination of ethanol and NGF caused Ca2+]i to increase with 100 mg% and 400 mg% ethanol and to decrease to a lower level with 200 mg% ethanol. These data were compared to data from previously published similar aged medial septal (MS) neurons (B. Webb, S.S. Suarez, M.B. Heaton, D.W. Walker, Clin. Exp. Res. 20 (1996) 1385-1394) and with embryonic gestational day 21 (E21) SH neurons (B. Webb, S.S. Suarez, M.B. Heaton, D.W. Walker, Brain Res. 729 (1996) 176-189). Differences in Ca2+]i responses were observed in ethanol and NGF-treated postnatal SH neurons compared with P0 MS neurons and E21 SH neurons. Of these differences, most occurred during the combined treatment with ethanol and NGF compared with either treatment alone.