Effect of Alcohol, Acetaldehyde, and Salsolinol on β‐Endorphin Secretion from the Hypothalamic Neurons in Primary Cultures

The effect of ethanol, acetaldehyde, and salsolinol on hypothalamic β‐endorphin secreting neurons is studied by using rat fetal hypothalamic neurons in primary culture. Exposure of these neuronal cells to different concentrations of ethanol (12.5–50 mM) and acetaldehyde (12.5‐50 μm) caused a concentration‐dependent increase in the secretion of β‐endorphin. Salsolinol (12.5–50 μm) did not cause any significant change in the secretion of β‐endorphin. Ethanol's effect was short‐lasting (2 hr). Acetaldehyde's effect on β‐endorphin secretion was greater and longer lasting, as compared with ethanol. Ethanol and salsolinol do not have any effect on cell viability, whereas higher concentrations of acetaldehyde appear to reduce the number of viable cells after 6 hr of treatment. None of the above treatments has any effect on cellular DNA content. These results suggest that ethanol is a potent stimulator of hypothalamic β‐endorphin. These results also show for the first time that ethanol's metabolite acetaldehyde is more potent in stimulating β‐endorphin secretion and may be significant in the ethanol regulated β‐endorphin secretion.