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Summary Physiological alcohol dependence is a key adaptation to chronic ethanol consumption that underlies withdrawal symptoms, is thought to directly contribute to alcohol addiction behaviors, and is associated with cognitive problems such as deficits in learning and memory [1–3]. Based on the idea that an ethanol-adapted (dependent) animal will perform better in a learning assay than an animal experiencing ethanol withdrawal will, we have used a learning paradigm to detect physiological ethanol dependence in Drosophila. Moderate ethanol consumption initially degrades the capacity of larvae to learn, but they eventually adapt and are able to learn as well as ethanol-naive animals. However, withholding ethanol from ethanol-adapted larvae impairs learning. Ethanol reinstatement restores the capacity to learn, thus demonstrating cognitive dependence on ethanol. The larval nervous system also shows ethanol withdrawal hyperexcitability. Larvae reach ethanol concentrations equivalent to 0.05 to 0.08 BAC—levels that would be mildly intoxicating in humans. These ethanol-induced changes in learning are not the product of sensory deficits or state-dependent learning. This is the first demonstration of cognitive ethanol dependence in an invertebrate genetic model system.

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The process of excitation and inhibition in the receptive fields (RF) of the ganglion cells and lateral geniculate body (LGB) of the cat were examined. The extent of the dependence of the magnitude of excitation and inhibition in RF on stimulus intensity was determined. This dependence is a power function with power indices of 0.15--0.20 (LGB) and 0.3--0.5 (retina) for excitation and 0.2--0.3 (LGB) and 0.5--0.6 (retina) for inhibition.