Abstract
The homotaurine derivate acamprosate has been proven to be efficient in reducing alcohol intake both in animal models and in human trials. However, the pharmacokinetic and pharmacodynamic properties of this drug in humans and its underlying mechanism of action are not well known. Earlier studies suggested that acamprosate is effective mainly by increasing GABAnergic neurotransmission. More recently the involvement of excitatory amino acid receptors has been discussed. Zeise et al. (1993) found in intracellular in vitro recordings from rat neocortical neurons that the discharge activity evoked by pulses of l-glutamate is reduced by acamprosate. Extracellular in vivo recordings from rat neocortical neurons revealed that excitatory and inhibitory postsynaptic potentials (EPSP, IPSP) as well as responses to locally administered excitatory amino acids [l-glutamate, l-aspartate, l-homocysteate, and N-methyl-d-aspartate (NMDA)] are reduced by acamprosate. Serotonergic effects of acamprosate may also be of importance. Acamprosate has been found to increase tryptamine-induced convulsions, to increase serotonin concentrations in both blood and cerebral tissue of rats, and to increase the binding capacity of serotonin 1d and 2 receptors (Nalpas et al. 1990; Daoust et al. 1989).
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© 1996 Springer-Verlag Berlin Heidelberg
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Hegerl, U. et al. (1996). Event-Related Potentials and EEG as Indicators of Central Neurophysiological Effects of Acamprosate. In: Soyka, M. (eds) Acamprosate in Relapse Prevention of Alcoholism. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-80193-8_6
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DOI: https://doi.org/10.1007/978-3-642-80193-8_6
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