Ethanol and brain plasticity: receptors and molecular networks of the postsynaptic density as targets of ethanol.

TL;DR: The identification and the understanding of the cellular and molecular mechanisms involved in ethanol toxicity might contribute to the development of treatments and/or therapeutic agents that could reduce or eliminate the deleterious effects of alcohol on the brain.

TL;DR: The potential for targeting the glutamate system as a novel pharmacotherapeutic approach to treating alcohol use disorders is discussed, focusing on five major components: the N-methyl-d-aspartate (NMDA) receptor and specific NMDA subunits, the glycineB site on the NMDA receptors (NMDAR), l-alpha-amino-3-hydroxy-5- methyl-isoxazole-4-propionic acid ionotropic (AMPA) and

TL;DR: This review outlines progressive neuroscience research into molecular and epigenetic mechanisms of alcoholism and several important CREB-related genes that may play a crucial role in the behavioral effects of ethanol and molecular changes in the specific neurocircuitry that underlie both alcohol addiction and a genetic predisposition to alcoholism.

TL;DR: This review summarizes the existing data implicating the Homer family of protein in acute behavioral and neurochemical sensitivity to drugs of abuse, the development of drug-induced neuroplasticity, as well as other behavioral and cognitive pathologies associated with an addicted state.

TL;DR: The application of molecular cloning technology to the study of the glutamate receptor system has led to an explosion of knowledge about the structure, expression, and function of this most important fast excitatory transmitter system in the mammalian brain.

TL;DR: Mechanistic studies based on the crystal structures of glutamate receptor domains include explanations for strikingly diverse phenomena, including the basis for subtype-specific agonist selectivity; mechanisms for desensitization and allosteric modulation; and mechanisms for partial agonist activity.

TL;DR: Genetic mutations that prevent persistent activation of CaMKII block LTP, experience-dependent plasticity and behavioural memory, making this kinase a leading candidate in the search for the molecular basis of memory.

TL;DR: After induction of long-lasting (but not short-lasting) functional enhancement of synapses in area CA1, new spines appear on the postsynaptic dendrite, whereas in control regions on the same dendrites or in slices where long-term potentiation was blocked, no significant spine growth occurred.