Download or read book Metabotropic Glutamate Receptors and Neurological/Psychiatric Disorders written by Enza Palazzo and published by Frontiers Media SA. This book was released on 2019-06-19 with total page 139 pages. Available in PDF, EPUB and Kindle. Book excerpt: Considering that neurological and psychiatric illnesses do not still have efficient therapies and are becoming increasingly widespread, the search for novel targets appears fundamental. Neuroinflammation, alterations in adult neurogenesis and excitotoxicity, all associated with glutamate transmission dysfunction, are key components of the pathogenetic mechanisms underlying neuropsychiatric illnesses. Counteracting the neurotoxic actions of glutamate through the modulatory actions of metabotropic glutamate receptors (mGluRs), represents a rational intervention that offers tolerability compatible with clinical therapy. Their suitability as targets for developing novel therapies is also based on the fact that mGluRs are found abundantly expressed in synapses of the central nervous system (CNS) that are considered critical in certain neurological and psychiatric disorders. Moreover, recently there has been an exponential development of selective ligands, especially positive and negative allosteric modulators, which by binding to less conserved transmembrane domain sequences ensure, besides a good permeability in the CNS, an adequate selectivity for each mGluR subtype. The eBook “Metabotropic Glutamate Receptors and Neurological/Psychiatric Disorders”, collects contributes (original and review articles) on the beneficial effects of positive and negative allosteric modulators of mGluRs in animal models of neurological and psychiatric diseases from renown experts in the field. The hope is that the effort of both Editors and Contributors of this eBook confirms the unlimited potential of mGluRs in CNS diseases and generate a collaborative discussion on the state of art, overall trends, novel strategies, and future direction of this attractive field of research.