Abstract
Major depression is a chronic and debilitating illness that effects approximately 1 in 5 people, but currently available treatments are limited by low rates of efficacy, therapeutic time lag, and undesirable side effects. Recent efforts have been directed towards investigating rapid-acting agents that reverse the behavioral and neuronal deficits of chronic stress and depression, notably the glutamate NMDA receptor antagonist ketamine. The cellular mechanisms underlying the rapid antidepressant actions of ketamine and related agents are discussed, as well as novel, selective glutamatergic receptor targets that are safer and have fewer side effects.
Copyright © 2016 Elsevier Ltd. All rights reserved.
MeSH terms
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Animals
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Antidepressive Agents / therapeutic use*
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Depression / drug therapy*
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Depression / metabolism
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Depression / physiopathology
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Depressive Disorder, Major / drug therapy*
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Depressive Disorder, Major / metabolism
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Depressive Disorder, Major / physiopathology
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Excitatory Amino Acid Agents / therapeutic use
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GABA-A Receptor Agonists / therapeutic use
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Glutamic Acid
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Humans
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Ketamine / therapeutic use
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Muscarinic Antagonists / therapeutic use
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Neuronal Plasticity
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Receptors, Metabotropic Glutamate / antagonists & inhibitors
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Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
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Scopolamine / therapeutic use
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Stress, Psychological / drug therapy
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Stress, Psychological / physiopathology
Substances
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Antidepressive Agents
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Excitatory Amino Acid Agents
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GABA-A Receptor Agonists
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Muscarinic Antagonists
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NR2B NMDA receptor
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Receptors, Metabotropic Glutamate
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Receptors, N-Methyl-D-Aspartate
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Glutamic Acid
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Ketamine
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Scopolamine