Modulation of glutamatergic synaptic transmission in the bed nucleus of the stria terminalis.

McElligott ZA, Winder DG
Prog Neuropsychopharmacol Biol Psychiatry. 2009 33 (8): 1329-35

PMID: 19524008 · PMCID: PMC2783684 · DOI:10.1016/j.pnpbp.2009.05.022

Glutamate, catecholamine and neuropeptide signaling within the bed nucleus of the stria terminalis (BNST) have all been identified as key participants in anxiety-like behaviors and behaviors related to withdrawal from exposure to substances of abuse. The BNST is thought to serve as a key relay between limbic cognitive centers and reward, stress and anxiety nuclei. Human studies and animal models have demonstrated that stressors and drugs of abuse can result in long term behavioral modifications that can culminate in psychological diseases such as addiction and post-traumatic stress disorder. The ability of catecholamines and neuropeptides to influence synaptic glutamatergic transmission (stemming from cognitive centers) within the BNST may have profound consequences over these behaviors. In this review we highlight studies examining synaptic plasticity and modulation of excitatory transmission within the BNST, emphasizing how such modulation may result in alterations in anxiety and reward related behavior.

MeSH Terms (10)

Animals Anxiety Glutamic Acid Humans Neuronal Plasticity Neurons Reward Septal Nuclei Synapses Synaptic Transmission

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