Metabotropic glutamate receptors in auditory processing.
Animals; Auditory Pathways/anatomy & histology/physiology; Auditory Perception/*physiology; auditory processing; excitotoxicity; Humans; Metabotropic Glutamate/*metabolism; mGluR; neuromodulation; neurotransmission; Receptors; synaptic plasticity
As the major excitatory neurotransmitter used in the vertebrate brain, glutamate activates ionotropic and metabotropic glutamate receptors (mGluRs), which mediate fast and slow neuronal actions, respectively. Important modulatory roles of mGluRs have been shown in many brain areas, and drugs targeting mGluRs have been developed for the treatment of brain disorders. Here, I review studies on mGluRs in the auditory system. Anatomical expression of mGluRs in the cochlear nucleus has been well characterized, while data for other auditory nuclei await more systematic investigations at both the light and electron microscopy levels. The physiology of mGluRs has been extensively studied using in vitro brain slice preparations, with a focus on the lower auditory brainstem in both mammals and birds. These in vitro physiological studies have revealed that mGluRs participate in neurotransmission, regulate ionic homeostasis, induce synaptic plasticity, and maintain the balance between excitation and inhibition in a variety of auditory structures. However, very few in vivo physiological studies on mGluRs in auditory processing have been undertaken at the systems level. Many questions regarding the essential roles of mGluRs in auditory processing still remain unanswered and more rigorous basic research is warranted.
Lu Y
Neuroscience
2014
2014-08
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.neuroscience.2014.05.057" target="_blank" rel="noreferrer noopener">10.1016/j.neuroscience.2014.05.057</a>
Protective Effects Of Ginsenoside Rg(2) Against Glutamate-induced Neurotoxicity In Pc12 Cells
Alzheimer's disease; apoptosis; beta peptide; calpain; damage; excitotoxicity; expression; Integrative & Complementary; ischemic neuronal death; Medicine; neuroprotection; nitric-oxide; Panax ginseng; Panax ginseng; Pharmacology & Pharmacy; Plant Sciences; receptors; system
We investigated the effect of ginsenoside Rg(2) on neurotoxic activities induced by glutamate in PC12 cells. The cells were incubated with glutamate (1 mmol/L), glutamate and ginsenoside Rg(2) (0.05, 0.1, 0.2 mmol/L) or nimodipine (5 mu mol/L for 24 h. The cellular viability was assessed by MTT assay. The lipid peroxidation products malondialdehyde (MDA) and nitrogen oxide (NO) were measured by a spectrophotometric method. Fura2/AM, as a cell permeable fluorescent probe for Ca2+, was used to detect intracellular Ca2+ concentration ([Ca2+](i)) using a monespectrofluorometer. Immunocytochemical techniques were employed to check the protein expression levels of calpain II, caspase-3 and beta-amyloid (A beta)1-40 in PC12 cells. The results showed that glutamate decreased the cell viability, increased [Ca2+](i), lipid peroxidation (the excessive production of MDA, NO) and the protein expression levels of calpain II, caspase-3 and A beta 1-40 in PC12 cells. Ginsenoside Rg(2) significantly attenuated glutamate-induced neurotoxic effects upon these parameters at all doses tested. Our study suggests that ginsenoside Rg(2) has a neuroprotective effect against glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis. In addition, the inhibitory effect of ginsenoside Rg(2) against the formation of A beta 1-40 suggests that ginsenoside Rg(2) may also represent a potential treatment strategy for Alzheimer's disease. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
Li N; Liu B; Dluzen D E; Jin Y
Journal of Ethnopharmacology
2007
2007-05
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/j.jep.2006.12.015" target="_blank" rel="noreferrer noopener">10.1016/j.jep.2006.12.015</a>