σ-Ligands and non-competitive NMDA antagonists inhibit glutamate release during cerebral ischemia
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2019, Handbook of Clinical NeurologyCitation Excerpt :They possess chaperone functions and appear to operate via protein–protein interactions to modulate the activity of various ion channels and signaling molecules to influence cellular activity and gene transcription (Hayashi and Su, 2007; Su et al., 2010). Sigma-1 agonists have also been shown to inhibit NMDA receptor activity and decrease glutamate release under certain conditions (Lobner and Lipton, 1990; Zhang et al., 2011). In addition to its direct inhibition of NMDA receptors, DM may thus further blunt NMDA receptor activity through sigma-1 receptors.
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2016, Pharmacology and TherapeuticsCitation Excerpt :The molecular targets responsible for this effect on phosphorylation remain to be determined. It may involve DM's agonist activity at sigma-1 receptors, as activation of these receptors can modulate the function of NMDA receptors (Lobner & Lipton, 1990; Pabba & Sibille, 2015). In addition, DM improved memory in the SNL animals (Morel et al., 2014), an effect likely due to the anti-amnestic effects conferred by sigma-1 activation (Maurice & Lockhart, 1997).
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2015, Journal of Pharmacological SciencesCitation Excerpt :Notably, sigma-1 receptors can respond to perturbations in ER calcium concentrations by promoting calcium entry into mitochondria through stabilization of type 3 inositol triphosphate (IP3) receptors (IP3R3) at the MAM (4). Activation of sigma-1 receptors has also been shown to attenuate the release of glutamate following ischemia (31), and under certain conditions inhibit NMDA receptors (32), which, among the glutamate receptor subtypes, appear to be the principal mediators of excitotoxic damage (10). The exact mechanisms by which sigma-1 receptors modulate the activity of NMDA receptors is unclear, but may involve direct interaction with specific subunits of the NMDA receptor (33) or indirect effects of other ion channel modulation (34).
Sigma receptors as potential therapeutic targets for neuroprotection
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