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Introduction: Epilepsy
Published in Candace M. Kent, David M. Chan, Analysis of a Model for Epilepsy, 2022
Candace M. Kent, David M. Chan
There are two types of receptors for the neurotransmitter glutamate, as well as for other neurotransmitters. They are the ionotropic glutamate receptors, iGluRs, and the metabotropic glutamate receptors, mGluRs. An ionotropic receptor is directly linked to an ion channel, and upon binding to the neurotransmitter quickly opens up the ion channel to the selective passage of ions into or out of the neuronal cell [3], [42]. The ionotropic receptors are said to mediate the neurotransmitters that they bind to [23]. A metabotropic receptor is indirectly linked, through a series of steps in a biochemical pathway, to an ion channel and upon binding to the neurotransmitter more slowly opens up the ion channel [3], [42]. The metabotropic receptors are said to modulate the neurotransmitters they bind to [23].
Glutathione and Glutathione Derivatives: Possible Modulators of Ionotropic Glutamate Receptors
Published in Christopher A. Shaw, Glutathione in the Nervous System, 2018
Réka Janáky, Vince Varga, Zsolt Jenei, Pirjo Saransaari, Simo S. Oja
The glutamate receptors fall into two families, ionotropic and metabotropic (Nakanishi 1992; Cunningham, Ferkany, and Enna 1994). The ionotropic receptors contain integral cation-specific ion channels. They are classified after the agonists N-methyl-d-aspartate (NMDA), 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), and kainate (KA), the last two receptor classes being collectively referred to as non-NMDA receptors (Récasens et al. 1992). The metabotropic receptors are coupled to G-proteins and functionally linked either to the turnover of inositol phosphates (Conn and Desai 1991) or to the metabolism of cyclic nucleotides (Nakanishi 1992). The glutamate receptors are probably homo- or heteromeric pentamers, consisting of subunits NR1 and NR2A-D (NMDA receptors), GluR1–4 (AMPA receptors), KA1, 2 and GluR5–7 (kainate receptors), and mGlu1–5 and 7, 8 (metabotropic receptors) (Nakanishi 1992; Stone 1993). One ionotropic receptor subunit has three transmembrane segments (TM1, 3, and 4) and one segment folding as a loop into the membrane from its intracellular surface (TM2). The amino acid side chains of the TM2 segments surrounding and forming the pore determine its ion selectivity. The metabotropic receptors have subunits with seven transmembrane segments (TM1 to 7). The pharmacological properties of the receptors are determined by their subunit composition, the structure of the receptor subunits, and the availability and charges of functional amino acid side chains in the receptor protein.
Control of blood vessels: extrinsic control by nerves and hormones
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
ATP is co-released with NAd in some large and small arteries. ATP stimulates postjunctional P2X purinergic receptors. These ‘ionotropic’ receptors are physically part of an ion channel protein (unlike ‘metabotropic’ a receptors, which activate enzyme cascades). Ligand-binding to the P2X receptor activates a cation conductance, partially selective for Ca2+ over Na+. The cation current causes a fast, brief depolarization of the myocyte (the fast excitatory junction potentials in Figures 14.3 and 12.9).
NBQX attenuates relapse of nicotine seeking but not nicotine and methamphetamine self-administration in rats
Published in The World Journal of Biological Psychiatry, 2021
Jana Ruda-Kucerova, Petra Amchova, Filip Siska, Yousef Tizabi
Recent progress in addiction’s neurobiology has identified the glutamatergic system as a significant player in various abused drugs, including nicotine (Polosa and Benowitz 2011; D’Souza 2015; Spencer and Kalivas 2017; Alasmari et al. 2018). Glutamate, a major excitatory neurotransmitter, acts on two broad categories of receptors, ionotropic and metabotropic. The ionotropic receptors are ligand-gated ion channels and are further classified into N-methyl-D-aspartate (NMDA), alpha- amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), and kainate receptors. The metabotropic receptors (mGluR), on the other hand, are G-protein coupled receptors and are further divided into eight subtypes (Karakas et al. 2015; Crupi et al. 2019). A significant amount of research has exploited the potential targeting of these receptors in drug addiction. In this regard, some recent reviews emphasise the possible use of both positive and negative allosteric modulators of metabotropic glutamate receptors in the prevention and/or treatment of drug of abuse with considerable preclinical evidence on self-administration and relapse in animals (Barnes et al. 2018; Caprioli et al. 2018; Levin et al. 2019). Besides, a role for glutamate transporters in drug addiction has been suggested (Spencer and Kalivas 2017).
Treatment Options for Anti-N-methyl-D-aspartate Receptor Encephalitis
Published in The Neurodiagnostic Journal, 2018
N-methyl-d-aspartate (NMDA) is an excitotoxin; it destroys nerve cells by overexciting them (Watkins 2015). This water-soluble artificial element is described as not typically found in organic issue (Masuko et al. 2008). NMDA receptors are a precise type of ionotropic glutamate receptor that controls synaptic plasticity and memory function and are ubiquitous throughout the body, primarily localized in the brain and spinal cord (Kadewaga et al. 2007; Watkins 2015). These receptors are indispensable for human interaction, judgment, and memory. Ionotropic receptors are also referred to as ligand-gated ion channels (Thompson et al. 2013). The receptors are a group of transmembrane ion channel proteins that permit ions such as Ca2+ and Na+ to cross through the membrane (Thompson et al. 2013).
Modulation of neuromuscular synapses and contraction in Drosophila 3rd instar larvae
Published in Journal of Neurogenetics, 2018
Kiel G. Ormerod, JaeHwan Jung, A. Joffre Mercier
The activation or inhibition of any neural pathway, ultimately depends on communication at chemical synapses, where neurotransmitters are released from presynaptic terminals, bind to receptors in the postsynaptic membrane (Figure 1) and alter electrical activity of the postsynaptic cell. ‘Classical’ neurotransmitters, such as acetylcholine, GABA and glutamate, bind to ionotropic receptors, chemically gated ion channels that directly alter the cell’s transmembrane potential. Other chemical signals, notably biogenic amines and neuropeptides, bind to metabotropic receptors that alter activity indirectly, typically through second messenger systems. Peptides and biogenic amines can be released as co-transmitters from presynaptic terminals to alter the effectiveness of ionotropic receptor activation (e.g. Adams & O’Shea, 1983; Fung et al., 1994; Nusbaum, Blitz, Swensen, Wood, & Marder, 2001), or they can be secreted by neuroendocrine cells and carried through the circulation to synapses, where they can alter transmitter release, postsynaptic responsiveness or both (e.g. Christie, Stemmler, & Dickinson, 2010; Ewer, 2005; Kravitz et al., 1980). These effects, which alter the efficacy of synaptic transmission, are referred to as ‘modulation’, and the signaling molecules that elicit them are often referred to as ‘modulators’ or ‘neuromodulators’. Thus, the ‘classical’ view of chemical synaptic transmission, in which a neurotransmitter acts directly to either depolarize or hyperpolarize a postsynaptic cell, represents only one component of synaptic communication; intercellular signaling in vivo involves many more components.