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A Neurochemical Approach to Elucidate Metabotropic vs. Ionotropic Glutamate Receptor Activities in Rat Hippocampal Slices
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Darryle D. Schoepp, Manisha A. Desai
One of the primary ways used to describe the functions of ionotropic glutamate receptors in hippocampus has been to study agonist-induced electrophysiological responses. However, distinct properties of these receptor subtypes have also been described with the use of a biochemical assay in which ionotropic glutamate receptor-induced neurotransmitter release is measured. In the hippocampus, ionotropic glutamate receptors modulate the release of a number of neurotransmitters that are either intrinsic to the hippocampal formation or that are released in the hippocampus from extrinsic afferents.49 For instance, studies measuring excitatory amino acid-induced release of 3-norepinephrine (3H-NE) have provided a great deal of information on the regulation of ionotropic glutamate receptors in the hippocampal formation.
Pharmacotherapy of Neurochemical Imbalances
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rupali Patil, Aman Upaganlawar, Suvarna Ingale
Glutamate receptors (Table 22.7) is composed of two families of receptors—ionotropic and metabotropic receptors. Ionotropic glutamate receptors are ion channels gated receptors which open/close upon agonist binding. Ionotropic glutamate receptors are of three types that are: N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), and kainate receptors. The metabotropic glutamate receptors are: G-protein-coupled receptors. There are 11 subtypes identified (Sharma and Sharma, 2017).
Herbal Medicines in Neuropsychiatric Illness: The Case of L-Stepholidine
Published in Vikas Kumar, Addepalli Veeranjaneyulu, Herbs for Diabetes and Neurological Disease Management, 2018
Nitin Sati, Kedar S. Prabhavalkr, Sridhar Natesan, Lokesh K. Bhatt
Glutamate receptors are broadly classified into two subtypes: ionotropic glutamate receptors which are ligand-gated ion channels and metabotropic glutamate receptors (mGlu receptors) which are coupled via G proteins to second messenger systems. When activated, ionotropic glutamate receptors produce an influx of cations into the cell, directly depolarizing the postsynaptic neuron and thus transmitting excitatory inputs into the synapse. In contrast, mGlu receptors function to modulate glutamatergic transmission by presynaptic and postsynaptic mechanisms.47 The mGlu receptors fall into three groups based on current pharmacology and the molecular properties of each receptor. Each mGlu receptor subtype is uniquely and differentially distributed in the CNS. Thus, the expression of mGlu receptors in different brain regions and selected synapses provides a mechanism for the CNS to modulate glutamatergic neuronal transmission within specific synapses.48 The availability of novel drugs that modulate glutamate neurotransmission provides a new prospect for the treatment of schizophrenia. Impairment of glutamate functioning has been hypothesized in etiology of schizophrenia.49
Dyskinesia and Parkinson’s disease: animal model, drug targets, and agents in preclinical testing
Published in Expert Opinion on Therapeutic Targets, 2022
Valentina Cesaroni, Fabio Blandini, Silvia Cerri
Glutamate is the most representative excitatory neurotransmitter of the central nervous system and there are extensive preclinical and clinical evidence suggesting changes in thalamo-cortical-striatal glutamatergic transmission and altered expression of both ionotropic and metabotropic receptors involved in LID development. Ionotropic glutamate receptors are ligand-gated ion channels involved in fast excitatory transmission in the central nervous system which are generally named according to their specific ligands: kainate, α-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA), and NMDA. NMDA receptors are formed by a tetrameric complex of different subunits (GluN1, GluN2, GluN3 or NR1, NR2, NR3), responsible for its biophysical and pharmacological properties. The observation of an increased activation of striatal NMDA receptors in experimental models of dyskinesia and in the brain of PD patients with LID [34,53] have suggested the use of antagonists and modulators of these receptors as potential anti-dyskinetic strategy. Similarly, preclinical studies on animal models of LID have reported a modification in the phosphorylation state of the AMPA receptors and their massive synaptic involvement in the striatum, proposing them to be a possible drug targets for ameliorating this side effect (see Table 2).
Ionotropic glutamate receptors in platelets: opposing effects and a unifying hypothesis
Published in Platelets, 2021
Maggie L. Kalev-Zylinska, Marie-Christine Morel-Kopp, Christopher M. Ward, James I. Hearn, Justin R. Hamilton, Anna Y. Bogdanova
Glutamate is the most abundant-free amino acid in the human body, involved in multiple metabolic pathways but best known for its role as a neurotransmitter [1]. Ionotropic glutamate receptors are ligand-gated cation channels that include three subtypes: α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), kainate receptors (KAR), and N-methyl-D-aspartate receptors (NMDAR) [2]. The primary role of these receptors in mammals is to mediate fast excitatory neurotransmission in the brain, spinal cord, and retina. In contrast, their purpose in peripheral tissues, including platelets is less clear [3]. The initial findings reporting expression and function of NMDAR in platelets [4–7] were not followed up for over a decade. The very low abundance of these receptors in platelets, together with high levels of plasma glutamate, created doubt over their biological relevance. However, subsequent work confirmed the important roles of glutamate receptors in platelets and renewed interest in this area. This review provides a detailed description of what has been learned about ionotropic glutamate receptors in platelets over the last 20–30 years to serve as a basis for further research in this developing field of platelet biology. Data on megakaryocytes will not be discussed as it was recently reviewed by us elsewhere [8].
Sex-dependent expression of N-cadherin-GluA1 pathway-related molecules in the prefrontal cortex mediates anxiety-like behavior in male offspring following prenatal stress
Published in Stress, 2021
Shuya Shao, Jing Li, Shengquan Chen, YanKai Dong, Shang Wang, Zhongliang Zhu, Longshan Xie, Hui Li
PS affects the function of the prefrontal cortex (PFC). Clinical studies showed that altered maturation within the PFC has been implicated in the pathogenesis of anxiety disorders in adolescents (Newman et al., 2016). In addition, some animal studies have demonstrated anxiety arises from synaptic deficits in the PFC (Liu et al., 2020; Pati et al., 2018). Studies have also implicated glutamatergic neuronal activity in the PFC in anxiety-like behavior (Corbett & Dunn, 1993; Karcz-Kubicha & Liljequist, 1995; Kotlinska & Liljequist, 1998). In the rodent brain, the majority of fast excitatory neurotransmission is carried out by α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-sensitive ionotropic glutamate receptors located at the post-synaptic density of glutamatergic synapses (Traynelis et al., 2010). AMPA receptors (AMPARs) are composed of a combination of four subunits, namely, GluA1–4, which can mediate anxiety, possibly by modulating network excitability in the PFC (Kiselycznyk et al., 2013). Studies have reported that decreased GluA1 and GluA2 expression in the PFC mediates anxiety-like behavior in males (Kiselycznyk et al., 2013). However, the role of AMPARs in sex difference in anxiety-like behavior in adolescent offspring exposed to PS remains unknown.