Metabotropic glutamatergic receptors and their ligands in drug addiction

Pomierny-Chamioło, Lucyna; Rup, Kinga; Pomierny, Bartosz; Niedzielska, Ewa; Kalivas, Peter W.; Filip, Małgorzata

doi:10.1016/j.pharmthera.2013.12.012

Cited by 74 publications

(52 citation statements)

References 383 publications

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“…The terminus of the mesolimbic dopaminergic pathway, the nucleus accumbens, is the key structure executing reward processes and serves to regulate motivation and learning processes (Di Chiara et al, 1999). It should be underlined that although impairment evoked by the abuse of addictive drugs starts in brain areas processing reward, the long-term drug intake disrupts the whole brain leading to dysfunctions of emotions, motivations, learning, memory, executive control, and cognitive awareness (Volkow, Fowler, & Wang, 2003) and appears to be under control of glutamatergic neurotransmission (reviewed by Kalivas, 2004;Pomierny-Chamioło et al, 2014;Tzschentke & Schmidt, 2003). Glutamate is a key mediator of synaptic plasticity, learning and memory processes, and the current notion of addiction, indicating that aberrant forms of drug-induced synaptic plasticity and learning drive compulsive relapsing behaviors (Dacher & Nugent, 2011).…”

Section: Chemistry and Pharmacology Of Psychostimulantsmentioning

confidence: 99%

“…There are extensive data supporting a role for this neurotransmitter in SUD. Repeated administration of psychostimulant drugs dysregulates brain glutamatergic systems in preclinical models (Pomierny-Chamioło et al, 2014). In clinical trials, ketamine, memantine, and N-acetylcysteine were/are currently being tested in psychostimulant use disorder.…”

Section: Glutamate-based Strategiesmentioning

confidence: 99%

“…Glutamatergic neurotransmission is mediated not only via ionotropic (NMDA, AMPA, and kainate) but also via eight subtypes of metabotropiclike receptors (mGluR 1-8 ) (Pomierny-Chamioło et al, 2014). So far, clinical studies have addressed the density of mGluR 5 receptors using [ 18 F]SP203 using PET in dependent individuals (clinicaltrials.gov; http://ClinicalTrials.…”

Section: N-acetylcysteinementioning

confidence: 99%

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Psychostimulants

McCreary

Müller

Filip

2015

International Review of Neurobiology

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Section: Chemistry and Pharmacology Of Psychostimulantsmentioning

confidence: 99%

Section: Glutamate-based Strategiesmentioning

confidence: 99%

Section: N-acetylcysteinementioning

confidence: 99%

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Psychostimulants

McCreary

Müller

Filip

2015

International Review of Neurobiology

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“…Both the etiology and proposed treatments of a number of neurological disorders involve chronic, long-term alterations in mGluR5 function (D'Antoni et al 2014;Dolen et al 2007;Nickols and Conn 2014;Pomierny-Chamiolo et al 2014;Yin and Niswender 2014). Interestingly, our unexpected finding that AMPAR-mediated evoked transmission is weakened with Grm5 deletion in light of the known role of mGluR5 in LTD is analogous to a paradox in synaptic phenotypes in the Fragile X model mouse, the Fmr1 KO.…”

Section: Discussionmentioning

confidence: 69%

Postsynaptic mGluR5 promotes evoked AMPAR-mediated synaptic transmission onto neocortical layer 2/3 pyramidal neurons during development

Loerwald

Patel

Huber

et al. 2015

Journal of Neurophysiology

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Loerwald KW, Patel AB, Huber KM, Gibson JR. Postsynaptic mGluR5 promotes evoked AMPAR-mediated synaptic transmission onto neocortical layer 2/3 pyramidal neurons during development. J Neurophysiol 113: 786 -795, 2015. First published November 12, 2014 doi:10.1152/jn.00465.2014.-Both short-and long-term roles for the group I metabotropic glutamate receptor number 5 (mGluR5) have been examined for the regulation of cortical glutamatergic synapses. However, how mGluR5 sculpts neocortical networks during development still remains unclear. Using a single cell deletion strategy, we examined how mGluR5 regulates glutamatergic synaptic pathways in neocortical layer 2/3 (L2/3) during development. Electrophysiological measurements were made in acutely prepared slices to obtain a functional understanding of the effects stemming from loss of mGluR5 in vivo. Loss of postsynaptic mGluR5 results in an increase in the frequency of action potential-independent synaptic events but, paradoxically, results in a decrease in evoked transmission in two separate synaptic pathways providing input to the same pyramidal neurons. Synaptic transmission through ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, but not N-methyl-D-aspartate (NMDA) receptors, is specifically decreased. In the local L2/3 pathway, the decrease in evoked transmission appears to be largely due to a decrease in cell-to-cell connectivity and not in the strength of individual cell-to-cell connections. This decrease in evoked transmission correlates with a decrease in the total dendritic length in a region of the dendritic arbor that likely receives substantial input from these two pathways, thereby suggesting a morphological correlate to functional alterations. These changes are accompanied by an increase in intrinsic membrane excitability. Our data indicate that total mGluR5 function, incorporating both short-and long-term processes, promotes the strengthening of AMPA receptor-mediated transmission in multiple neocortical pathways. metabotropic glutamate receptor; synapse; cortex GROUP I METABOTROPIC RECEPTORS (Gp1 mGluRs) consist of the two subtypes, mGluR1 and mGluR5. Over the first 4 wk of postnatal development, their expression and function are strong (Dudek and Bear 1989;Jia et al. 1995). The mGluR5 subtype is expressed in all layers of the rodent somatosensory cortex and peaks in expression during the first 3 wk of life (Munoz et al. 1999;Wijetunge et al. 2008).

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“…Here intracellular glutamate is exchanged for extracellular cystine. The stimulation of xc(À) modulates glutamate release from the presynaptic neurons [46]. xc(À) regulates glutamate homeostasis through the involvement of the presynaptic mGluR2/3.…”

Section: +mentioning

confidence: 99%

GABA and Glutamate: Their Transmitter Role in the CNS and Pancreatic Islets

Hampe¹,

Mitoma²,

Manto³

2018

GABA and Glutamate - New Developments in Neurotransmission Research

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Glutamate and gamma-aminobutyric acid (GABA) are the major neurotransmitters in the mammalian brain. Inhibitory GABA and excitatory glutamate work together to control many processes, including the brain's overall level of excitation. The contributions of GABA and glutamate in extra-neuronal signaling are by far less widely recognized. In this chapter, we first discuss the role of both neurotransmitters during development, emphasizing the importance of the shift from excitatory to inhibitory GABAergic neurotransmission. The second part summarizes the biosynthesis and role of GABA and glutamate in neurotransmission in the mature brain, and major neurological disorders associated with glutamate and GABA receptors and GABA release mechanisms. The final part focuses on extra-neuronal glutamatergic and GABAergic signaling in pancreatic islets of Langerhans, and possible associations with type 1 diabetes mellitus.

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Metabotropic glutamatergic receptors and their ligands in drug addiction

Cited by 74 publications

References 383 publications

Psychostimulants

Psychostimulants

Postsynaptic mGluR5 promotes evoked AMPAR-mediated synaptic transmission onto neocortical layer 2/3 pyramidal neurons during development

GABA and Glutamate: Their Transmitter Role in the CNS and Pancreatic Islets

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