Induction of LTP in the hippocampus needs synaptic activation of glutamate metabotropic receptors

Nature ◽  
1993 ◽  
Vol 363 (6427) ◽  
pp. 347-350 ◽  
Author(s):  
Zafar I. Bashir ◽  
Zuner A. Bortolotto ◽  
Ceri H. Davies ◽  
Nicola Berretta ◽  
Andrew J. Irving ◽  
...  
Keyword(s):  
Synaptic Activation ◽  
Metabotropic Receptors

scholarly journals Prefrontal synaptic activation during hippocampal memory reactivation

Cell Reports ◽  
2021 ◽  
Vol 34 (12) ◽  
pp. 108885
Author(s):  
Yuya Nishimura ◽  
Yuji Ikegaya ◽  
Takuya Sasaki
Keyword(s):  
Synaptic Activation ◽  
Memory Reactivation

scholarly journals The Effects of N-Acetylcysteine on the Rat Mesocorticolimbic Pathway: Role of mGluR5 Receptors and Interaction with Ethanol

2021 ◽  
Vol 14 (6) ◽  
pp. 593
Author(s):  
Sandra Fernández-Rodríguez ◽  
Claudia Esposito-Zapero ◽  
Teodoro Zornoza ◽  
Ana Polache ◽  
Luis Granero ◽  
...  
Keyword(s):  
Behavioral Activation ◽  
Ethanol Administration ◽  
Metabotropic Receptors ◽  
Negative Allosteric Modulator ◽  
High Doses ◽  
Cell Expression ◽  
Mucolytic Agent ◽  
Different Doses

N-acetylcysteine (NAC) is a prodrug that is marketed as a mucolytic agent and used for the treatment of acetaminophen overdose. Over the last few decades, evidence has been gathered that suggests the potential use of NAC as a new pharmacotherapy for alcohol use disorder (AUD), although its mechanism of action is already being debated. In this paper, we set out to assess both the potential involvement of the glutamate metabotropic receptors (mGluR) in the possible dual effect of NAC administered at two different doses and NAC’s effect on ethanol-induced activation. To this aim, 30 or 120 mg/kg of NAC was intraperitoneally administered to rats with the presence or absence of the negative allosteric modulator of mGluR5 (MTEP 0.1 mg/kg). Thereafter, the cFOS IR-cell expression was analyzed. Secondly, we explored the effect of 120 mg/kg of NAC on the neurochemical and behavioral activation induced by intra-VTA ethanol administration (150 nmol). Our results showed that the high NAC dose stimulated cFOS expression in the NAcc, and that this effect was suppressed in the presence of MTEP, thus suggesting the implication of mGluR5. Additionally, high doses could attenuate the ethanol-induced increase in cFOS-expression in the NAcc, probably due to a phenomenon based on the long-term depression of the MSNs. Additional experiments are required to corroborate our hypothesis.

scholarly journals A Role for Xanthurenic Acid in the Control of Brain Dopaminergic Activity

2021 ◽  
Vol 22 (13) ◽  
pp. 6974
Author(s):  
Omar Taleb ◽  
Mohammed Maammar ◽  
Christian Klein ◽  
Michel Maitre ◽  
Ayikoe Guy Mensah-Nyagan
Keyword(s):  
Dopamine Release ◽  
Intraperitoneal Administration ◽  
Glutamate Transporter ◽  
Fold Increase ◽  
Xanthurenic Acid ◽  
Metabotropic Receptors ◽  
Parent Molecule ◽  
Dopaminergic Activity ◽  
The Brain

Xanthurenic acid (XA) is a metabolite of the kynurenine pathway (KP) synthetized in the brain from dietary or microbial tryptophan that crosses the blood-brain barrier through carrier-mediated transport. XA and kynurenic acid (KYNA) are two structurally related compounds of KP occurring at micromolar concentrations in the CNS and suspected to modulate some pathophysiological mechanisms of neuropsychiatric and/or neurodegenerative diseases. Particularly, various data including XA cerebral distribution (from 1 µM in olfactory bulbs and cerebellum to 0.1–0.4 µM in A9 and A10), its release, and interactions with G protein-dependent XA-receptor, glutamate transporter and metabotropic receptors, strongly support a signaling and/or neuromodulatory role for XA. However, while the parent molecule KYNA is considered as potentially involved in neuropsychiatric disorders because of its inhibitory action on dopamine release in the striatum, the effect of XA on brain dopaminergic activity remains unknown. Here, we demonstrate that acute local/microdialysis-infusions of XA dose-dependently stimulate dopamine release in the rat prefrontal cortex (four-fold increase in the presence of 20 µM XA). This stimulatory effect is blocked by XA-receptor antagonist NCS-486. Interestingly, our results show that the peripheral/intraperitoneal administration of XA, which has been proven to enhance intra-cerebral XA concentrations (about 200% increase after 50 mg/kg XA i.p), also induces a dose-dependent increase of dopamine release in the cortex and striatum. Furthermore, our in vivo electrophysiological studies reveal that the repeated/daily administrations of XA reduce by 43% the number of spontaneously firing dopaminergic neurons in the ventral tegmental area. In the substantia nigra, XA treatment does not change the number of firing neurons. Altogether, our results suggest that XA may contribute together with KYNA to generate a KYNA/XA ratio that may crucially determine the brain normal dopaminergic activity. Imbalance of this ratio may result in dopaminergic dysfunctions related to several brain disorders, including psychotic diseases and drug dependence.

scholarly journals Increased cortical synaptic activation of TrkB and downstream signaling markers in a mouse model of Down Syndrome

2015 ◽  
Vol 77 ◽  
pp. 173-190 ◽  
Author(s):  
R.L. Nosheny ◽  
P.V. Belichenko ◽  
B.L. Busse ◽  
A.M. Weissmiller ◽  
V. Dang ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Synaptic Activation ◽  
Downstream Signaling

Activation of Presynaptic Group III Metabotropic Receptors Enhances Glutamate Release in Rat Entorhinal Cortex

2000 ◽  
Vol 83 (5) ◽  
pp. 2519-2525 ◽  
Author(s):  
D. Ieuan Evans ◽  
Roland S. G. Jones ◽  
Gavin Woodhall
Keyword(s):  
Synaptic Transmission ◽  
Entorhinal Cortex ◽  
Metabotropic Glutamate Receptors ◽  
Glutamate Release ◽  
Facilitatory Effect ◽  
Metabotropic Receptors ◽  
Patch Clamp Technique ◽  
Group Iii ◽  
Bath Application ◽  
Layer V

The role of group III metabotropic glutamate receptors (mGluRs) in modulating excitatory synaptic transmission was investigated in the rat entorhinal cortex (EC) in vitro. AMPA receptor-mediated excitatory postsynaptic currents (EPSCs) were recorded in the whole cell configuration of the patch-clamp technique from visually identified neurons in layers V and II. In layer V, bath application of the specific group III mGluR agonist L(+)-2-amino-4-phosphonobutyric acid (L-AP4, 500 μM) resulted in a marked facilitation of both spontaneous and activity-independent “miniature” (s/mEPSC) event frequency. The facilitatory effect of L-AP4 (100 μM) on sEPSC frequency prevailed in the presence ofdl−2-amino-5-phosphonopentanoic acid (100 μM) but was abolished by the group III antagonist (RS)-cyclopropyl-4-phosphonophenylglycine (20 μM). These data confirmed that group III mGluRs, and not N-methyl-d-aspartate (NMDA) receptors were involved in the response to L-AP4. Bath application of the specific mGluR4a agonist (1S,3R,4S)-1-aminocyclopentane-1,2,4-tricarboxylic acid (20 μM) also had a facilitatory effect on sEPSC frequency, suggesting involvement of mGluR4a. In layer II neurons, L-AP4 caused a reduction in sEPSC frequency but did not affect mEPSCs recorded in the presence of tetrodotoxin. These findings suggest that a group III mGluR with mGluR4a-like pharmacology is involved in modulating synaptic transmission in layer V cells of the EC. The effect on mEPSCs suggests that this receptor is located presynaptically and that its activation results in a direct facilitation of glutamate release. This novel facilitatory effect is specific to layer V and, to our knowledge, is the first report of a direct facilitatory action of group III mGluRs on synaptic transmission. In layer II, L-AP4 had an inhibitory effect on glutamate release similar to that reported in other brain regions.

Glutamate receptors in cortical plasticity: molecular and cellular biology

1997 ◽  
Vol 77 (1) ◽  
pp. 217-255 ◽  
Author(s):  
L. Kaczmarek ◽  
M. Kossut ◽  
J. Skangiel-Kramska
Keyword(s):  
Glutamate Receptors ◽  
Cortical Neurons ◽  
Cortical Plasticity ◽  
Excitatory Input ◽  
Cellular Biology ◽  
Metabotropic Receptors ◽  
Functional Studies ◽  
Neuron Response ◽  
Plastic Changes ◽  
Protein Immunoreactivity

Glutamate receptors (GluRs) provide the major excitatory input to cortical neurons. Four main subtypes of GluRs are distinguished, namely, N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, kainate, and metabotropic receptors. All of them have been implicated in neuronal plasticity, and this paper reviews data that may be pertinent to the role played by GluRs in neocortical plasticity both in adult animals as well as during postnatal development. Emphasis is given to receptor distribution analyzed by various means, such as physiological responses, ligand binding as revealed by receptor autoradiography, and expression of receptor subunits at both mRNA and protein (immunoreactivity) levels. Possible mechanisms of involvement of GluRs in plastic changes on cortical neuron response are reviewed, and data on up- and downregulation of GluRs in neocortical plasticity are summarized. Functional studies involving either activation or blocking, and effects of such manipulation on cortical plasticity are discussed.

Metabotropic receptors for glutamate and GABA in pain

2009 ◽  
Vol 60 (1) ◽  
pp. 43-56 ◽  
Author(s):  
Cyril Goudet ◽  
Valerio Magnaghi ◽  
Marc Landry ◽  
Frédéric Nagy ◽  
Robert W. Gereau ◽  
...  
Keyword(s):  
Metabotropic Receptors

Varicosity-Schwann Cell Interactions Mediated by ATP in the Mouse Vas Deferens

2005 ◽  
Vol 93 (5) ◽  
pp. 2787-2796 ◽  
Author(s):  
Y. Q. Lin ◽  
M. R. Bennett
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Vas Deferens ◽  
P2y Receptors ◽  
Autonomic Nerve ◽  
Nerve Terminals ◽  
Metabotropic Receptors ◽  
Mouse Vas Deferens ◽  
Endogenous Release ◽  
Autonomic Nerve Terminals

Schwann cells, from a variety of sources, are known to possess P2Y purinergic metabotropic receptors. However, it is not known if Schwann cells associated with autonomic nerve terminals possess such receptors and if so whether these receptors are activated by the endogenous release of ATP from the nerve terminals. We show that such Schwann cells in the vas deferens give evoked calcium transients on nerve stimulation. These transients are mediated, at least in part, by the endogenous release of ATP, which acts on Schwann cell P2Y receptors to release calcium from within the cells. This work suggests the possibility that Schwann cells are active participants in the process of junctional transmission in the autonomic nervous system.

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