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Excitatory glutamate receptors

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https://www.readbyqxmd.com/read/28921378/chemistry-and-chemical-equilibrium-dynamics-of-bmaa-and-its-carbamate-adducts
#1
Pedro Diaz-Parga, Joy J Goto, V V Krishnan
Beta-N-methylamino-L-alanine (BMAA) has been demonstrated to contribute to the onset of the ALS/Parkinsonism-dementia complex (ALS/PDC) and is implicated in the progression of other neurodegenerative diseases. While the role of BMAA in these diseases is still debated, one of the suggested mechanisms involves the activation of excitatory glutamate receptors. In particular, the excitatory effects of BMAA are shown to be dependent on the presence of bicarbonate ions, which in turn forms carbamate adducts in physiological conditions...
September 18, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28916137/oxytocin-induces-penile-erection-and-yawning-when-injected-into-the-bed-nucleus-of-the-stria-terminalis-involvement-of-glutamic-acid-dopamine-and-nitric-oxide
#2
Fabrizio Sanna, Jessica Bratzu, Antonio Argiolas, Maria Rosaria Melis
Oxytocin (5-100ng), but not Arg(8)-vasopressin (100ng), injected unilaterally into the bed nucleus of the stria terminalis (BNST) induces penile erection and yawning in a dose-dependent manner in male rats. The minimal effective dose was 20ng for penile erection and 5ng for yawning. Oxytocin responses were abolished not only by the oxytocin receptor antagonist d(CH2)5Tyr(Me)(2)-Orn(8)-vasotocin (1μg), but also by (+) MK-801 (1μg), an excitatory amino acid receptor antagonist of the N-methyl-d-aspartic acid (NMDA) subtype, SCH 23390 (1μg), a D1 receptor antagonist, but not haloperidol (1μg), a D2 receptor antagonist, and SMTC (40μg), an inhibitor of neuronal nitric oxide synthase, injected into the BNST 15min before oxytocin...
September 12, 2017: Hormones and Behavior
https://www.readbyqxmd.com/read/28904092/map1b-light-chain-modulates-synaptic-transmission-via-ampa-receptor-intracellular-trapping
#3
Rocío Palenzuela, Yolanda Gutiérrez, Jonathan E Draffin, Argentina Lario, Marion Benoist, José A Esteban
The regulated transport of AMPA-type glutamate receptors (AMPARs) to the synaptic membrane is a key mechanism to determine the strength of excitatory synaptic transmission in the brain. In this work, we uncovered a new role for the microtubule-associated protein MAP1B, in modulating the access of AMPARs to the postsynaptic membrane. Using mice and rats of either sex, we show that MAP1B light chain (LC) accumulates in the somatodendritic compartment of hippocampal neurons, where it forms immobile complexes on microtubules that limit vesicular transport...
September 13, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28902836/hippocampal-ltp-and-contextual-learning-require-surface-diffusion-of-ampa-receptors
#4
A C Penn, C L Zhang, F Georges, L Royer, C Breillat, E Hosy, J D Petersen, Y Humeau, D Choquet
Long-term potentiation (LTP) of excitatory synaptic transmission has long been considered a cellular correlate for learning and memory. Early LTP (less than 1 h) had initially been explained either by presynaptic increases in glutamate release or by direct modification of postsynaptic AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor function. Compelling models have more recently proposed that synaptic potentiation can occur by the recruitment of additional postsynaptic AMPA receptors (AMPARs), sourced either from an intracellular reserve pool by exocytosis or from nearby extra-synaptic receptors pre-existing on the neuronal surface...
September 13, 2017: Nature
https://www.readbyqxmd.com/read/28899919/astrocyte-mediated-neuronal-synchronisation-properties-revealed-by-false-gliotransmitter-release
#5
Tiina M Pirttimaki, Robert E Sims, Gregory Saunders, Serena A Antonio, Neela Krushna Codadu, H Rheinallt Parri
Astrocytes spontaneously release glutamate as a gliotransmitter (GT) resulting in the generation of extrasynaptic NMDA-R mediated slow inward currents (SICs) in neighbouring neurons, which can increase local neuronal excitability. However, there is a deficit in our knowledge of the factors that control spontaneous astrocyte GT release, and the extent of its influence. We found that in rat brain slices, increasing the supply of the physiological transmitter glutamate increased the frequency and signalling charge of SICs over an extended period...
September 12, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28899729/serotonin-gating-of-cortical-and-thalamic-glutamate-inputs-onto-principal-neurons-of-the-basolateral-amygdala
#6
Ji-Dong Guo, Brendan M O'Flaherty, Donald G Rainnie
The basolateral amygdala (BLA) is a key site for crossmodal association of sensory stimuli and an important relay in the neural circuitry of emotion. Indeed, the BLA receives substantial glutamatergic inputs from multiple brain regions including the prefrontal cortex and thalamic nuclei. Modulation of glutamatergic transmission in the BLA regulates stress- and anxiety-related behaviors. Serotonin (5-HT) also plays an important role in regulating stress-related behavior through activation of both pre- and postsynaptic 5-HT receptors...
September 9, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28895001/regulation-of-hypothalamo-pituitary-adrenocortical-responses-to-stressors-by-the-nucleus-of-the-solitary-tract-dorsal-vagal-complex
#7
REVIEW
James P Herman
Hindbrain neurons in the nucleus of the solitary tract (NTS) are critical for regulation of hypothalamo-pituitary-adrenocortical (HPA) responses to stress. It is well known that noradrenergic (as well as adrenergic) neurons in the NTS send direct projections to hypophysiotropic corticotropin-releasing hormone (CRH) neurons and control activation of HPA axis responses to acute systemic (but not psychogenic) stressors. Norepinephrine (NE) signaling via alpha1 receptors is primarily excitatory, working either directly on CRH neurons or through presynaptic activation of glutamate release...
September 11, 2017: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/28887876/cell-specific-gain-modulation-by-synaptically-released-zinc-in-cortical-circuits-of-audition
#8
Charles T Anderson, Manoj Kumar, Shanshan Xiong, Thanos Tzounopoulos
In many excitatory synapses, mobile zinc is found within glutamatergic vesicles and is coreleased with glutamate. Ex vivo studies established that synaptically released (synaptic) zinc inhibits excitatory neurotransmission at lower frequencies of synaptic activity but enhances steady state synaptic responses during higher frequencies of activity. However, it remains unknown how synaptic zinc affects neuronal processing in vivo. Here, we imaged the sound-evoked neuronal activity of the primary auditory cortex in awake mice...
September 9, 2017: ELife
https://www.readbyqxmd.com/read/28886985/pannexin-1-channels-in-epilepsy
#9
REVIEW
Mark S Aquilino, Paige Whyte-Fagundes, Georg Zoidl, Peter L Carlen
Pannexin-1 (Panx1) expression is raised in several animal seizure models and in resected human epileptic brain tissue, suggesting relevance to epilepsy. Multiple factors that are characteristic of seizures are thought to regulate Panx1 channel opening, including elevated levels of extracellular K(+). Panx1, when open, 1) releases ATP, glutamate, and other metabolites into the extracellular medium, and 2) may depolarize the membrane due to a channel reversal potential around 0mV. Resultant ATP release from stimulated Panx1 can activate purinergic receptors, including P2X7 receptors...
September 5, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28886343/dominant-mutations-in-grm1-cause-spinocerebellar-ataxia-type-44
#10
Lauren M Watson, Elizabeth Bamber, Ricardo Parolin Schnekenberg, Jonathan Williams, Conceição Bettencourt, Jennifer Lickiss, Katherine Fawcett, Samuel Clokie, Yvonne Wallis, Penny Clouston, David Sims, Henry Houlden, Esther B E Becker, Andrea H Németh
The metabotropic glutamate receptor 1 (mGluR1) is abundantly expressed in the mammalian central nervous system, where it regulates intracellular calcium homeostasis in response to excitatory signaling. Here, we describe heterozygous dominant mutations in GRM1, which encodes mGluR1, that are associated with distinct disease phenotypes: gain-of-function missense mutations, linked in two different families to adult-onset cerebellar ataxia, and a de novo truncation mutation resulting in a dominant-negative effect that is associated with juvenile-onset ataxia and intellectual disability...
September 7, 2017: American Journal of Human Genetics
https://www.readbyqxmd.com/read/28882644/postsynaptic-n-type-or-p-q-type-calcium-channels-mediate-long-term-potentiation-by-group-i-metabotropic-glutamate-receptors-in-the-trigeminal-oralis
#11
Haein Weon, Tae Wan Kim, Dong-Ho Youn
AIMS: Both N-type and P/Q-type voltage-gated Ca(2+) channels (VGCCs) are involved in the induction of long-term potentiation (LTP), the long-lasting increase of synaptic strength, in the central nervous system. To provide further information on the roles of N-type and P/Q-type VGCCs in the induction of LTP at excitatory synapses of trigeminal primary afferents in the spinal trigeminal subnucleus oralis (Vo), we investigated whether they contribute to the induction of LTP by activation of group I metabotropic glutamate receptors (mGluRs)...
September 4, 2017: Life Sciences
https://www.readbyqxmd.com/read/28880414/levodopa-treatment-and-dendritic-spine-pathology
#12
REVIEW
Haruo Nishijima, Tatsuya Ueno, Yukihisa Funamizu, Shinya Ueno, Masahiko Tomiyama
Parkinson's disease (PD) is a neurodegenerative disorder associated with the progressive loss of nigrostriatal dopaminergic neurons. Levodopa is the most effective treatment for the motor symptoms of PD. However, chronic oral levodopa treatment can lead to various motor and nonmotor complications because of nonphysiological pulsatile dopaminergic stimulation in the brain. Examinations of autopsy cases with PD have revealed a decreased number of dendritic spines of striatal neurons. Animal models of PD have revealed altered density and morphology of dendritic spines of neurons in various brain regions after dopaminergic denervation or dopaminergic denervation plus levodopa treatment, indicating altered synaptic transmission...
September 7, 2017: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/28875233/glutamate-dependent-translational-control-of-glutamine-synthetase-in-bergmann-glia-cells
#13
Reynaldo Tiburcio-Félix, Miguel Escalante-López, Bruno López-Bayghen, Daniel Martínez, Luisa C Hernández-Kelly, Samuel Zinker, Dinorah Hernández-Melchor, Esther López-Bayghen, Tatiana N Olivares-Bañuelos, Arturo Ortega
Glutamate is the major excitatory transmitter of the vertebrate brain. It exerts its actions through the activation of specific plasma membrane receptors expressed both in neurons and in glial cells. Recent evidence has shown that glutamate uptake systems, particularly enriched in glia cells, trigger biochemical cascades in a similar fashion as receptors. A tight regulation of glutamate extracellular levels prevents neuronal overstimulation and cell death, and it is critically involved in glutamate turnover...
September 5, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28870203/the-dlgap-family-neuronal-expression-function-and-role-in-brain-disorders
#14
REVIEW
Andreas H Rasmussen, Hanne B Rasmussen, Asli Silahtaroglu
The neurotransmitter glutamate facilitates neuronal signalling at excitatory synapses. Glutamate is released from the presynaptic membrane into the synaptic cleft. Across the synaptic cleft glutamate binds to both ion channels and metabotropic glutamate receptors at the postsynapse, which expedite downstream signalling in the neuron. The postsynaptic density, a highly specialized matrix, which is attached to the postsynaptic membrane, controls this downstream signalling. The postsynaptic density also resets the synapse after each synaptic firing...
September 4, 2017: Molecular Brain
https://www.readbyqxmd.com/read/28868122/allicin-attenuates-tunicamycin-induced-cognitive-deficits-in-rats-via-its-synaptic-plasticity-regulatory-activity
#15
Qiong Xiang, Xian-Hui Li, Bo Yang, Xin-Xing Fang, Jing Jia, Jie Ren, Yu-Chun Dong, Cheng Ou-Yang, Guang-Cheng Wang
OBJECTIVES: To illuminate the functional effects of allicin on rats with cognitive deficits induced by tunicamycin (TM) and the molecular mechanism of this process. MATERIALS AND METHODS: 200-250 g male SD rats were divided into three groups at random: control group (n=12), TM group (5 μl, 50 μM, ICV, n=12), and allicin treatment group (180 mg/kg/d with chow diet, n=12). After 16 weeks of allicin treatment, the learning ability and memory were tested using novel object recognition (NOR) testing on rats with 72 hr TM treatment (5 μl, 50 μM, ICV); meanwhile, the variation of field excitatory postsynaptic potential (fEPSP) in the Schaffer Collateral (SC)-CA1 synapse was detected by extracellular electrophysiological recordings and the morphology of dendritic spine was observed by Golgi staining as well as detecting several synaptic plasticity-related proteins by Western blot...
June 2017: Iranian Journal of Basic Medical Sciences
https://www.readbyqxmd.com/read/28852612/bisphenol-a-impairs-synaptic-plasticity-by-both-pre-and-postsynaptic-mechanisms
#16
Fan Hu, Tingting Li, Huarui Gong, Zhi Chen, Yan Jin, Guangwei Xu, Ming Wang
Bisphenol A (BPA), an environmental xenoestrogen, has been reported to induce learning and memory impairments in rodent animals. However, effects of BPA exposure on synaptic plasticity and the underlying physiological mechanisms remain elusive. Our behavioral and electrophysiological analyses show that BPA obviously perturbs hippocampal spatial memory of juvenile Sprague-Dawley rats after four weeks exposure, with significantly impaired long-term potentiation (LTP) in the hippocampus. These effects involve decreased spine density of pyramidal neurons, especially the apical dendritic spine...
August 2017: Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
https://www.readbyqxmd.com/read/28844473/the-challenge-of-interpreting-glutamate-receptor-ion-channel-structures
#17
REVIEW
Mark L Mayer
Ion channels activated by glutamate mediate excitatory synaptic transmission in the central nervous system. Similar to other ligand-gated ion channels, their gating cycle begins with transitions from a ligand-free closed state to glutamate-bound active and desensitized states. In an attempt to reveal the molecular mechanisms underlying gating, numerous structures for glutamate receptors have been solved in complexes with agonists, antagonists, allosteric modulators, and auxiliary proteins. The embarrassingly rich library of structures emerging from this work reveals very dynamic molecules with a more complex conformational spectrum than anticipated from functional studies...
August 24, 2017: Biophysical Journal
https://www.readbyqxmd.com/read/28831734/interactions-of-hallucinogens-with-the-glutamatergic-system-permissive-network-effects-mediated-through-cortical-layer-v-pyramidal-neurons
#18
Gerard J Marek
Recordings made from layer V (L5) pyramidal cells of the prefrontal cortex (PFC) and neocortex in rodent slice preparations have shown that serotonin (5-hydroxytryptamine, 5-HT) and serotonergic hallucinogens induce an increase in the frequency of spontaneous excitatory postsynaptic currents (EPSCs) in the apical dendritic field by activating 5-HT2A receptors. Serotonergic hallucinogens induce late EPSCs and increase recurrent network activity when subcortical or mid-cortical regions are stimulated at low frequencies (e...
August 23, 2017: Current Topics in Behavioral Neurosciences
https://www.readbyqxmd.com/read/28828612/regulation-of-glutamate-transporter-expression-in-glial-cells
#19
Donají Chi-Castañeda, Edna Suárez-Pozos, Arturo Ortega
Glutamate (Glu) is the major excitatory neurotransmitter in the vertebrate central nervous system. During synaptic activity, Glu is released into the synaptic cleft and binds to Glu receptors activating a wide variety of signal transduction cascades. Extracellular Glu concentrations are maintained exclusively within physiological levels mainly by glial Glu transporters. Inefficient clearance of synaptic Glu may be neurotoxic owing to prolonged hyperactivation of postsynaptic Glu receptors, causing a multitude of intracellular events in the postsynaptic neuron, which ultimately results in neuronal cell death...
2017: Advances in Neurobiology
https://www.readbyqxmd.com/read/28828611/glial-glutamate-transporters-as-signaling-molecules
#20
Edna Suárez-Pozos, Donají Chi-Castañeda, Arturo Ortega
One of the most important processes of the synaptic transmission is neurotransmitter uptake, which is critical for the good performance of the nervous system by maintaining the neurotransmitter's baseline levels after its release. The major excitatory neurotransmitter in the central nervous system is glutamate; its extracellular levels are tightly regulated through high-affinity plasma membrane transporters. Most of the brain glutamate uptake activity is carried out by glial transporters that until recently have been regarded as important for the recycling of this excitatory amino acid...
2017: Advances in Neurobiology
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