The role of RIM1α in BDNF-enhanced glutamate release

2008 ◽  
Vol 55 (1) ◽  
pp. 27-34 ◽  
Author(s):  
Fatma Simsek-Duran ◽  
György Lonart
Keyword(s):  
Glutamate Release

scholarly journals The G Protein-Coupled Glutamate Receptors as Novel Molecular Targets in Schizophrenia Treatment—A Narrative Review

2021 ◽  
Vol 10 (7) ◽  
pp. 1475
Author(s):  
Waldemar Kryszkowski ◽  
Tomasz Boczek
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Glutamate Release ◽  
Molecular Targets ◽  
Brain Regions ◽  
Psychotic Symptoms ◽  
Unknown Etiology ◽  
Metabotropic Glutamate ◽  
G Protein Coupled

Schizophrenia is a severe neuropsychiatric disease with an unknown etiology. The research into the neurobiology of this disease led to several models aimed at explaining the link between perturbations in brain function and the manifestation of psychotic symptoms. The glutamatergic hypothesis postulates that disrupted glutamate neurotransmission may mediate cognitive and psychosocial impairments by affecting the connections between the cortex and the thalamus. In this regard, the greatest attention has been given to ionotropic NMDA receptor hypofunction. However, converging data indicates metabotropic glutamate receptors as crucial for cognitive and psychomotor function. The distribution of these receptors in the brain regions related to schizophrenia and their regulatory role in glutamate release make them promising molecular targets for novel antipsychotics. This article reviews the progress in the research on the role of metabotropic glutamate receptors in schizophrenia etiopathology.

scholarly journals Brain-Specific SNAP-25 Deletion Leads to Elevated Extracellular Glutamate Level and Schizophrenia-Like Behavior in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Hua Yang ◽  
Mengjie Zhang ◽  
Jiahao Shi ◽  
Yunhe Zhou ◽  
Zhipeng Wan ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Mouse Model ◽  
Glutamate Release ◽  
Critical Role ◽  
Conditional Knockout ◽  
Snare Complex ◽  
Extracellular Glutamate ◽  
Glutamate Level

Several studies have associated reduced expression of synaptosomal-associated protein of 25 kDa (SNAP-25) with schizophrenia, yet little is known about its role in the illness. In this paper, a forebrain glutamatergic neuron-specific SNAP-25 knockout mouse model was constructed and studied to explore the possible pathogenetic role of SNAP-25 in schizophrenia. We showed that SNAP-25 conditional knockout (cKO) mice exhibited typical schizophrenia-like phenotype. A significantly elevated extracellular glutamate level was detected in the cerebral cortex of the mouse model. Compared with Ctrls, SNAP-25 was dramatically reduced by about 60% both in cytoplasm and in membrane fractions of cerebral cortex of cKOs, while the other two core members of SNARE complex: Syntaxin-1 (increased ~80%) and Vamp2 (increased ~96%) were significantly increased in cell membrane part. Riluzole, a glutamate release inhibitor, significantly attenuated the locomotor hyperactivity deficits in cKO mice. Our findings provide in vivo functional evidence showing a critical role of SNAP-25 dysfunction on synaptic transmission, which contributes to the developmental of schizophrenia. It is suggested that a SNAP-25 cKO mouse, a valuable model for schizophrenia, could address questions regarding presynaptic alterations that contribute to the etiopathophysiology of SZ and help to consummate the pre- and postsynaptic glutamatergic pathogenesis of the illness.

scholarly journals Amperometric Measurement of Glutamate Release Modulation by Gabapentin and Pregabalin in Rat Neocortical Slices: Role of Voltage-Sensitive Ca2+ α2δ-1 Subunit

2011 ◽  
Vol 338 (1) ◽  
pp. 240-245 ◽  
Author(s):  
Jorge E. Quintero ◽  
David J. Dooley ◽  
François Pomerleau ◽  
Peter Huettl ◽  
Greg A. Gerhardt
Keyword(s):  
Glutamate Release

scholarly journals The Role of Glutamate Release on Voltage-Dependent Anion Channels (VDAC)-Mediated Apoptosis in an Eleven Vessel Occlusion Model in Rats

PLoS ONE ◽  
2010 ◽  
Vol 5 (12) ◽  
pp. e15192 ◽  
Author(s):  
Eunkuk Park ◽  
Gi-Ja Lee ◽  
Samjin Choi ◽  
Seok-Keun Choi ◽  
Su-Jin Chae ◽  
...  
Keyword(s):  
Glutamate Release ◽  
Anion Channels ◽  
Vessel Occlusion ◽  
Occlusion Model ◽  
Voltage Dependent

scholarly journals Alpha-1 Adrenergic Receptors Modulate Glutamate and GABA Neurotransmission onto Ventral Tegmental Dopamine Neurons during Cocaine Sensitization

2020 ◽  
Vol 21 (3) ◽  
pp. 790 ◽  
Author(s):  
Maria Carolina Velasquez-Martinez ◽  
Bermary Santos-Vera ◽  
Maria E. Velez-Hernandez ◽  
Rafael Vazquez-Torres ◽  
Carlos A. Jimenez-Rivera
Keyword(s):  
Glutamate Release ◽  
Cell Voltage ◽  
Gaba Release ◽  
Dopamine Neurons ◽  
Gamma Aminobutyric Acid ◽  
Gabaergic Neurotransmission ◽  
Cocaine Administration ◽  
Ventral Tegmental ◽  
Gaba Neurotransmission

The ventral tegmental area (VTA) plays an important role in the reward and motivational processes that facilitate the development of drug addiction. Presynaptic α1-AR activation modulates glutamate and Gamma-aminobutyric acid (GABA) release. This work elucidates the role of VTA presynaptic α1-ARs and their modulation on glutamatergic and GABAergic neurotransmission during cocaine sensitization. Excitatory and inhibitory currents (EPSCs and IPSCs) measured by a whole cell voltage clamp show that α1-ARs activation increases EPSCs amplitude after 1 day of cocaine treatment but not after 5 days of cocaine injections. The absence of a pharmacological response to an α1-ARs agonist highlights the desensitization of the receptor after repeated cocaine administration. The desensitization of α1-ARs persists after a 7-day withdrawal period. In contrast, the modulation of α1-ARs on GABA neurotransmission, shown by decreases in IPSCs’ amplitude, is not affected by acute or chronic cocaine injections. Taken together, these data suggest that α1-ARs may enhance DA neuronal excitability after repeated cocaine administration through the reduction of GABA inhibition onto VTA dopamine (DA) neurons even in the absence of α1-ARs’ function on glutamate release and protein kinase C (PKC) activation. α1-AR modulatory changes in cocaine sensitization increase our knowledge of the role of the noradrenergic system in cocaine addiction and may provide possible avenues for therapeutics.

scholarly journals APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Tomas Fanutza ◽  
Dolores Del Prete ◽  
Michael J Ford ◽  
Pablo E Castillo ◽  
Luciano D’Adamio
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transmitter Release ◽  
Glutamate Release ◽  
Hippocampal Slices ◽  
Synaptic Release ◽  
Hippocampal Synapses ◽  
A Cell ◽  
Acute Hippocampal Slices

The amyloid precursor protein (APP), whose mutations cause familial Alzheimer’s disease, interacts with the synaptic release machinery, suggesting a role in neurotransmission. Here we mapped this interaction to the NH2-terminal region of the APP intracellular domain. A peptide encompassing this binding domain -named JCasp- is naturally produced by a γ-secretase/caspase double-cut of APP. JCasp interferes with the APP-presynaptic proteins interaction and, if linked to a cell-penetrating peptide, reduces glutamate release in acute hippocampal slices from wild-type but not APP deficient mice, indicating that JCasp inhibits APP function.The APP-like protein-2 (APLP2) also binds the synaptic release machinery. Deletion of APP and APLP2 produces synaptic deficits similar to those caused by JCasp. Our data support the notion that APP and APLP2 facilitate transmitter release, likely through the interaction with the neurotransmitter release machinery. Given the link of APP to Alzheimer’s disease, alterations of this synaptic role of APP could contribute to dementia.

scholarly journals Estrogenic-dependent glutamatergic neurotransmission from kisspeptin neurons governs feeding circuits in females

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Jian Qiu ◽  
Heidi M Rivera ◽  
Martha A Bosch ◽  
Stephanie L Padilla ◽  
Todd L Stincic ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Arcuate Nucleus ◽  
Neuronal Excitability ◽  
Glutamate Release ◽  
Metabotropic Receptors ◽  
Hypothalamic Arcuate Nucleus ◽  
17Β Estradiol ◽  
Arcuate Neurons ◽  
Feeding Circuits

The neuropeptides tachykinin2 (Tac2) and kisspeptin (Kiss1) in hypothalamic arcuate nucleus Kiss1 (Kiss1ARH) neurons are essential for pulsatile release of GnRH and reproduction. Since 17β-estradiol (E2) decreases Kiss1 and Tac2 mRNA expression in Kiss1ARH neurons, the role of Kiss1ARH neurons during E2-driven anorexigenic states and their coordination of POMC and NPY/AgRP feeding circuits have been largely ignored. Presently, we show that E2 augmented the excitability of Kiss1ARH neurons by amplifying Cacna1g, Hcn1 and Hcn2 mRNA expression and T-type calcium and h-currents. E2 increased Slc17a6 mRNA expression and glutamatergic synaptic input to arcuate neurons, which excited POMC and inhibited NPY/AgRP neurons via metabotropic receptors. Deleting Slc17a6 in Kiss1 neurons eliminated glutamate release and led to conditioned place preference for sucrose in E2-treated KO female mice. Therefore, the E2-driven increase in Kiss1 neuronal excitability and glutamate neurotransmission may play a key role in governing the motivational drive for palatable food in females.

Deciphering the Role of Glutamate Signaling in Glioblastoma Multiforme: Current Therapeutic Modalities and Future Directions

2020 ◽  
Vol 26 (37) ◽  
pp. 4777-4788 ◽  
Author(s):  
Hamid Mollazadeh ◽  
Elmira Mohtashami ◽  
Seyed H. Mousavi ◽  
Mohammad Soukhtanloo ◽  
Mohammad M. Vahedi ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Current Knowledge ◽  
Glutamate Release ◽  
Receptor Activation ◽  
Invasion And Migration ◽  
Glutamate Signaling ◽  
Therapeutic Modalities ◽  
Glutamatergic Signaling ◽  
And Migration

As the most popular intrinsic neoplasm throughout the brain, glioblastoma multiforme (GBM) is resistant to existing therapies. Due to its invasive nature, GBM shows a poor prognosis despite aggressive surgery and chemoradiation. Therefore, identifying and understanding the critical molecules of GBM can help develop new therapeutic strategies. Glutamatergic signaling dysfunction has been well documented in neurodegenerative diseases as well as in GBM. Inhibition of glutamate receptor activation or extracellular glutamate release by specific antagonists inhibits cell development, invasion, and migration and contributes to apoptosis and autophagy in GBM cells. This review outlines the current knowledge of glutamate signaling involvement and current therapeutic modalities for the treatment of GBM.

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