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Neurotransmitter Glutamate (neurotransmitter + glutamate)
Kinds of Neurotransmitter Glutamate Selected AbstractsSynapse-specific localization of vesicular glutamate transporters in the rat olfactory bulbEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2007Marie-Madeleine Gabellec Abstract Vesicular glutamate transporters (VGLUTs) mediate the packaging of the excitatory neurotransmitter glutamate into synaptic vesicles. Three VGLUT subtypes have so far been identified, with distinct expression patterns in the adult brain. Here, we investigated the spatial distribution of the three VGLUTs in the rat olfactory bulb, a brain region containing a variety of glutamate synapses, both axodendritic and dendrodendritic. Using multilabelling confocal microscopy and electron microscopic immunocytochemistry, we showed that each VGLUT isoform has a highly selective localization in olfactory bulb synapses. VGLUT1 is present at dendrodendritic synapses established by the output neurones (mitral and tufted cells) with bulbar interneurones in the glomerular layer and external plexiform layer, as well as in axonal synapses of the granule cell layer. By contrast, VGLUT2 is strongly expressed in axon terminals of olfactory sensory neurones, which establish synapses with second-order neurones in the glomerular neuropil. VGLUT2 is also found in the outer part of the external plexiform layer and in the granule cell layer but colocalizes only partially with VGLUT1. Finally, we showed that VGLUT3 is exclusively located in the glomerular neuropil, where it colocalizes extensively with the vesicular inhibitory amino acid transporter vesicular GABA transporter, suggesting that it is associated with a subset of inhibitory synapses. Together, these observations extend previous findings on VGLUT distribution in the forebrain, and suggest that each VGLUT subtype has a specific function in the distinct features of axodendritic and dendrodendritic synapses that characterize the olfactory bulb circuit. [source] Glutamatergic neurons are present in the rat ventral tegmental areaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2007Tsuyoshi Yamaguchi Abstract The ventral tegmental area (VTA) is thought to play an important role in reward function. Two populations of neurons, containing either dopamine (DA) or ,-amino butyric acid (GABA), have been extensively characterized in this area. However, recent electrophysiological studies are consistent with the notion that neurons that utilize neurotransmitters other than DA or GABA are likely to be present in the VTA. Given the pronounced phenotypic diversity of neurons in this region, we have proposed that additional cell types, such as those that express the neurotransmitter glutamate may also be present in this area. Thus, by using in situ hybridization histochemistry we investigated whether transcripts encoded by genes for the two vesicular glutamate transporters, VGluT1 or VGluT2, were expressed in the VTA. We found that VGluT2 mRNA but not VGluT1 mRNA is expressed in the VTA. Neurons expressing VGluT2 mRNA were differentially distributed throughout the rostro-caudal and medio-lateral aspects of the VTA, with the highest concentration detected in rostro-medial areas. Phenotypic characterization with double in situ hybridization of these neurons indicated that they rarely co,expressed mRNAs for tyrosine hydroxylase (TH, marker for DAergic neurons) or glutamic acid decarboxylase (GAD, marker for GABAergic neurons). Based on the results described here, we concluded that the VTA contains glutamatergic neurons that in their vast majority are clearly non-DAergic and non-GABAergic. [source] Glutamate regulates retinal progenitors cells proliferation during developmentEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2006Rodrigo A. P. Martins Abstract The precise coordination of cell cycle exit and cell fate specification is essential for generating the correct proportion of retinal cell types during development. The decision to exit the cell cycle is regulated by intrinsic and extrinsic cues. There is growing evidence that neurotransmitters can regulate cell proliferation and cell fate specification during the early stages of CNS development prior to the formation of synaptic connections. We found that the excitatory neurotransmitter glutamate regulates retinal progenitor cell proliferation during embryonic development of the mouse. AMPA/kainate and N -methyl- d -aspartate receptors are expressed in embryonic retinal progenitor cells. Addition of exogenous glutamate leads to a dose-dependent decrease in cell proliferation without inducing cell death or activating the p53 pathway. Activation of AMPA/kainate receptors induced retinal progenitor cells to prematurely exit the cell cycle. Using a replication-incompetent retrovirus to follow the clonal expansion of individual retinal progenitor cells, it was observed that blockade of AMPA/kainate receptors increased the proportion of large clones, showing that modulation of endogenous glutamatergic activity can have long-term consequences on retinal cell proliferation. Real time reverse transcriptase-polymerase chain reaction and immunoblot analyses demonstrated that glutamate does not alter the levels of the mRNA and proteins that regulate the G1/S-phase transition. Instead, the activity of the Cdk2 kinase is reduced in the presence of glutamate. These data indicate that glutamate regulates retinal progenitor cell proliferation by post-translational modulation of cyclin/Cdk2 kinase activity. [source] Heterogeneous distribution of AMPA glutamate receptor subunits at the photoreceptor synapses of rodent retinaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2001Iris Hack Abstract In the retina the segregation of different aspects of visual information starts at the first synapse in signal transfer from the photoreceptors to the second-order neurons, via the neurotransmitter glutamate. We examined the distribution of the four AMPA glutamate receptor subunits GluR1,GluR4 at the photoreceptor synapses in mouse and rat retinae by light and immunoelectron microscopy and serial section reconstructions. On the dendrites of OFF-cone bipolar cells, which make flat, noninvaginating contacts postsynaptic at cone synaptic terminals, the subunits GluR1 and GluR2 were predominantly found. Horizontal cell processes postsynaptic at both rod and cone synaptic terminals preferentially expressed the subunits GluR2, GluR2/3 and GluR4. An intriguing finding was the presence of GluR2/3 and GluR4 subunits on dendrites of putative rod bipolar cells, which are thought to signal through the sign-inverting metabotropic glutamate receptor 6, mGluR6. Furthermore, at the rod terminals, horizontal cell processes and rod bipolar cell dendrites showed labelling for the AMPA receptor subunits at the ribbon synaptic site or perisynaptically at their site of invagination into the rod terminal. The wide distribution of AMPA receptor subunits at the photoreceptor synapses suggests that AMPA receptors play an important role in visual signal transfer from the photoreceptors to their postsynaptic partners. [source] Effect of exogenous glutamate and N-Methyl-D-aspartic acid on spontaneous activity of isolated human ureterINTERNATIONAL JOURNAL OF UROLOGY, Issue 9 2007Slobodan M Jankovic Objectives: While the neurotransmitter role of glutamate in the gastrointestinal tract has been shown, its effects on smooth muscle of the human ureter have not previously been investigated. In our study we have investigated the effects of exogenous glutamate on the spontaneous activity of isolated human ureter, taken from 14 adult patients after nephrectomy. Methods: The segment of ureter, excised 3 cm distal from the pyeloureteral junction, was isolated in an organ bath. Both longitudinal tension and intraluminal pressure of the segment were recorded simultaneously. Results: Glutamate administered in the lumen of the isolated ureteral segments (7.8 × 10,7 M/L,3.5 × 10,2 M/L) was ineffective. When added to the isolated organ bath from the serous side of the ureteral segment, glutamate (7.9 × 10,6 M/L,10.6 × 10,3 M/L) and N-Methyl-D-aspartic acid (NMDA) (9.1 × 10,8 M/L,3.1 × 10,5 M/L) produced a concentration-dependent increase in spontaneous activity of the isolated preparations, while kainic acid (6.3 × 10,8 M/L,10.5 × 10,5 M/L) and (+/,)- trans -1-Aminocyclopentane- trans -1,3-dicarboxylic acid (ACPD) (7.7 × 10,8 M/L ,6.5 × 10,5 M/L) were ineffective. Conclusions: The results of our study suggest that an excitatory neurotransmitter glutamate stimulates spontaneous activity of the human ureter through activation of NMDA ionotropic receptors, located on smooth muscle cells or intramural nerve fibers [source] The glutamate/GABA-glutamine cycle: aspects of transport, neurotransmitter homeostasis and ammonia transferJOURNAL OF NEUROCHEMISTRY, Issue 3 2006Lasse K. Bak Abstract Neurons are metabolically handicapped in the sense that they are not able to perform de novo synthesis of neurotransmitter glutamate and ,-aminobutyric acid (GABA) from glucose. A metabolite shuttle known as the glutamate/GABA-glutamine cycle describes the release of neurotransmitter glutamate or GABA from neurons and subsequent uptake into astrocytes. In return, astrocytes release glutamine to be taken up into neurons for use as neurotransmitter precursor. In this review, the basic properties of the glutamate/GABA-glutamine cycle will be discussed, including aspects of transport and metabolism. Discussions of stoichiometry, the relative role of glutamate vs. GABA and pathological conditions affecting the glutamate/GABA-glutamine cycling are presented. Furthermore, a section is devoted to the accompanying ammonia homeostasis of the glutamate/GABA-glutamine cycle, examining the possible means of intercellular transfer of ammonia produced in neurons (when glutamine is deamidated to glutamate) and utilized in astrocytes (for amidation of glutamate) when the glutamate/GABA-glutamine cycle is operating. A main objective of this review is to endorse the view that the glutamate/GABA-glutamine cycle must be seen as a bi-directional transfer of not only carbon units but also nitrogen units. [source] Fast food delivery: the response of nursing astrocytes to an exciting call from neuronsJOURNAL OF NEUROCHEMISTRY, Issue 2003L. Pellerin It was suggested long time ago that astrocytes might play a prominent role in the distribution of energy substrates to neurons but convincing evidence was lacking. More recently, the excitatory neurotransmitter glutamate was shown to enhance aerobic glycolysis in cultured cortical astrocytes by a mechanism involving glial glutamate transporters. Using specific knockout mice for these transporters, it was demonstrated that a classical metabolic response to neuronal activation in the whisker-to-barrel system, 2-deoxyglucose accumulation, was disrupted in the somatosensory cortex of these animals at postnatal day 10. From these data, it was concluded that a net transfer of some energy substrate, preferentially lactate, must be taking place in order to fulfill increasing neuronal energy needs during periods of enhanced activity. In support of this concept, the presence of specific transporters for lactate, known as monocarboxylate transporters, was recently described both on astrocytes and neurons in vitro as well as in vivo. [source] Postnatal changes of vesicular glutamate transporter (VGluT)1 and VGluT2 immunoreactivities and their colocalization in the mouse forebrainTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 3 2005Kouichi Nakamura Abstract Vesicular glutamate transporter 1 (VGluT1) and VGluT2 accumulate neurotransmitter glutamate into synaptic vesicles at presynaptic terminals, and their antibodies are thus considered to be a good marker for glutamatergic axon terminals. In the present study, we investigated the postnatal development and maturation of glutamatergic neuronal systems by single- and double-immunolabelings for VGluT1 and VGluT2 in mouse forebrain including the telencephalon and diencephalon. VGluT2 immunoreactivity was widely distributed in the forebrain, particularly in the diencephalon, from postnatal day 0 (P0) to adulthood, suggesting relatively early maturation of VGluT2-loaded glutamatergic axons. In contrast, VGluT1 immunoreactivity was intense only in the limbic regions at P0, and drastically increased in the other telencephalic and diencephalic regions during three postnatal weeks. Interestingly, VGluT1 immunoreactivity was frequently colocalized with VGluT2 immunoreactivity at single axon terminal-like profiles in layer IV of the primary somatosensory area from P5 to P10 and in the ventral posteromedial thalamic nucleus from P0 to P14. This was in sharp contrast to the finding that almost no colocalization was found in glomeruli of the olfactory bulb, patchy regions of the caudate-putamen, and the ventral posterolateral thalamic nucleus, where moderate to intense immunoreactivities for VGluT1 and VGluT2 were intermingled with each other in neuropil during postnatal development. The present results indicate that VGluT2-loaded glutamatergic axons maturate earlier than VGluT1-laden axons in the mouse telencephalic and diencephalic regions, and suggest that VGluT1 plays a transient developmental role in some glutamatergic systems that mainly use VGluT2 in the adulthood. J. Comp. Neurol. 492:263,288, 2005. © 2005 Wiley-Liss, Inc. [source] Modulation of synaptic plasticity by stress and antidepressantsBIPOLAR DISORDERS, Issue 3 2002Maurizio Popoli Recent preclinical and clinical studies have shown that mechanisms underlying neuronal plasticity and survival are involved in both the outcome of stressful experiences and the action of antidepressants. Whereas most antidepressants predominantly affect the brain levels of monoamine neurotransmitters, it is increasingly appreciated that they also modulate neurotransmission at synapses using the neurotransmitter glutamate (the most abundant in the brain). In the hippocampus, a main area of the limbic system involved in cognitive functions as well as attention and affect, specific molecules enriched at glutamatergic synapses mediate major changes in synaptic plasticity induced by stress paradigms or antidepressant treatments. We analyze here the modifications induced by stress or antidepressants in the strength of synaptic transmission in hippocampus, and the molecular modifications induced by antidepressants in two main mediators of synaptic plasticity: the N -methyl- D -aspartate (NMDA) receptor complex for glutamate and the Ca2+/calmodulin-dependent protein kinase II (CaM kinase II). Both stress and antidepressants induce alterations in long-term potentiation of hippocampal glutamatergic synapses, which may be partly accounted for by the influence of environmental or drug-induced stimulation of monoaminergic pathways projecting to the hippocampus. In the course of antidepressant treatments significant changes have been described in both the NMDA receptor and CaM kinase II, which may account for the physiological changes observed. A central role in these synaptic changes is exerted by brain-derived neurotrophic factor (BDNF), which modulates both synaptic plasticity and its molecular mediators, as well as inducing morphological synaptic changes. The role of these molecular effectors in synaptic plasticity is discussed in relation to the action of antidepressants and the search for new molecular targets of drug action in the therapy of mood disorders. [source] | |||||||||||||