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Journal articles on the topic 'GABA, glutamate,synapses'

Author: Grafiati

Published: 14 March 2023

Last updated: 31 July 2025

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1

Khatri, Shailesh N., Wan-Chen Wu, Ying Yang, and Jason R. Pugh. "Direction of action of presynaptic GABAA receptors is highly dependent on the level of receptor activation." Journal of Neurophysiology 121, no. 5 (2019): 1896–905. http://dx.doi.org/10.1152/jn.00779.2018.

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Many synapses, including parallel fiber synapses in the cerebellum, express presynaptic GABAA receptors. However, reports of the functional consequences of presynaptic GABAA receptor activation are variable across synapses, from inhibition to enhancement of transmitter release. We find that presynaptic GABAA receptor function is bidirectional at parallel fiber synapses depending on GABA concentration and modulation of GABAA receptors in mice. Activation of GABAA receptors by low GABA concentrations enhances glutamate release, whereas activation of receptors by higher GABA concentrations inhibi

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2

Gundersen, Vidar, Frode Fonnum, Ole Petter Ottersen, and Jon Storm-Mathisen. "Redistribution of Neuroactive Amino Acids in Hippocampus and Striatum during Hypoglycemia: A Quantitative Immunogold Study." Journal of Cerebral Blood Flow & Metabolism 21, no. 1 (2001): 41–51. http://dx.doi.org/10.1097/00004647-200101000-00006.

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Postembedding immunocytochemistry was used to localize aspartate, glutamate, gamma-aminobutyric acid (GABA), and glutamine in hippocampus and striatum during normo- and hypoglycemia in rat. In both brain regions, hypoglycemia caused aspartatelike immunoreactivity to increase. In hippocampus, this increase was evident particularly in the terminals of known excitatory afferents—in GABA-ergic neurons and myelinated axons. Aspartate was enriched along with glutamate in nerve terminals forming asymmetric synapses on spines and with GABA in terminals forming symmetric synapses on granule and pyramid

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3

Kaneda, Katsuyuki, and Hitoshi Kita. "Synaptically Released GABA Activates Both Pre- and Postsynaptic GABAB Receptors in the Rat Globus Pallidus." Journal of Neurophysiology 94, no. 2 (2005): 1104–14. http://dx.doi.org/10.1152/jn.00255.2005.

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The globus pallidus (GP) contains abundant GABAergic synapses and GABAB receptors. To investigate whether synaptically released GABA can activate pre- and postsynaptic GABAB receptors in the GP, physiological recordings were performed using rat brain slice preparations. Cell-attached recordings from GABAA antagonist-treated preparations revealed that repetitive local stimulation induced a GABAB antagonist-sensitive pause in spontaneous firings of GP neurons. Whole cell recordings revealed that the repetitive stimulation evoked fast excitatory postsynaptic potentials followed by a slow inhibito

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DeFazio, R. Anthony, Ami P. Raval, Hung W. Lin, Kunjan R. Dave, David Della-Morte та Miguel A. Perez-Pinzon. "GABA Synapses Mediate Neuroprotection after Ischemic and εPKC Preconditioning in Rat Hippocampal Slice Cultures". Journal of Cerebral Blood Flow & Metabolism 29, № 2 (2008): 375–84. http://dx.doi.org/10.1038/jcbfm.2008.126.

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Delayed neuroprotection against ischemic challenges is conferred by both ischemic preconditioning (IPC) and preconditioning by activation of the ε-isoform of protein kinase C (εPKC-PC). In vivo, ischemic preconditioning enhances GABA release and ameliorates glutamate release during lethal cerebral ischemia. We tested the hypothesis that IPC and εPKC-PC confer neuroprotection by GABA synapses in rat organotypic hippocampal slices. Ischemic preconditioning or εPKC-PC was induced with 15 mins oxygen-glucose deprivation (OGD) or ψεRACK, a selective εPKC activator; and test ischemia consisted of 40

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Walls, Anne B., Elvar M. Eyjolfsson, Olav B. Smeland, et al. "Knockout of GAD65 has Major Impact on Synaptic GABA Synthesized from Astrocyte-Derived Glutamine." Journal of Cerebral Blood Flow & Metabolism 31, no. 2 (2010): 494–503. http://dx.doi.org/10.1038/jcbfm.2010.115.

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γ-Aminobutyric acid (GABA) synthesis from glutamate is catalyzed by glutamate decarboxylase (GAD) of which two isoforms, GAD65 and GAD67, have been identified. The GAD65 has repeatedly been shown to be important during intensified synaptic activity. To specifically elucidate the significance of GAD65 for maintenance of the highly compartmentalized intracellular and intercellular GABA homeostasis, GAD65 knockout and corresponding wild-type mice were injected with [1-13C]glucose and the astrocyte-specific substrate [1,2-13C]acetate. Synthesis of GABA from glutamine in the GABAergic synapses was

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Liao, Fei, Haitao Liu, Santiago Milla-Navarro, Pedro de la Villa, and Francisco Germain. "Origin of Retinal Oscillatory Potentials in the Mouse, a Tool to Specifically Locate Retinal Damage." International Journal of Molecular Sciences 24, no. 4 (2023): 3126. http://dx.doi.org/10.3390/ijms24043126.

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To determine the origin of oscillatory potentials (OPs), binocular electroretinogram (ERG) recordings were performed under light and dark adaptation on adult healthy C57BL/6J mice. In the experimental group, 1 μL of PBS was injected into the left eye, while the right eye was injected with 1 μL of PBS containing different agents: APB, GABA, Bicuculline, TPMPA, Glutamate, DNQX, Glycine, Strychnine, or HEPES. The OP response depends on the type of photoreceptors involved, showing their maximum response amplitude in the ERG induced by mixed rod/cone stimulation. The oscillatory components of the O

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Sethuramanujam, Santhosh, and Malcolm M. Slaughter. "Disinhibitory recruitment of NMDA receptor pathways in retina." Journal of Neurophysiology 112, no. 1 (2014): 193–203. http://dx.doi.org/10.1152/jn.00817.2013.

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Glutamate release at bipolar to ganglion cell synapses activates NMDA and AMPA/kainic acid (KA) ionotropic glutamate receptors. Their relative strength determines the output signals of the retina. We found that this balance is tightly regulated by presynaptic inhibition that preferentially suppresses NMDA receptor (NMDAR) activation. In transient ON-OFF neurons, block of GABA and glycine feedback enhanced total NMDAR charge by 35-fold in the ON response and 9-fold in the OFF compared with a 1.7-fold enhancement of AMPA/KA receptors. Blocking only glycine receptors enhanced the NMDAR excitatory

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8

Yamamoto, Ryo, Takafumi Furuyama, Tokio Sugai, Munenori Ono, Denis Pare, and Nobuo Kato. "Serotonergic control of GABAergic inhibition in the lateral amygdala." Journal of Neurophysiology 123, no. 2 (2020): 670–81. http://dx.doi.org/10.1152/jn.00500.2019.

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Much evidence implicates the serotonergic regulation of the amygdala in anxiety. Thus the present study was undertaken to characterize the influence of serotonin (5-HT) on principal neurons (PNs) of the rat lateral amygdala (LA), using whole cell recordings in vitro. Because inhibition is a major determinant of PN activity, we focused on the control of GABAergic transmission by 5-HT. IPSCs were elicited by local electrical stimulation of LA in the presence of glutamate receptor antagonists. We found that 5-HT reduces GABAA inhibitory postsynaptic currents (IPSCs) via presynaptic 5-HT1B recepto

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Nurullin, L. F., N. D. Almazov, and E. M. Volkov. "Immunofluorescent Identification of GABAergic Structures in the Somatic Muscle of the Earthworm <i>Lumbricus terrestris</i>." Биологические мембраны Журнал мембранной и клеточной биологии 40, no. 6 (2023): 449–55. http://dx.doi.org/10.31857/s0233475523060075.

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Using the immunofluorescence confocal microscopy, we detected the following GABAergic structures in the somatic muscle of the body wall of the earthworm: neurotransmitter gamma-aminobutyric acid (GABA); the enzyme responsible for synthesis of GABA, glutamate decarboxylase; type 1, 2, and 3 membrane transporters of GABA providing its reuptake; pre- and postsynaptic type A (ionotropic) and type B (metabotropic) GABA receptors. These structures are localized in the areas of cholinergic neuromuscular synapses. We assume that GABA can participate in modulation of motor activity of the earthworm som

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10

Chéry, Nadège, and Yves De Koninck. "GABAB Receptors Are the First Target of Released GABA at Lamina I Inhibitory Synapses in the Adult Rat Spinal Cord." Journal of Neurophysiology 84, no. 2 (2000): 1006–11. http://dx.doi.org/10.1152/jn.2000.84.2.1006.

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We have previously provided functional evidence that glycine and GABA are contained in the same synaptic vesicles and coreleased at the same synapses in lamina I of the rat spinal dorsal horn. However, whereas both glycine receptors (GlyRs) and GABAA receptors (GABAARs) are expressed on the postsynaptic target, under certain conditions inhibitory events appeared to be mediated by GlyRs only. We therefore wanted to test whether GABAB receptors could be activated in conditions where GABA released was insufficient to activate GABAARs. Focal stimulation in the vicinity of visually identified lamin

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Aroniadou-Anderjaska, Vassiliki, Fu-Ming Zhou, Catherine A. Priest, Matthew Ennis, and Michael T. Shipley. "Tonic and Synaptically Evoked Presynaptic Inhibition of Sensory Input to the Rat Olfactory Bulb Via GABABHeteroreceptors." Journal of Neurophysiology 84, no. 3 (2000): 1194–203. http://dx.doi.org/10.1152/jn.2000.84.3.1194.

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Olfactory receptor neurons of the nasal epithelium send their axons, via the olfactory nerve (ON), to the glomeruli of the olfactory bulb (OB), where the axon terminals form glutamatergic synapses with the apical dendrites of mitral and tufted cells, the output cells of the OB, and with juxtaglomerular (JG) interneurons. Many JG cells are GABAergic. Here we show that, despite the absence of conventional synapses, GABA released from JG cells activates GABAB receptors on ON terminals and inhibits glutamate release both tonically and in response to ON stimulation. Field potential recordings and c

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Wang, Huaixing, and Julie S. Haas. "GABABR Modulation of Electrical Synapses and Plasticity in the Thalamic Reticular Nucleus." International Journal of Molecular Sciences 22, no. 22 (2021): 12138. http://dx.doi.org/10.3390/ijms222212138.

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Two distinct types of neuronal activity result in long-term depression (LTD) of electrical synapses, with overlapping biochemical intracellular signaling pathways that link activity to synaptic strength, in electrically coupled neurons of the thalamic reticular nucleus (TRN). Because components of both signaling pathways can also be modulated by GABAB receptor activity, here we examined the impact of GABAB receptor activation on the two established inductors of LTD in electrical synapses. Recording from patched pairs of coupled rat neurons in vitro, we show that GABAB receptor inactivation its

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Case, Daniel T., and Deda C. Gillespie. "Pre- and postsynaptic properties of glutamatergic transmission in the immature inhibitory MNTB-LSO pathway." Journal of Neurophysiology 106, no. 5 (2011): 2570–79. http://dx.doi.org/10.1152/jn.00644.2010.

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The lateral superior olive (LSO) integrates excitatory inputs driven by sound arriving at the ipsilateral ear with inhibitory inputs driven by sound arriving at the contralateral ear in order to compute interaural intensity differences needed for localizing high-frequency sound sources. Specific mechanisms necessary for developmental refinement of the inhibitory projection, which arises from the medial nucleus of the trapezoid body (MNTB), have only been partially deciphered. The demonstration that immature MNTB-LSO synapses release glutamate has led to a model in which early glutamate neurotr

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Lalo, Ulyana, Jemma Andrew, Oleg Palygin, and Yuriy Pankratov. "Ca2+-dependent modulation of GABAA and NMDA receptors by extracellular ATP: implication for function of tripartite synapse." Biochemical Society Transactions 37, no. 6 (2009): 1407–11. http://dx.doi.org/10.1042/bst0371407.

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The importance of communication between neuronal and glial cells for brain function is recognized by a modern concept of ‘tripartite synapse’. Astrocytes enwrap synapses and can modulate their activity by releasing gliotransmitters such as ATP, glutamate and D-serine. One of the regulatory pathways in the tripartite synapse is mediated by P2X purinoreceptors. Release of ATP from synaptic terminals and astrocytes activates Ca2+ influx via P2X purinoreceptors which co-localize with NMDA (N-methyl-D-aspartate) and GABA (γ-aminobutyric acid) receptors and can modulate their activity via intracellu

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15

Ben-Ari, Yehezkel, Jean-Luc Gaiarsa, Roman Tyzio, and Rustem Khazipov. "GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations." Physiological Reviews 87, no. 4 (2007): 1215–84. http://dx.doi.org/10.1152/physrev.00017.2006.

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Developing networks follow common rules to shift from silent cells to coactive networks that operate via thousands of synapses. This review deals with some of these rules and in particular those concerning the crucial role of the neurotransmitter γ-aminobuytric acid (GABA), which operates primarily via chloride-permeable GABAAreceptor channels. In all developing animal species and brain structures investigated, neurons have a higher intracellular chloride concentration at an early stage leading to an efflux of chloride and excitatory actions of GABA in immature neurons. This triggers sodium sp

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Hoffpauir, Brian K., and Evanna L. Gleason. "Activation of mGluR5 Modulates GABAA Receptor Function in Retinal Amacrine Cells." Journal of Neurophysiology 88, no. 4 (2002): 1766–76. http://dx.doi.org/10.1152/jn.2002.88.4.1766.

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Amacrine cells in the vertebrate retina receive glutamatergic input from bipolar cells and make synapses onto bipolar cells, ganglion cells, and other amacrine cells. Recent studies indicate that amacrine cells express metabotropic glutamate receptors (mGluRs) and that signaling within the inner plexiform layer (IPL) of the retina might be modulated by mGluR activity. This study tests the hypothesis that activation of mGluR5 modulates GABAA receptor function in retinal amacrine cells. Whole cell voltage-clamp recordings were combined with pharmacology to establish the identity of the ionotropi

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17

Moulder, K. L., X. Jiang, A. A. Taylor, W. Shin, K. D. Gillis, and S. Mennerick. "Vesicle Pool Heterogeneity at Hippocampal Glutamate and GABA Synapses." Journal of Neuroscience 27, no. 37 (2007): 9846–54. http://dx.doi.org/10.1523/jneurosci.2803-07.2007.

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18

Hirasawa, Hajime, Massimo Contini, and Elio Raviola. "Extrasynaptic release of GABA and dopamine by retinal dopaminergic neurons." Philosophical Transactions of the Royal Society B: Biological Sciences 370, no. 1672 (2015): 20140186. http://dx.doi.org/10.1098/rstb.2014.0186.

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In the mouse retina, dopaminergic amacrine (DA) cells synthesize both dopamine and GABA. Both transmitters are released extrasynaptically and act on neighbouring and distant retinal neurons by volume transmission. In simultaneous recordings of dopamine and GABA release from isolated perikarya of DA cells, a proportion of the events of dopamine and GABA exocytosis were simultaneous, suggesting co-release. In addition, DA cells establish GABAergic synapses onto AII amacrine cells, the neurons that transfer rod bipolar signals to cone bipolars. GABA A but not dopamine receptors are clustered in t

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Keable, Ryan, Iryna Leshchyns’ka, and Vladimir Sytnyk. "Trafficking and Activity of Glutamate and GABA Receptors: Regulation by Cell Adhesion Molecules." Neuroscientist 26, no. 5-6 (2020): 415–37. http://dx.doi.org/10.1177/1073858420921117.

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The efficient targeting of ionotropic receptors to postsynaptic sites is essential for the function of chemical excitatory and inhibitory synapses, constituting the majority of synapses in the brain. A growing body of evidence indicates that cell adhesion molecules (CAMs), which accumulate at synapses at the earliest stages of synaptogenesis, are critical for this process. A diverse variety of CAMs assemble into complexes with glutamate and GABA receptors and regulate the targeting of these receptors to the cell surface and synapses. Presynaptically localized CAMs provide an additional level o

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Otis, T. S., and I. Mody. "Differential activation of GABAA and GABAB receptors by spontaneously released transmitter." Journal of Neurophysiology 67, no. 1 (1992): 227–35. http://dx.doi.org/10.1152/jn.1992.67.1.227.

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1. Whole-cell patch-clamp techniques were used to record from dentate gyrus granule cells in adult rat brain slices when N-methyl-D-aspartate (NMDA) and non-NMDA type glutamate receptors were blocked by D-2-amino-5-phosphonovaleric acid (D-AP5) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), respectively. Spontaneous inhibitory postsynaptic currents (sIPSCs), each presumably due to vesicular release of gamma-aminobutyric acid (GABA), selectively activated GABAA-type receptors. None of the individual sIPSCs showed a slow-onset potassium current characteristic of GABAB receptor activation. 2. I

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Verkhratsky, Alexei, and Maiken Nedergaard. "The homeostatic astroglia emerges from evolutionary specialization of neural cells." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1700 (2016): 20150428. http://dx.doi.org/10.1098/rstb.2015.0428.

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Evolution of the nervous system progressed through cellular diversification and specialization of functions. Conceptually, the nervous system is composed from electrically excitable neuronal networks connected with chemical synapses and non-excitable glial cells that provide for homeostasis and defence. Astrocytes are integrated into neural networks through multipartite synapses; astroglial perisynaptic processes closely enwrap synaptic contacts and control homeostasis of the synaptic cleft, supply neurons with glutamate and GABA obligatory precursor glutamine and contribute to synaptic plasti

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Stewart, R. R., D. J. Zou, J. M. Treherne, K. Mollgard, N. R. Saunders, and J. G. Nicholls. "The intact central nervous system of the newborn opossum in long-term culture: fine structure and GABA-mediated inhibition of electrical activity." Journal of Experimental Biology 161, no. 1 (1991): 25–41. http://dx.doi.org/10.1242/jeb.161.1.25.

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1. The entire central nervous system (CNS) of the newly born, South American opossum (Monodelphis domestica) was isolated and maintained in basal medium, Eagle's (BME) with 0.2% foetal calf serum and antibiotics. Isolated CNS preparations remained electrically excitable for up to 10 days. The fine structure of the spinal cord was normal after 5 days in culture: axons, synapses, dendrites and glia were virtually unchanged. Signs of degeneration were evident only in dorsal areas of the spinal cord, which had been denervated by removal of the dorsal root ganglia during dissection. 2. Amino acid t

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Speed, Haley E., and Lynn E. Dobrunz. "Developmental Decrease in Short-Term Facilitation at Schaffer Collateral Synapses in Hippocampus Is mGluR1 Sensitive." Journal of Neurophysiology 99, no. 2 (2008): 799–813. http://dx.doi.org/10.1152/jn.00625.2007.

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Developmental changes can occur in the dynamic properties of synapses, known as short-term plasticity. Using rat acute hippocampal slices at room temperature, we have previously shown a decrease in short-term facilitation at Schaffer collateral synapses from young adults compared with juveniles in response to temporally complex natural stimulus patterns such as synapses receive in vivo. Here we show that this developmental decrease in facilitation is also seen at 32°C and investigate the underlying mechanism. Addition of the mGluR1 antagonist LY367385 increases short-term facilitation in respo

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LIN, BIN, PAUL R. MARTIN, and ULRIKE GRÜNERT. "Expression and distribution of ionotropic glutamate receptor subunits on parasol ganglion cells in the primate retina." Visual Neuroscience 19, no. 4 (2002): 453–65. http://dx.doi.org/10.1017/s0952523802194077.

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The response properties of postreceptoral sensory neurones are determined by the properties of their input neurones, by intrinsic membrane properties, and by the properties of neurotransmitter receptors on the soma and dendritic tree. We previously showed that inhibitory neurotransmitter (GABAA and glycine) receptors on a well-characterised sensory neurone, the parasol ganglion cell in the primate retina, are segregated towards the distal part of the dendritic tree. Here we studied the distribution of excitatory ionotropic glutamate receptor subunits on the dendrites of parasol cells in the re

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Heinmiller, Andrew, Ryan Ting-A-Kee, Hector Vargas-Perez, Andrew Yeh, and Derek van der Kooy. "Tegmental pedunculopontine glutamate and GABA-B synapses mediate morphine reward." Behavioral Neuroscience 123, no. 1 (2009): 145–55. http://dx.doi.org/10.1037/a0014015.

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Ghatpande, Ambarish S., and Alan Gelperin. "Presynaptic Muscarinic Receptors Enhance Glutamate Release at the Mitral/Tufted to Granule Cell Dendrodendritic Synapse in the Rat Main Olfactory Bulb." Journal of Neurophysiology 101, no. 4 (2009): 2052–61. http://dx.doi.org/10.1152/jn.90734.2008.

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The mammalian olfactory bulb receives multiple modulatory inputs, including a cholinergic input from the basal forebrain. Understanding the functional roles played by the cholinergic input requires an understanding of the cellular mechanisms it modulates. In an in vitro olfactory bulb slice preparation we demonstrate cholinergic muscarinic modulation of glutamate release onto granule cells that results in γ-aminobutyric acid (GABA) release onto mitral/tufted cells. We demonstrate that the broad-spectrum cholinergic agonist carbachol triggers glutamate release from mitral/tufted cells that acti

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Han, Victor Z., Kirsty Grant, and Curtis C. Bell. "Rapid Activation of GABAergic Interneurons and Possible Calcium Independent GABA Release in the Mormyrid Electrosensory Lobe." Journal of Neurophysiology 83, no. 3 (2000): 1592–604. http://dx.doi.org/10.1152/jn.2000.83.3.1592.

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The primary afferent fibers from the electroreceptors of mormyrid electric fish terminate centrally in the granular layer of the electrosensory lobe (ELL). This study examines the excitatory and inhibitory processes that take place in this layer using an in vitro slice preparation and field potentials evoked by stimulation of primary afferent fibers in the deep fiber layer of ELL. The postsynaptic response to stimulation of the afferent fibers was still present after blocking chemical transmission in three different ways: by adding glutamate receptor antagonists to the medium, by substituting

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Strecker, George J., Jean-Pierre Wuarin, and F. Edward Dudek. "GABAA-Mediated Local Synaptic Pathways Connect Neurons in the Rat Suprachiasmatic Nucleus." Journal of Neurophysiology 78, no. 4 (1997): 2217–20. http://dx.doi.org/10.1152/jn.1997.78.4.2217.

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Strecker, George J., Jean-Pierre Wuarin, and F. EdwardDudek. GABAA-mediated local synaptic pathways connect neurons in the rat suprachiasmatic nucleus. J. Neurophysiol. 78: 2217–2220, 1997. The suprachiasmatic nucleus (SCN) in mammals functions as the biological clock controlling circadian rhythms, but the synaptic circuitry of the SCN is largely unexplored. Most SCN neurons use the neurotransmitter γ-aminobutyric acid (GABA), and anatomic studies indicate many GABAergic synapses and local axon collaterals; however, physiological evidence for synaptic communication among SCN neurons is indirec

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Redman, Stephen J., and Robert Porter. "David Roderick Curtis 1927–2017." Historical Records of Australian Science 31, no. 2 (2020): 152. http://dx.doi.org/10.1071/hr19016.

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David Curtis was a pioneer in the identification of excitatory and inhibitory transmitters released at synapses in the central nervous system. He made major contributions to the identification of gamma-amino butyric acid (GABA) and glycine as inhibitory transmitters released at inhibitory synapses. His work laid the foundation for the subsequent acceptance that L-glutamate was the major excitatory transmitter. David’s scientific work led to him receiving many accolades and honours, including Fellowships of the Australian Academy of Sciences, the Royal Society and a Companion of the Order of Au

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Dai, Shuiping, Misha Perouansky, and Robert A. Pearce. "Isoflurane Enhances Both Fast and Slow Synaptic Inhibition in the Hippocampus at Amnestic Concentrations." Anesthesiology 116, no. 4 (2012): 816–23. http://dx.doi.org/10.1097/aln.0b013e31824be0e3.

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Background Inhibition mediated by γ-aminobutyric acid type A (GABA A) receptors has long been considered an important target for a variety of general anesthetics. In the hippocampus, two types of phasic GABA A receptor-mediated inhibition coexist: GABA A,fast, which is expressed primarily at peri-somatic sites, and GABAA,slow, which is expressed primarily in the dendrites. Their spatial segregation suggests distinct functions: GABA A,slow may control plasticity of dendritic synapses, whereas GABA A,fast controls action potential initiation at the soma. We examined modulation of GABA A,fast and

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LINDSTROM, SARAH H., NASON AZIZI, CYNTHIA WELLER, and MARTIN WILSON. "Retinal input to efferent target amacrine cells in the avian retina." Visual Neuroscience 27, no. 3-4 (2010): 103–18. http://dx.doi.org/10.1017/s0952523810000155.

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AbstractThe bird visual system includes a substantial projection, of unknown function, from a midbrain nucleus to the contralateral retina. Every centrifugal, or efferent, neuron originating in the midbrain nucleus makes synaptic contact with the soma of a single unique amacrine cell, the target cell (TC). By labeling efferent neurons in the midbrain, we have been able to identify their terminals in retinal slices and make patch-clamp recordings from TCs. TCs generate Na+-based action potentials (APs) triggered by spontaneous EPSPs originating from multiple classes of presynaptic neurons. Exog

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Giustizieri, Michela, Giorgio Bernardi, Nicola B. Mercuri, and Nicola Berretta. "Distinct Mechanisms of Presynaptic Inhibition at GABAergic Synapses of the Rat Substantia Nigra Pars Compacta." Journal of Neurophysiology 94, no. 3 (2005): 1992–2003. http://dx.doi.org/10.1152/jn.00171.2005.

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We investigated the mechanisms of presynaptic inhibition of GABAergic neurotransmission by group III metabotropic glutamate receptors (mGluRs) and GABAB receptors, in dopamine (DA) neurons of the substantia nigra pars compacta (SNc). Both the group III mGluRs agonist l-(+)-2-amino-4-phosphonobutyric acid (AP4, 100 μM) and the GABAB receptor agonist baclofen (10 μM) reversibly depressed the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) to 48.5 ± 2.7 and 79.3 ± 1.6% (means ± SE) of control, respectively. On the contrary, the frequency of action potential-independent miniatur

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El Khoueiry, Corinne, Cristina Alba-Delgado, Myriam Antri та ін. "GABAA and Glycine Receptor-Mediated Inhibitory Synaptic Transmission onto Adult Rat Lamina IIi PKCγ-Interneurons: Pharmacological but Not Anatomical Specialization". Cells 11, № 8 (2022): 1356. http://dx.doi.org/10.3390/cells11081356.

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Mechanical allodynia (pain to normally innocuous tactile stimuli) is a widespread symptom of inflammatory and neuropathic pain. Spinal or medullary dorsal horn (SDH or MDH) circuits mediating tactile sensation and pain need to interact in order to evoke mechanical allodynia. PKCγ-expressing (PKCγ+) interneurons and inhibitory controls within SDH/MDH inner lamina II (IIi) are pivotal in connecting touch and pain circuits. However, the relative contribution of GABA and glycine to PKCγ+ interneuron inhibition remains unknown. We characterized inhibitory inputs onto PKCγ+ interneurons by combining

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Gao, Fan, Bruce R. Maple, and Samuel M. Wu. "I4AA-Sensitive Chloride Current Contributes to the Center Light Responses of Bipolar Cells in the Tiger Salamander Retina." Journal of Neurophysiology 83, no. 6 (2000): 3473–82. http://dx.doi.org/10.1152/jn.2000.83.6.3473.

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Light-evoked currents in depolarizing and hyperpolarizing bipolar cells (DBCs and HBCs) were recorded under voltage-clamp conditions in living retinal slices of the larval tiger salamander. Responses to illumination at the center of the DBCs' and HBCs' receptive fields were mediated by two postsynaptic currents: Δ I C, a glutamate-gated cation current with a reversal potential near 0 mV, and Δ I Cl, a chloride current with a reversal potential near −60 mV. In DBCs Δ I C was suppressed byl-2-amino-4-phosphonobutyric acid (l-AP4), and in HBCs it was suppressed by 6,7-dinitroquinoxaline-2,3-dione

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Ulrich, Daniel, Valérie Besseyrias, and Bernhard Bettler. "Functional Mapping of GABAB-Receptor Subtypes in the Thalamus." Journal of Neurophysiology 98, no. 6 (2007): 3791–95. http://dx.doi.org/10.1152/jn.00756.2007.

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The thalamus plays an important role in attention mechanisms and the generation of brain rhythms. γ-Aminobutyric acid type B (GABAB) receptors are known to regulate the main output neurons of the thalamus, the thalamocortical relay (TCR) cells. However, the contributions of the two predominant GABAB-receptor subtypes, GABAB(1a,2) and GABAB(1b,2), to the control of TCR cell activity are unknown. Here, we used genetic and electrophysiological methods to investigate subtype-specific GABAB effects at the inputs to TCR cells. We found that mainly GABAB(1a,2) receptors inhibit the release of glutama

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Pinal, Noelia. "A four PDZ domain-containing splice variant form of GRIP1 is localized in GABAergic and glutamatergic synapses in the brain." J Biol Chem 297, no. (37) (2004): 38978–90. https://doi.org/10.1074/jbc.M405786200.

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We have isolated, from a rat brain cDNA library, a clone corresponding to a 2779-bp cDNA encoding a novel splice form of the glutamate receptor interacting protein-1 (GRIP1). We call this 696-amino acid splice form GRIP1c 4-7 to differentiate it from longer splice forms of GRIP1a/b containing seven PDZ domains. The four PDZ domains of GRIP1c 4-7 are identical to PDZ domains 4-7 of GRIP1a/b. GRIP1c 4-7 also contains 35 amino acids at the N terminus and 12 amino acids at the C terminus that are different from GRIP1a/b. In transfected HEK293 cells, a majority of GRIP1c 4-7 was associated with the

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Farzana, F., R. Zalm, N. Chen, et al. "Neurobeachin Regulates Glutamate- and GABA-Receptor Targeting to Synapses via Distinct Pathways." Molecular Neurobiology 53, no. 4 (2015): 2112–23. http://dx.doi.org/10.1007/s12035-015-9164-8.

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Masugi-Tokita, Miwako, and Ryuichi Shigemoto. "High-resolution quantitative visualization of glutamate and GABA receptors at central synapses." Current Opinion in Neurobiology 17, no. 3 (2007): 387–93. http://dx.doi.org/10.1016/j.conb.2007.04.012.

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Palmer, Mary J., and Jenni Harvey. "Honeybee Kenyon cells are regulated by a tonic GABA receptor conductance." Journal of Neurophysiology 112, no. 8 (2014): 2026–35. http://dx.doi.org/10.1152/jn.00180.2014.

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The higher cognitive functions of insects are dependent on their mushroom bodies (MBs), which are particularly large in social insects such as honeybees. MB Kenyon cells (KCs) receive multisensory input and are involved in associative learning and memory. In addition to receiving sensory input via excitatory nicotinic synapses, KCs receive inhibitory GABAergic input from MB feedback neurons. Cultured honeybee KCs exhibit ionotropic GABA receptor currents, but the properties of GABA-mediated inhibition in intact MBs are currently unknown. Here, using whole cell recordings from KCs in acutely is

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Redman, S. J., and R. Porter. "David Roderick Curtis. 3 June 1927—11 December 2017." Biographical Memoirs of Fellows of the Royal Society 69 (August 26, 2020): 133–43. http://dx.doi.org/10.1098/rsbm.2020.0025.

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David Curtis was a pioneer in the identification of excitatory and inhibitory transmitters released at synapses in the central nervous system. He made major contributions to the identification of gamma-amino butyric acid (GABA) and glycine as inhibitory transmitters released at inhibitory synapses. His work laid the foundation for the subsequent acceptance that l -glutamate was the major excitatory transmitter. David's scientific work led to him receiving many accolades and honours, including fellowships of the Australian Academy of Sciences and the Royal Society and a Companion of the Order o

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Wagner, Julia, Svenja Tetzlaff, Ekin Reyhan, and Varun Venkataramani. "CNSC-56. DIVERSE, FUNCTIONAL NEUROTRANSMITTER RECEPTOR EXPRESSION ON GLIOBLASTOMA CELLS ENABLES EXTENSIVE NEURON-TO-GLIOMA COMMUNICATION." Neuro-Oncology 26, Supplement_8 (2024): viii53—viii54. http://dx.doi.org/10.1093/neuonc/noae165.0212.

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Abstract Glioblastomas are invasive yet incurable brain tumors. Recent data have shown that glutamatergic neuron-to-glioma synapses drive glioblastoma proliferation and invasion. In this study, we set out to investigate whether glioblastoma could communicate with neurons via various neuron-derived neurotransmitters through a functional neurotransmitter receptor screening. For this purpose, we stably transduced glioblastoma cells with a genetically encoded calcium indicator and sequentially and locally applied eight different neurotransmitters to glioblastoma cells in neuron-glioma co-cultures.

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Wang, Na, and Junyu Xu. "Functions of Kinesin Superfamily Proteins in Neuroreceptor Trafficking." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/639301.

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Synaptic plasticity is widely regarded as the cellular basis of learning and memory. Understanding the molecular mechanism of synaptic plasticity has been one of center pieces of neuroscience research for more than three decades. It has been well known that the trafficking ofα-amino-3-hydroxy-5-methylisoxazoloe-4-propionic acid- (AMPA-) type, N-methyl-D-aspartate- (NMDA-) type glutamate receptors to and from synapses is a key molecular event underlying many forms of synaptic plasticity. Kainate receptors are another type of glutamate receptors playing important roles in synaptic transmission.

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Martinello, Katiuscia, Addolorata Mascia, Sara Casciato та ін. "α4β2^* nicotinic acetylcholine receptors drive human temporal glutamate/GABA balance toward inhibition". Journal of Physiology 603, № 6 (2025): 1645–62. https://doi.org/10.1113/jp285689.

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AbstractHeteromeric nicotinic acetylcholine nAChRs (nAChRs) containing the α4 and β2 subunits (α4β2* nAChRs) modulate neurotransmitter release in several regions of the brain. In temporal lobe epilepsy, inhibitory GABAergic neurotransmission is altered, whereas no evidence of nicotinic dysfunction has been reported. Here, we investigated, in human epileptic cortical tissues, the ability of α4β2* nAChRs to modulate synaptic transmission. An increased expression of α4 and β2 subunits was observed in the temporal cortex of epileptic patients. We then recorded excitatory and inhibitory postsynapti

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Kim, Jieun, Ju Hwan Yang, In Soo Ryu, Sumin Sohn, Sunghyun Kim, and Eun Sang Choe. "Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration." International Journal of Molecular Sciences 20, no. 12 (2019): 2943. http://dx.doi.org/10.3390/ijms20122943.

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Nicotine causes tobacco dependence, which may result in fatal respiratory diseases. The striatum is a key structure of forebrain basal nuclei associated with nicotine dependence. In the striatum, glutamate release is increased when α7 nicotinic acetylcholine receptors expressed in the glutamatergic terminals are exposed to nicotine, and over-stimulates glutamate receptors in gamma amino-butyric acid (GABA)ergic neurons. These receptor over-stimulations in turn potentiate GABAergic outputs to forebrain basal nuclei and contribute to the increase in psychomotor behaviors associated with nicotine

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Colbert, C. M., and W. B. Levy. "Electrophysiological and pharmacological characterization of perforant path synapses in CA1: mediation by glutamate receptors." Journal of Neurophysiology 68, no. 1 (1992): 1–8. http://dx.doi.org/10.1152/jn.1992.68.1.1.

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1. With the use of hippocampal slices from adult rats, we studied monosynaptic potentials in CA1 evoked by stimulating either the perforant pathway or the Schaffer collaterals. Excision of region CA3 and the dentate gyrus prevented polysynaptic excitation of CA1 and facilitated interpretation of the extracellular potentials. 2. Laminar profiles distinguished the population excitatory postsynaptic potentials (pEPSPs) in CA1 evoked by stimulating the Schaffer collaterals and the perforant path. Stimulating the perforant path evoked short-latency negative-going pEPSPs in s. lacunosum-moleculare o

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Kang, Ning, Li Jiang, Wei He, Jun Xu, Maiken Nedergaard, and Jian Kang. "Presynaptic Inactivation of Action Potentials and Postsynaptic Inhibition of GABAA Currents Contribute to KA-Induced Disinhibition in CA1 Pyramidal Neurons." Journal of Neurophysiology 92, no. 2 (2004): 873–82. http://dx.doi.org/10.1152/jn.01231.2003.

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Kainate-type glutamate ionotropic receptors (KAR) mediate either depression or potentiation of inhibitory transmission. The mechanisms underlying the depressant effect of KAR agonists have been controversial. Under dual patch-clamp recording techniques in synaptically coupled pairs of CA1 interneurons and pyramidal neurons in hippocampal slices, micromolar concentrations of KAR agonists, kainic acid (KA, 10 μM) and ATPA (10 μM), induced inactivation of action potentials (APs) in 58 and 50% of presynaptic interneurons, respectively. Inactivation of interneuronal APs might have significantly con

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Egashira, Yoshihiro, Miki Takase, Shoji Watanabe, et al. "Unique pH dynamics in GABAergic synaptic vesicles illuminates the mechanism and kinetics of GABA loading." Proceedings of the National Academy of Sciences 113, no. 38 (2016): 10702–7. http://dx.doi.org/10.1073/pnas.1604527113.

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GABA acts as the major inhibitory neurotransmitter in the mammalian brain, shaping neuronal and circuit activity. For sustained synaptic transmission, synaptic vesicles (SVs) are required to be recycled and refilled with neurotransmitters using an H+ electrochemical gradient. However, neither the mechanism underlying vesicular GABA uptake nor the kinetics of GABA loading in living neurons have been fully elucidated. To characterize the process of GABA uptake into SVs in functional synapses, we monitored luminal pH of GABAergic SVs separately from that of excitatory glutamatergic SVs in culture

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Huang, M. H., F. M. Smith, and J. A. Armour. "Amino acids modify activity of canine intrinsic cardiac neurons involved in cardiac regulation." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 4 (1993): H1275—H1282. http://dx.doi.org/10.1152/ajpheart.1993.264.4.h1275.

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The effects of amino acids on intrinsic cardiac neuronal activity identified in 10 anesthetized dogs were investigated. Local injection of small volumes (1-10 microliters) of the excitatory amino acids, glutamate (100 mM) and aspartate (10 mM), and the inhibitory amino acids, gamma-aminobutyric acid (GABA; 10 mM) and glycine (10 mM), modified the activity of 39 of 50 identified neurons. Spontaneous activity of eight neurons was modified by both excitatory and inhibitory amino acids. Cardiodynamic responses accompanied neuronal activity modification in 15 instances. After acute decentralization

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Llewellyn-Smith, I. J., J. B. Minson, P. M. Pilowsky, L. F. Arnolda, and J. P. Chalmers. "The One Hundred Percent Hypothesis: Glutamate Or Gaba in Synapses on Sympathetic Preganglionic Neurons." Clinical and Experimental Hypertension 17, no. 1-2 (1995): 323–33. http://dx.doi.org/10.3109/10641969509087074.

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Zhao, Liangfang, and Eric S. Levine. "BDNF-endocannabinoid interactions at neocortical inhibitory synapses require phospholipase C signaling." Journal of Neurophysiology 111, no. 5 (2014): 1008–15. http://dx.doi.org/10.1152/jn.00554.2013.

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Endogenous cannabinoids (endocannabinoids) and neurotrophins, particularly brain-derived neurotrophic factor (BDNF), are potent synaptic modulators that are expressed throughout the forebrain and play critical roles in many behavioral processes. Although the effects of BDNF at excitatory synapses have been well characterized, the mechanisms of action of BDNF at inhibitory synapses are not well understood. Previously we have found that BDNF suppresses presynaptic GABA release in layer 2/3 of the neocortex via postsynaptic tropomyosin-related kinase receptor B (trkB) receptor-induced release of

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