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Journal articles on the topic 'Presynaptic kainate receptors'

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Published: 14 March 2023

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1

Liu, Qing-Song, Peter R. Patrylo, Xiao-Bing Gao, and Anthony N. van den Pol. "Kainate Acts at Presynaptic Receptors to Increase GABA Release From Hypothalamic Neurons." Journal of Neurophysiology 82, no. 2 (August 1, 1999): 1059–62. http://dx.doi.org/10.1152/jn.1999.82.2.1059.

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Recent reports suggest that kainate acting at presynaptic receptors reduces the release of the inhibitory transmitter GABA from hippocampal neurons. In contrast, in the hypothalamus in the presence of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) receptor antagonists [1-(4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466) and d,l-2-amino-5-phosphonopentanoic acid (AP5)], kainate increased GABA release. In the presence of tetrodotoxin, the frequency, but not the amplitude, of GABA-mediated miniature inhibitory postsynaptic currents (IPSCs) was enhanced by kainate, consistent with a presynaptic site of action. Postsynaptic activation of kainate receptors on cell bodies/dendrites was also found. In contrast to the hippocampus where kainate increases excitability by reducing GABA release, in the hypothalamus where a much higher number of GABAergic cells exist, kainate-mediated activation of transmitter release from inhibitory neurons may reduce the level of neuronal activity in the postsynaptic cell.

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2

Sun, H. Y., A. F. Bartley, and L. E. Dobrunz. "Calcium-Permeable Presynaptic Kainate Receptors Involved in Excitatory Short-Term Facilitation Onto Somatostatin Interneurons During Natural Stimulus Patterns." Journal of Neurophysiology 101, no. 2 (February 2009): 1043–55. http://dx.doi.org/10.1152/jn.90286.2008.

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Schaffer collateral synapses in hippocampus show target-cell specific short-term plasticity. Using GFP-expressing Inhibitory Neuron (GIN) transgenic mice that express enhanced green fluorescent protein (EGFP) in a subset of somatostatin-containing interneurons (SOM interneurons), we previously showed that Schaffer collateral synapses onto SOM interneurons in stratum (S.) radiatum have unusually large (up to 6-fold) paired-pulse facilitation. This results from a low initial release probability and the enhancement of facilitation by synaptic activation of presynaptic kainate receptors. Here we further investigate the properties of these kainate receptors and examine their effects on short-term facilitation during physiologically derived stimulation patterns, using excitatory postsynaptic currents recorded in S. radiatum interneurons during Schaffer collateral stimulation in acute slices from juvenile GIN mice. We find that GluR5 and GluR6 antagonists decrease short-term facilitation at Schaffer collateral synapses onto SOM interneurons with no additive effects, suggesting that the presynaptic kainate receptors are heteromers containing both GluR5 and GluR6 subunits. The calcium-permeable receptor antagonist 1-napthyl acetyl spermine (NASPM) both mimics and occludes the effect of the kainate receptor antagonists, indicating that the presynaptic kainate receptors are calcium permeable. Furthermore, Schaffer collateral synapses onto SOM interneurons show up to 11-fold short-term facilitation during physiologically derived stimulus patterns, in contrast to other interneurons that have less than 1.5-fold facilitation. Blocking the kainate receptors reduces facilitation in SOM interneurons by ∼50% during the physiologically derived patterns and reduces the dynamic range. Activation of calcium-permeable kainate receptors containing GluR5/GluR6 causes a dramatic increase in short-term facilitation during physiologically derived stimulus patterns, a mechanism likely to be important in regulating the strength of Schaffer collateral synapses onto SOM interneurons in vivo.

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3

Bortolotto, Zuner A., Sari Lauri, John T. R. Isaac, and Graham L. Collingridge. "Kainate receptors and the induction of mossy fibre long-term potentiation." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1432 (April 29, 2003): 657–66. http://dx.doi.org/10.1098/rstb.2002.1216.

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There is intense interest in understanding the molecular mechanisms involved in long-term potentiation (LTP) in the hippocampus. Significant progress in our understanding of LTP has followed from studies of glutamate receptors, of which there are four main subtypes ( α -amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), N -methyl-D-aspartate (NMDA), mGlu and kainate). This article summarizes the evidence that the kainate subtype of glutamate receptor is an important trigger for the induction of LTP at mossy fibre synapses in the CA3 region of the hippocampus. The pharmacology of the first selective kainate receptor antagonists, in particular the GLU K5 subunit selective antagonist LY382884, is described. LY382884 selectively blocks the induction of mossy fibre LTP, in response to a variety of different high-frequency stimulation protocols. This antagonist also inhibits the pronounced synaptic facilitation of mossy fibre transmission that occurs during high-frequency stimulation. These effects are attributed to the presence of presynaptic GLU K5 -subunit-containing kainate receptors at mossy fibre synapses. Differences in kainate receptor-dependent synaptic facilitation of AMPA and NMDA receptor-mediated synaptic transmission are described. These data are discussed in the context of earlier reports that glutamate receptors are not involved in mossy fibre LTP and more recent experiments using kainate receptor knockout mice, that argue for the involvement of GLU K6 but not GLU K5 kainate receptor subunits. We conclude that activation of presynaptic GLU K5 -containing kainate receptors is an important trigger for the induction of mossy fibre LTP in the hippocampus.

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4

Kullmann, Dimitri M. "Presynaptic Kainate Receptors in the Hippocampus." Neuron 32, no. 4 (November 2001): 561–64. http://dx.doi.org/10.1016/s0896-6273(01)00507-4.

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5

Lauri, Sari, and Tomi Taira. "Kainate receptors in developing presynaptic terminals." Wiley Interdisciplinary Reviews: Membrane Transport and Signaling 1, no. 1 (October 19, 2011): 45–55. http://dx.doi.org/10.1002/wmts.3.

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6

Kerchner, Geoffrey A., Timothy J. Wilding, Ping Li, Min Zhuo, and James E. Huettner. "Presynaptic Kainate Receptors Regulate Spinal Sensory Transmission." Journal of Neuroscience 21, no. 1 (January 1, 2001): 59–66. http://dx.doi.org/10.1523/jneurosci.21-01-00059.2001.

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7

Charara, A., E. Blankstein, and Y. Smith. "Presynaptic kainate receptors in the monkey striatum." Neuroscience 91, no. 4 (July 1999): 1195–200. http://dx.doi.org/10.1016/s0306-4522(99)00099-8.

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8

Crowder, Tara L., and Jeff L. Weiner. "Functional Characterization of Kainate Receptors in the Rat Nucleus Accumbens Core Region." Journal of Neurophysiology 88, no. 1 (July 1, 2002): 41–48. http://dx.doi.org/10.1152/jn.2002.88.1.41.

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The nucleus accumbens, a brain region involved in motivation, attention, and reward, receives substantial glutamatergic innervation from many limbic structures. This excitatory glutamatergic input plays an integral role in both normal and pathophysiological states. Despite the importance of glutamatergic transmission in the nucleus accumbens, the specific receptor subtypes that mediate glutamatergic signaling in this brain region have not been fully characterized. The current study sought to examine the possible role of the kainate subclass of glutamate receptor in the nucleus accumbens. Kainate receptors are relatively poorly understood members of the ionotropic glutamate receptor family and are highly expressed in the nucleus accumbens. Recent studies have highlighted a number of novel pre- and postsynaptic functions of kainate receptors in several other brain regions. Using the whole cell patch-clamp technique, we report the first demonstration of functional kainate receptors on neurons within the core region of the nucleus accumbens. In addition, we present evidence that activation of kainate receptors in this brain region inhibits excitatory synaptic transmission via a presynaptic mechanism.

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9

Schmitz, D., J. Mellor, M. Frerking, and R. A. Nicoll. "Presynaptic kainate receptors at hippocampal mossy fiber synapses." Proceedings of the National Academy of Sciences 98, no. 20 (September 25, 2001): 11003–8. http://dx.doi.org/10.1073/pnas.191351498.

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10

HARVEY, D. M., and D. J. CALKINS. "Localization of kainate receptors to the presynaptic active zone of the rod photoreceptor in primate retina." Visual Neuroscience 19, no. 5 (September 2002): 681–92. http://dx.doi.org/10.1017/s0952523802195137.

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Visual information is encoded at the photoreceptor synapse by modulation of the tonic release of glutamate from one or more electron-dense ribbons. This release is highest in the dark, when photoreceptors are depolarized, and decreases in grades when photoreceptors hyperpolarize with increasing light. Functional diversity between neurons postsynaptic at the synaptic ribbon arises in part from differential expression of both metabotropic (G-protein-gated) and ionotropic (ligand-gated) glutamate receptor. In the brain, different subunits also modulate the presynaptic active zone. In hippocampus, ionotropic kainate receptors localize to the presynaptic membrane of glutamatergic axon terminals and facilitate depolarization of the synapse (e.g. Lauri et al., 2001). Such facilitation may be helpful in the retina, where consistent depolarization of the photoreceptor axon terminal is necessary to maintain glutamate release in the dark. We investigated whether such a mechanism could be present in primate retina by using electron microscopy to examine the localization of the kainate subunits GluR6/7 at the rod axon terminal, where only a single ribbon synapse mediates glutamate release. We scored 54 rod axon terminals whose postsynaptic space contained one or more GluR6/7-labeled processes and traced these processes through serial sections to determine their identity. Of 68 labeled processes, 63% originated from narrow “fingers” of cytoplasm extending from the presynaptic axon terminal into the postsynaptic cleft. Each rod terminal typically inserts 4–6 presynaptic fingers, and we scored several instances where multiple fingers contained label. Such consistency suggests that each presynaptic finger expresses GluR6/7. The physiological properties of kainate receptors and the geometry of the rod axon terminal suggest that presynaptic GluR6/7 could provide a steady inward current to maintain consistent depolarization of the rod synapse in the long intervals between photons in the dark.

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11

Kerchner, Geoffrey A., and Min Zhuo. "Presynaptic Suppression of Dorsal Horn Inhibitory Transmission by μ-Opioid Receptors." Journal of Neurophysiology 88, no. 1 (July 1, 2002): 520–22. http://dx.doi.org/10.1152/jn.2002.88.1.520.

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Opioids modify sensory experience at many levels in the CNS. The mechanisms of this action, including the ways opioid receptors affect synaptic transmission, are not yet fully understood. Here we show that the selective activation of μ-opioid receptors suppressed inhibitory transmission between spinal cord dorsal horn neurons in vitro. μ-Opioid receptor activation reduced evoked inhibitory postsynaptic current (eIPSC) amplitude by acting presynaptically, because it altered the paired-pulse ratio, did not affect GABA-evoked currents, and decreased miniature IPSC (mIPSC) frequency. The mechanism of this effect was independent both of presynaptic Ca2+ entry and of the pathway linking presynaptic kainate (KA) receptors to suppression of inhibitory transmission in the same cells. These data identify μ-opioid receptors as important presynaptic modulators of dorsal horn inhibitory transmission.

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12

Partovi, Dara, and Matthew Frerking. "Presynaptic inhibition by kainate receptors converges mechanistically with presynaptic inhibition by adenosine and GABAB receptors." Neuropharmacology 51, no. 6 (November 2006): 1030–37. http://dx.doi.org/10.1016/j.neuropharm.2006.06.010.

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13

Yang, Xiong-Li, and Samuel M. Wu. "Effects of CNQX, APB, PDA, and kynurenate on horizontal cells of the tiger salamander retina." Visual Neuroscience 3, no. 3 (September 1989): 207–12. http://dx.doi.org/10.1017/s0952523800009962.

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AbstractEffects of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 2-amino-4-phosphonobutyrate (APB), cis-2,3-piperidine dicarboxylic acid (PDA), and kynurenate (KYN) on the depolarizing actions of glutamate and kainate on horizontal cells (HCs) were studied in the larval tiger salamander retina. APB, PDA, and KYN hyperpolarized the HCs, but they failed to block either the actions of glutamate and kainate, or the HC light responses. APB and PDA did not cause membrane polarizations in either rods or cones, suggesting that the HC hyperpolarizations were not mediated by presynaptic actions of these compounds. CNQX, the newly synthesized non-NMDA (N-Methyl-D-Aspartate) receptor antagonist, blocked the HC light responses and the action of kainate, but not that of glutamate. These results suggest that the synaptic receptors in the tiger salamander HCs are probably non-NMDA although extra-synaptic NMDA receptors may exist in these cells.

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14

LIU, QING-SONG, QIWU XU, JIAN KANG, and MAIKEN NEDERGAARD. "Astrocyte activation of presynaptic metabotropic glutamate receptors modulates hippocampal inhibitory synaptic transmission." Neuron Glia Biology 1, no. 4 (November 2004): 307–16. http://dx.doi.org/10.1017/s1740925x05000190.

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In the CNS, fine processes of astrocytes often wrap around dendrites, axons and synapses, which provides an interface where neurons and astrocytes might interact. We have reported previously that selective Ca2+ elevation in astrocytes, by photolysis of caged Ca2+ by o-nitrophenyl-EGTA (NP-EGTA), causes a kainite receptor-dependent increase in the frequency of spontaneous inhibitory post-synaptic potentials (sIPSCs) in neighboring interneurons in hippocampal slices. However, tetrodotoxin (TTX), which blocks action potentials, reduces the frequency of miniature IPSCs (mIPSCs) in interneurons during Ca2+ uncaging by an unknown presynaptic mechanism. In this study we investigate the mechanism underlying the presynaptic inhibition. We show that Ca2+ uncaging in astrocytes is accompanied by a decrease in the amplitude of evoked IPSCs (eIPSCs) in neighboring interneurons. The decreases in eIPSC amplitude and mIPSC frequency are prevented by CPPG, a group II/III metabotropic glutamate receptor (mGluR) antagonist, but not by the AMPA/kainate and NMDA receptor antagonists CNQX/CPP. Application of either the group II mGluR agonist DCG IV or the group III mGluR agonist L-AP4 decreased the amplitude of eIPSCs by a presynaptic mechanism, and both effects are blocked by CPPG. Thus, activation of mGluRs mediates the effects of Ca2+ uncaging on mIPSCs and eIPSCs. Our results indicate that Ca2+-dependent release of glutamate from astrocytes can activate distinct classes of glutamate receptors and differentially modulate inhibitory synaptic transmission in hippocampal interneurons.

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15

Nakamura, Michiko, Il-Sung Jang, Hitoshi Ishibashi, Shigenori Watanabe, and Norio Akaike. "Possible Roles of Kainate Receptors on GABAergic Nerve Terminals Projecting to Rat Substantia Nigra Dopaminergic Neurons." Journal of Neurophysiology 90, no. 3 (September 2003): 1662–70. http://dx.doi.org/10.1152/jn.01165.2002.

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GABAergic afferent inputs are thought to play an important role in the control of the firing pattern of substantia nigra pars compacta (SNc) dopaminergic neurons. We report here the actions of presynaptic kainite (KA) receptors in GABAergic transmission of rat SNc dopaminergic neurons. In mechanically dissociated rat SNc dopaminergic neurons attached with native presynaptic nerve terminals, GABAergic miniature inhibitory postsynaptic currents (mIPSCs) were recorded by use of conventional whole cell patch recording mode. In the voltage-clamp condition, KA (3 μM) significantly increased GABAergic mIPSC frequency without affecting the current amplitude. This facilitatory effect of KA was not affected in the presence of 20 μM GYKI52466, a selective AMPA receptor antagonist, but was completely inhibited in the presence of 20 μM CNQX, an AMPA/KA receptor antagonist. Presynaptic KA receptors on GABAergic terminals were mainly permeable to Na+ but impermeable to Ca2+ because KA-induced facilitation of mIPSC frequency was completely suppressed in either Na+-free or Ca2+-free external solutions, and in the presence of 200 μM Cd2+, a general voltage-dependent Ca2+ channel blocker. In the slice preparation, KA increased GABAergic spontaneous mIPSC frequency, but significantly suppressed evoked IPSC (eIPSC) amplitude. However, this inhibitory action on eIPSCs was reversed by 10 μM CGP55845 , a selective GABAB receptor antagonist, implicating the possible involvement of GABAB autoreceptors in KA-induced modulation of GABAergic transmission. Thus presynaptic KA receptors on GABAergic nerve terminals synapsing onto SNc neurons may play functional roles contributing the fine control of neuronal excitability and firing pattern of SNc.

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16

Crépel, Francis. "Role of Presynaptic Kainate Receptors at Parallel Fiber–Purkinje Cell Synapses in Induction of Cerebellar LTD: Interplay With Climbing Fiber Input." Journal of Neurophysiology 102, no. 2 (August 2009): 965–73. http://dx.doi.org/10.1152/jn.00269.2009.

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Until recently, except for A1 adenosine, N-methyl-d-aspartate, and cannabinoid receptors, little effort has been made to unravel possible roles of parallel fiber (PF) presynaptic receptors in long-term depression (LTD) of synaptic transmission at PF–Purkinje cell (PC) synapses. Presynaptic kainate (KA) receptors are also present on PFs and might also influence LTD induction by modulating glutamate (Glu) release at PF–PC synapses. This hypothesis was tested by comparing the efficacy of two pairing protocols in inducing LTD in adult wild-type and knock-out mice for the Glu receptor 6 (GluR6) subunit of KA receptors. Activation of presynaptic KA receptors was unnecessary for LTD induction when PF inputs were paired with climbing fiber (CF) stimulation but became crucial when CF input was replaced by direct depolarization of PCs. By comparing basal paired-pulse facilitation of PF-excitatory postsynaptic currents (EPSCs) and depolarization-induced suppression of excitation in adult wild-type and GluR6 knock-out mice, it was shown that the participation of PF presynaptic KA receptors in LTD induction was likely to mainly result from their tonic activation by basal extracellular Glu, rather than from their activation by retrograde release of Glu by PCs during pairing protocols. Finally, this study suggests that, in adult mice, CFs not only participate in LTD induction by depolarizing postsynaptic cells but also by activating postsynaptic mGluR1α metabotropic glutamate receptors at CF–PC synapses.

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17

Todd, Keith J., Carrie A. B. Slatter, and Declan W. Ali. "Activation of Ionotropic Glutamate Receptors on Peripheral Axons of Primary Motoneurons Mediates Transmitter Release at the Zebrafish NMJ." Journal of Neurophysiology 91, no. 2 (February 2004): 828–40. http://dx.doi.org/10.1152/jn.00599.2003.

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The development and function of the vertebrate neuromuscular junction (NMJ) is continually being redefined. Previous studies have indicated that glutamate may play a role in the development or function of the NMJ by associating with presynaptic receptors. We have used larval zebrafish ( Danio rerio) to investigate the presence of presynaptic ionotropic glutamate receptors (iGluRs) at the NMJ in vivo. In whole-mount zebrafish larvae, antibody staining directed to NR2A subunits colocalized with specific staining of motoneuron axon tracts. Whole cell voltage-clamp recordings of miniature endplate currents (mEPCs) from axial white muscle were performed during application of iGluR agonists and antagonists. Local perfusion of the NMJ with iGluR agonists resulted in significant increases in the frequency of spontaneous acetylcholine (ACh) release. These increases were blocked by the N-methyl-d-aspartate (NMDA) receptor antagonist d-(-)-2-amino-5-phosphonopentanoic acid (50 μM) and by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxalene-2,3-dione (50 μM). Further pharmacological investigation revealed no effect of the kainate receptor-specific antagonist (2S,4R)-4-methylglutamate (10 μM) on kainate-induced rises in the frequency of spontaneous ACh release. However, these were blocked with the AMPA receptor-specific antagonist 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (50 μM). Application of glutamate (1 mM) in the presence of the glutamate uptake inhibitor d-threo-β-benzyloxyaspartate(200 μM) resulted in a significant increase in the frequency of mEPCs. These results suggest the presence of AMPA and NMDA receptors in association with motoneuron axons of larval zebrafish.

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18

Chittajallu, Ramesh, Michel Vignes, Kumlesh K. Dev, Janine M. Barnes, Graham L. Collingridge, and Jeremy M. Henley. "Regulation of glutamate release by presynaptic kainate receptors in the hippocampus." Nature 379, no. 6560 (January 1996): 78–81. http://dx.doi.org/10.1038/379078a0.

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19

Lucifora, Simona, Helen H. Willcockson, Chun-Rong Lu, Melanie Darstein, Kris D. Phend, Juli G. Valtschanoff, and Aldo Rustioni. "Presynaptic low- and high-affinity kainate receptors in nociceptive spinal afferents." Pain 120, no. 1-2 (January 2006): 97–105. http://dx.doi.org/10.1016/j.pain.2005.10.018.

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20

Schmitz, Dietmar, Matthew Frerking, and Roger A. Nicoll. "Synaptic Activation of Presynaptic Kainate Receptors on Hippocampal Mossy Fiber Synapses." Neuron 27, no. 2 (August 2000): 327–38. http://dx.doi.org/10.1016/s0896-6273(00)00040-4.

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21

Nakamura, Michiko, Kyu-Hyung Choi, Sung-Keun Choi, Chung-Sik Do, Ju-Hye Jun, Hyung-Kook Kwon, So-Min Lee, Ryu-Jin Moon, Ki-Joung Yi, and Il-Sung Jang. "Presynaptic kainate receptors increase GABAergic neurotransmission in rat periaqueductal gray neurons." European Journal of Pharmacology 635, no. 1-3 (June 2010): 72–78. http://dx.doi.org/10.1016/j.ejphar.2010.03.004.

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22

Nair, Ramya, Juliane Lauks, SangYong Jung, Nancy E. Cooke, Heidi de Wit, Nils Brose, Manfred W. Kilimann, Matthijs Verhage, and JeongSeop Rhee. "Neurobeachin regulates neurotransmitter receptor trafficking to synapses." Journal of Cell Biology 200, no. 1 (December 31, 2012): 61–80. http://dx.doi.org/10.1083/jcb.201207113.

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The surface density of neurotransmitter receptors at synapses is a key determinant of synaptic efficacy. Synaptic receptor accumulation is regulated by the transport, postsynaptic anchoring, and turnover of receptors, involving multiple trafficking, sorting, motor, and scaffold proteins. We found that neurons lacking the BEACH (beige-Chediak/Higashi) domain protein Neurobeachin (Nbea) had strongly reduced synaptic responses caused by a reduction in surface levels of glutamate and GABAA receptors. In the absence of Nbea, immature AMPA receptors accumulated early in the biosynthetic pathway, and mature N-methyl-d-aspartate, kainate, and GABAA receptors did not reach the synapse, whereas maturation and surface expression of other membrane proteins, synapse formation, and presynaptic function were unaffected. These data show that Nbea regulates synaptic transmission under basal conditions by targeting neurotransmitter receptors to synapses.

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23

Miwa, A., H. P. Robinson, and N. Kawai. "Presynaptic glutamate receptors depress inhibitory postsynaptic transmission in lobster neuromuscular synapse." Journal of Neurophysiology 70, no. 3 (September 1, 1993): 1159–67. http://dx.doi.org/10.1152/jn.1993.70.3.1159.

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1. We examined the functional role of GTP-coupled glutamate receptor (GluB-R) in the presynaptic membrane of lobster neuromuscular synapse. 2. Injection of guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S), a hydrolysis-resistant analogue of GTP, into the excitatory axon mimicked the presynaptic glutamate response and effectively suppressed excitatory postsynaptic potentials or excitatory postsynaptic currents (EPSCs). 3. Statistical analysis revealed that the coefficient of variation (standard deviation divided by the mean of EPSC amplitude) was increased after injection of GTP gamma S into the excitatory axon, indicating a presynaptic inhibition of transmitter release. 4. The effect of glutamate on inhibitory postsynaptic potentials (IPSPs) or inhibitory postsynaptic currents (IPSCs) was studied when the postsynaptic glutamate receptors were blocked by the Joro spider toxin (JSTX). Glutamate depressed IPSPs or IPSCs in the JSTX-treated preparation. Furthermore, repetitive stimulation of the excitatory nerve produced effective inhibition of IPSCs. 5. Quisqualate and kainate suppressed IPSCs in a similar way to glutamate. In contrast, N-methyl-D-aspartate, ibotenic acid, trans-D,L-1-amino-1,3-cyclopentanedicarboxyloc acid, and 2-amino-4-phosphonobutanate had no effect on GluB-R. 6. Our results indicate that GluB-R, which exists in both excitatory and inhibitory nerve terminals, regulates transmitter release by a presynaptic inhibitory mechanism.

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24

Lourenço, Joana, Astrid Cannich, Mario Carta, Françoise Coussen, Christophe Mulle, and Giovanni Marsicano. "Synaptic activation of kainate receptors gates presynaptic CB1 signaling at GABAergic synapses." Nature Neuroscience 13, no. 2 (January 17, 2010): 197–204. http://dx.doi.org/10.1038/nn.2481.

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25

Clarke, V. R. J., S. M. Molchanova, T. Hirvonen, T. Taira, and S. E. Lauri. "Activity-Dependent Upregulation of Presynaptic Kainate Receptors at Immature CA3-CA1 Synapses." Journal of Neuroscience 34, no. 50 (December 10, 2014): 16902–16. http://dx.doi.org/10.1523/jneurosci.1842-14.2014.

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26

Li, Huifang, Anita E. Bandrowski, and David A. Prince. "Cortical Injury Affects Short-Term Plasticity of Evoked Excitatory Synaptic Currents." Journal of Neurophysiology 93, no. 1 (January 2005): 146–56. http://dx.doi.org/10.1152/jn.00665.2004.

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The hypothesis that plastic changes in the efficacy of excitatory neurotransmission occur in areas of chronic cortical injury was tested by assessing short-term plasticity of evoked excitatory synaptic currents (EPSCs) in neurons of partially isolated neocortical islands (undercut cortex). Whole cell recordings were obtained from layer V pyramidal neurons of sensorimotor cortical slices prepared from P36–P43 control and undercut rats. AMPA/kainate receptor-mediated EPSCs elicited by stimuli delivered at 40 to 66.7 Hz exhibited more paired-pulse depression (PPD) in undercut cortex than control, the time constant of depression evoked by trains of 20- to 66.7-Hz stimuli was faster, and the steady-state amplitude of EPSCs reached after five to seven EPSCs was lower. An antagonist of the glutamate autoreceptor, group II mGluR, increased the steady-state amplitude of EPSCs from undercut but not control cortex, suggesting that activation of presynaptic receptors by released glutamate is more prominent in undercut cortex. In contrast, the GABAB receptor antagonist (2S)-3-[[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl](phenylmethyl)phosphinic acid had no effect. Increasing [Ca2+]o from 2 to 4 mM increased PPD, with a smaller effect in neurons of the undercut. The I-V relationship of AMPA/kainate receptor-mediated EPSCs was close to linear in both control and undercut neurons, and spermine had no significant effect on the EPSCs, suggesting that decreases in postsynaptic glutamate receptors containing the GluR2 subunit were not involved in the alterations in short-term plasticity. Results are compatible with an increase in the probability of transmitter release at excitatory synapses in undercut cortex due to functional changes in presynaptic terminals.

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27

Negrete-Díaz, José V., Talvinder S. Sihra, José M. Delgado-García, and Antonio Rodríguez-Moreno. "Kainate Receptor–Mediated Inhibition of Glutamate Release Involves Protein Kinase A in the Mouse Hippocampus." Journal of Neurophysiology 96, no. 4 (October 2006): 1829–37. http://dx.doi.org/10.1152/jn.00280.2006.

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The mechanisms involved in the inhibition of glutamate release mediated by the activation of presynaptic kainate receptors (KARs) at the hippocampal mossy fiber–CA3 synapse are not well understood. We have observed a long-lasting inhibition of CA3 evoked excitatory postsynaptic currents (eEPSCs) after a brief application of kainate (KA) at concentrations ranging from 0.3 to 10 μM. The inhibition outlasted the change in holding current caused by the activation of ionotropic KARs in CA3 pyramidal cells, indicating that this action is not contingent on the opening of the receptor channels. The inhibition of the eEPSCs by KA was prevented by G protein and protein kinase A (PKA) inhibitors and was enhanced after stimulation of the adenylyl cyclase (AC) with forskolin. We conclude that KARs present at mossy fiber terminals mediate the inhibition of glutamate release through a metabotropic mechanism that involves the activation of an AC-second messenger cAMP-PKA signaling cascade.

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28

Pinheiro, P. S., R. J. Rodrigues, N. Rebola, S. Xapelli, C. R. Oliveira, and J. O. Malva. "Presynaptic kainate receptors are localized close to release sites in rat hippocampal synapses." Neurochemistry International 47, no. 5 (October 2005): 309–16. http://dx.doi.org/10.1016/j.neuint.2005.05.007.

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Cossart, R., R. Tyzio, C. Dinocourt, M. Esclapez, J. C. Hirsch, Y. Ben-Ari, and C. Bernard. "Presynaptic Kainate Receptors that Enhance the Release of GABA on CA1 Hippocampal Interneurons." Neuron 29, no. 2 (February 2001): 497–508. http://dx.doi.org/10.1016/s0896-6273(01)00221-5.

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Sadiq, Sanah, Zena Ghazala, Arnab Chowdhury, and Dietrich Büsselberg. "Metal Toxicity at the Synapse: Presynaptic, Postsynaptic, and Long-Term Effects." Journal of Toxicology 2012 (2012): 1–42. http://dx.doi.org/10.1155/2012/132671.

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Metal neurotoxicity is a global health concern. This paper summarizes the evidence for metal interactions with synaptic transmission and synaptic plasticity.Presynapticallymetal ions modulate neurotransmitter release through their interaction with synaptic vesicles, ion channels, and the metabolism of neurotransmitters (NT). Many metals (e.g., , , and ) also interact with intracellular signaling pathways.Postsynaptically, processes associated with the binding of NT to their receptors, activation of channels, and degradation of NT are altered by metals. , , , , , , , , and methylmercury modulate NMDA, AMPA/kainate, and/or GABA receptors activity. , , , and also impairsynaptic plasticityby targeting molecules such as CaM, PKC, and NOS as well as the transcription machinery involved in the maintenance of synaptic plasticity. The multiple effects of metals might occur simultaneously and are based on the specific metal species, metal concentrations, and the types of neurons involved.

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Crepel, Francis, and Hervé Daniel. "Developmental Changes in Agonist-Induced Retrograde Signaling at Parallel Fiber–Purkinje Cell Synapses: Role of Calcium-Induced Calcium Release." Journal of Neurophysiology 98, no. 5 (November 2007): 2550–65. http://dx.doi.org/10.1152/jn.00376.2007.

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In cerebellar Purkinje cells (PCs), activation of postsynaptic mGluR1 receptors inhibits parallel fiber (PF) to PC synaptic transmission by retrograde signaling. However, results were conflicting with respect to whether endocannabinoids or glutamate (Glu) is the retrograde messenger involved. Experiments in cerebellar slices from 10- to 12-day-old rats and mice confirmed that suppression of PF-excitatory postsynaptic currents (EPSCs) by mGluR1 agonists was entirely blocked by cannabinoid receptor antagonists at this early developmental stage. In contrast, suppression of PF-EPSCs by mGluR1 agonists was only partly blocked by cannabinoid receptor antagonists in 18- to 22-day-old rats, and the remaining suppression was accompanied by an increase in paired-pulse facilitation. This endocannnabinoidindependent suppression of PF-EPSCs was potentiated by the Glu uptake inhibitor d-threo-β-benzyloxyaspartate (d-TBOA) and blocked by the desensitizing kainate (KA) receptors agonist SYM 2081, by nonsaturating concentrations of 6-cyano-7-nitroquinoxaline-2-3-dione (CNQX) [but not by GYKI 52466 hydrochloride (GYKI)] and by dialyzing PCs with guanosine 5′-[β-thio]diphosphate (GDP-βS). An endocannnabinoid-independent suppression of PF-EPSCs was also present in nearly mature wild-type mice but was absent in GluR6−/− mice. The endocannnabinoid-independent suppression of PF-EPSCs induced by mGluR1 agonists and the KA-dependent component of depolarization-induced suppression of excitation (DSE) were blocked by ryanodine acting at a presynaptic level. We conclude that retrograde release of Glu by PCs participates in mGluR1 agonist-induced suppression of PF-EPSCs at nearly mature PF-PC synapses and that Glu operates through activation of presynaptic KA receptors located on PFs and prolonged release of calcium from presynaptic internal calcium stores.

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32

Liu, Yan, Shan Wang, Jun Kan, Jingzhi Zhang, Lisa Zhou, Yuli Huang, and Yunlong Zhang. "Chinese Herbal Medicine Interventions in Neurological Disorder Therapeutics by Regulating Glutamate Signaling." Current Neuropharmacology 18, no. 4 (March 20, 2020): 260–76. http://dx.doi.org/10.2174/1570159x17666191101125530.

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Glutamate is the major excitatory neurotransmitter in the central nervous system, and its signaling is critical for excitatory synaptic transmission. The well-established glutamate system involves glutamate synthesis, presynaptic glutamate release, glutamate actions on the ionotropic glutamate receptors (NMDA, AMPA, and kainate receptors) and metabotropic glutamate receptors, and glutamate uptake by glutamate transporters. When the glutamate system becomes dysfunctional, it contributes to the pathogenesis of neurodegenerative and neuropsychiatric diseases such as Alzheimer's disease, Parkinson's disease, depression, epilepsy, and ischemic stroke. In this review, based on regulating glutamate signaling, we summarize the effects and underlying mechanisms of natural constituents from Chinese herbal medicines on neurological disorders. Natural constituents from Chinese herbal medicine can prevent the glutamate-mediated excitotoxicity via suppressing presynaptic glutamate release, decreasing ionotropic and metabotropic glutamate receptors expression in the excitatory synapse, and promoting astroglial glutamate transporter expression to increase glutamate clearance from the synaptic cleft. However, some natural constituents from Chinese herbal medicine have the ability to restore the collapse of excitatory synapses by promoting presynaptic glutamate release and increasing ionotropic and metabotropic glutamate receptors expression. These regulatory processes involve various signaling pathways, which lead to different mechanistic routes of protection against neurological disorders. Hence, our review addresses the underlying mechanisms of natural constituents from Chinese herbal medicines that regulate glutamate systems and serve as promising agents for the treatment of the above-mentioned neurological disorders.

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Schmitz, Dietmar, Jack Mellor, Joerg Breustedt, and Roger A. Nicoll. "Presynaptic kainate receptors impart an associative property to hippocampal mossy fiber long-term potentiation." Nature Neuroscience 6, no. 10 (August 31, 2003): 1058–63. http://dx.doi.org/10.1038/nn1116.

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Kerchner, Geoffrey A., Guo-Du Wang, Chang-Shen Qiu, James E. Huettner, and Min Zhuo. "Direct Presynaptic Regulation of GABA/Glycine Release by Kainate Receptors in the Dorsal Horn." Neuron 32, no. 3 (November 2001): 477–88. http://dx.doi.org/10.1016/s0896-6273(01)00479-2.

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35

Jin, X. T., and Y. Smith. "Activation of presynaptic kainate receptors suppresses GABAergic synaptic transmission in the rat globus pallidus." Neuroscience 149, no. 2 (October 2007): 338–49. http://dx.doi.org/10.1016/j.neuroscience.2007.07.017.

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36

Brammer, M. J., S. Richmond, J. Z. Xiang, P. Adamson, I. Hajimohammadreza, M. A. Silva, and I. C. Campbell. "Kainate and quisqualate effects on rat presynaptic cortical receptors are metabotropic and non-additive." Neuroscience Letters 128, no. 2 (July 1991): 231–34. http://dx.doi.org/10.1016/0304-3940(91)90267-w.

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Wyeth, Megan S., Kenneth A. Pelkey, Xiaoqing Yuan, Geoffrey Vargish, April D. Johnston, Steven Hunt, Calvin Fang, et al. "Neto Auxiliary Subunits Regulate Interneuron Somatodendritic and Presynaptic Kainate Receptors to Control Network Inhibition." Cell Reports 20, no. 9 (August 2017): 2156–68. http://dx.doi.org/10.1016/j.celrep.2017.08.017.

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38

Christenson, J., and S. Grillner. "Primary afferents evoke excitatory amino acid receptor-mediated EPSPs that are modulated by presynaptic GABAB receptors in lamprey." Journal of Neurophysiology 66, no. 6 (December 1, 1991): 2141–49. http://dx.doi.org/10.1152/jn.1991.66.6.2141.

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1. The primary afferent neurons (dorsal cells) are of two types in lamprey, which are fast (touch) and slowly adapting (pressure), respectively. Intracellular stimulation of such sensory neurons evokes mono- and polysynaptic excitatory postsynaptic potentials (EPSPs) in spinobulbar neurons (giant interneurons) and in unidentified interneurons. Paired intracellular recordings between identified sensory cells and spinobulbar neurons made it possible to study the synaptic transmission in detail. It is shown that both touch and pressure primary afferents utilize excitatory amino acid (EAA) transmission and, furthermore, that these effects are subject to a presynaptic GABAB receptor modulation. 2. The monosynaptic mixed electrical and chemical EPSPs in giant interneurons had a mean peak amplitude of 3.2 +/- 1.3 (SD) mV, a time to peak of 4.7 +/- 1.2 ms, and a duration at one-half peak amplitude of 9.4 +/- 3.2 ms. Corresponding results were obtained with dorsal root or dorsal column stimulation. Seventy percent of the fast-adapting dorsal cells of the "touch" type evoked monosynaptic mixed EPSPs in giant interneurons, whereas only 3% of the slowly adapting "pressure" dorsal cells did. 3. The chemical part of the monosynaptic EPSPs evoked in giant interneurons was, in all cases tested, blocked by application of EAA antagonists, like the nonselective antagonist kynurenic acid (KYAC; 2 mM). The selective kainate/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 5 microM) had a similar effect, whereas the selective N-methyl-D-aspartate (NMDA) receptor antagonist 2-aminophosphono-5-valeric acid (AP-5; 200-400 microM) did not change the EPSP, even in the absence of magnesium ions. 4. The monosynaptic excitatory synaptic transmission was modulated by application of the selective GABAB receptor agonist L-baclofen (5-10 mM local droplet application or 100-1,000 microM bath applied) or by gamma-aminobutyric acid (GABA; 100-1,000 microM), also when GABAA receptor-evoked effects were blocked by bicuculline (10 microM). L-baclofen or GABA in combination with bicuculline did not evoke any effects in the postsynaptic neuron on membrane potential, input resistance, or spike threshold. Therefore the effects of the GABAB receptor activation most likely occurs at the presynaptic afferent level. 5. In conclusion, the monosynaptic excitation from skin mechanoreceptors evoked in spinobulbar neurons is mediated by EAA receptors of the kainate/AMPA type. GABAB receptor activation causes a depression of this EPSP, most likely because of a presynaptic action. GABA interneurons are known to form close appositions on sensory axons in the lamprey.

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39

Angulo, Maria Cecilia, Jean Rossier, and Etienne Audinat. "Postsynaptic Glutamate Receptors and Integrative Properties of Fast-Spiking Interneurons in the Rat Neocortex." Journal of Neurophysiology 82, no. 3 (September 1, 1999): 1295–302. http://dx.doi.org/10.1152/jn.1999.82.3.1295.

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The glutamate-mediated synaptic responses of neocortical pyramidal cell to fast-spiking interneuron (pyramidal-FS) connections were studied by performing paired recordings at 30–33°C in acute slices of 14- to 35-day-old rats ( n = 39). Postsynaptic fast-spiking (FS) cells were recorded in whole cell configuration with a patch pipette, and presynaptic pyramidal cells were impaled with sharp intracellular electrodes. At a holding potential of −72 mV (near the resting membrane potential), unitary excitatory postsynaptic potentials (EPSPs) had a mean amplitude of 2.1 ± 1.3 mV and a mean width at half-amplitude of 10.5 ± 3.7 ms ( n = 18). Bath application of the N-methyl-d-aspartate (NMDA) receptor antagonist d(−)2-amino-5-phosphonovaleric acid (d-AP5) had minor effects on both the amplitude and the duration of unitary EPSPs, whereas the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA)/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) almost completely blocked the synaptic responses. In voltage-clamp mode, the selective antagonist of AMPA receptors 1-(4-aminophenyl)-3-methylcarbamyl-4-methyl-7,8-methylenedioxy-3,4-dihydro-5H-2,3-benzodiazepine (GYKI 53655; 40–66 μM) blocked 96 ± 1.9% ofd-AP5–insensitive unitary excitatory postsynaptic currents (EPSCs), confirming the predominance of AMPA receptors, as opposed to kainate receptors, at pyramidal-FS connections ( n = 3). Unitary EPSCs mediated by AMPA receptors had fast rise times (0.29 ± 0.04 ms) and amplitude-weighted decay time constants (2 ± 0.8 ms; n = 16). In the presence of intracellular spermine, these currents showed the characteristic rectifying current-voltage ( I-V) curve of calcium-permeable AMPA receptors. A slower component mediated by NMDA receptors was observed when unitary synaptic currents were recorded at a membrane potential more positive than −50 mV. In response to short trains of moderately high-frequency (67 Hz) presynaptic action potentials, we observed only a limited temporal summation of unitary EPSPs, probably because of the rapid kinetics of AMPA receptors and the absence of NMDA component in these subthreshold synaptic responses. By combining paired recordings with extracellular stimulations ( n = 11), we demonstrated that EPSPs elicited by two different inputs were summed linearly by FS interneurons at membrane potentials below the action potential threshold. We estimated that, in our in vitro recording conditions, 8 ± 5 pyramidal cells ( n = 18) should be activated simultaneously to make FS interneurons fire an action potential from −72 mV. The low level of temporal summation and the linear summation of excitatory inputs in FS cells favor the role of coincidence detectors of these interneurons in neocortical circuits.

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Crepel, Francis. "Developmental Changes in Retrograde Messengers Involved in Depolarization-Induced Suppression of Excitation at Parallel Fiber-Purkinje Cell Synapses in Rodents." Journal of Neurophysiology 97, no. 1 (January 2007): 824–36. http://dx.doi.org/10.1152/jn.00735.2006.

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At parallel fiber (PF) to Purkinje cell (PC) synapses, depolarization-induced suppression of excitation (DSE) and suppression of PF-excitatory postsynaptic currents (EPSCs) by activation of postsynaptic mGluR1 glutamate (Glu) receptors involve retrograde release of endocannabinoids. However, Levenes et al. suggested instead that Glu was the retrograde messenger in this latter case. Because the study by Levenes et al. was performed in nearly mature rats, whereas most others were performed in juvenile animals, DSE was re-investigated in juvenile versus nearly mature rats and mice. Indeed, DSE was preferred here to agonist-induced suppression of PF-EPSCs, to avoid possible indirect effects in this latter case. In 10- to 12-day-old rats, DSE of PF-EPSCs was entirely mediated through retrograde release of endocannabinoids. In 18- to 22-day-old-rats, DSE was partly resistant to CB1 cannabinoid receptor antagonists. The remaining component was potentiated by the Glu uptake inhibitor d-threo-beta-benzyloxyaspartate (d-TBOA) and blocked by the desensitizing kainate (KA) receptor agonist (2S,4R)-4-methylglutamic acid (SYM 2081). This SYM-2081-sensitive component of DSE was accompanied by a paired-pulse facilitation increase that was also potentiated by d-TBOA and blocked by SYM 2081. In nearly mature wild-type and GluR6 −/− mice, results fully confirmed the presence of an endocannabinoid-independent component of DSE that involves retrograde release of Glu and activation of presynaptic KA receptors including GluR6 receptor subunits. Therefore retrograde release of Glu by PCs participates to DSE at PF-PC synapses in nearly mature rodents but not in juvenile ones, and Glu probably operates through activation of presynaptic KA receptors that include GluR6 receptor subunits.

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Xu, Hui, Long-Jun Wu, Ming-Gao Zhao, Hiroki Toyoda, Kunjumon I. Vadakkan, Yongheng Jia, Raphael Pinaud, and Min Zhuo. "Presynaptic Regulation of the Inhibitory Transmission by GluR5-Containing Kainate Receptors in Spinal Substantia Gelatinosa." Molecular Pain 2 (June 5, 2006): 1744–8069. http://dx.doi.org/10.1186/1744-8069-2-29.

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42

Cunha, Rodrigo A., J. A. Ribeiro, and João O. Malva. "Presynaptic kainate receptors modulating glutamatergic transmission in the rat hippocampus are inhibited by arachidonic acid." Neurochemistry International 44, no. 5 (April 2004): 371–79. http://dx.doi.org/10.1016/s0197-0186(03)00167-0.

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43

Jouhanneau, Jean-Sébastien, Simon M. Ball, Elek Molnár, and John T. R. Isaac. "Mechanisms of bi-directional modulation of thalamocortical transmission in barrel cortex by presynaptic kainate receptors." Neuropharmacology 60, no. 6 (May 2011): 832–41. http://dx.doi.org/10.1016/j.neuropharm.2010.12.023.

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44

Fiszman, Mónica L., Ferenc Erdélyi, Gábor Szabó, and Stefano Vicini. "Presynaptic AMPA and kainate receptors increase the size of GABAergic terminals and enhance GABA release." Neuropharmacology 52, no. 8 (June 2007): 1631–40. http://dx.doi.org/10.1016/j.neuropharm.2007.03.010.

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45

A. Cunha, Rodrigo, João O. Malva, and J. A. Ribeiro. "Pertussis toxin prevents presynaptic inhibition by kainate receptors of rat hippocampal [3 H]GABA release." FEBS Letters 469, no. 2-3 (March 8, 2000): 159–62. http://dx.doi.org/10.1016/s0014-5793(00)01272-2.

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46

Hwang, Se Jin, Silvia Pagliardini, Aldo Rustioni, and Juli G. Valtschanoff. "Presynaptic kainate receptors in primary afferents to the superficial laminae of the rat spinal cord." Journal of Comparative Neurology 436, no. 3 (2001): 275–89. http://dx.doi.org/10.1002/cne.1067.

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Kullmann, Dimitri M., Ming-Yuan Min, Fredrik Asztely, and Dmitri A. Rusakov. "Extracellular glutamate diffusion determines the occupancy of glutamate receptors at CA1 synapses in the hippocampus." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (February 28, 1999): 395–402. http://dx.doi.org/10.1098/rstb.1999.0392.

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Following exocytosis at excitatory synapses in the brain, glutamate binds to several subtypes of postsynaptic receptors. The degree of occupancy of AMPA and NMDA receptors at hippocampal synapses is, however, not known. One approach to estimate receptor occupancy is to examine quantal amplitude fluctuations of postsynaptic signals in hippocampal neurons studied in vitro . The results of such experiments suggest that NMDA receptors at CA1 synapses are activated not only by glutamate released from the immediately apposed presynaptic terminals, but also by glutamate spillover from neighbouring terminals. Numerical simulations point to the extracellular diffusion coefficient as a critical parameter that determines the extent of activation of receptors positioned at different distances from the release site. We have shown that raising the viscosity of the extracellular medium can modulate the diffusion coefficient, providing an experimental tool to investigate the role of diffusion in activation of synaptic and extrasynaptic receptors. Whether intersynaptic cross–talk mediated by NMDA receptors occurs in vivo remains to be determined. The theoretical and experimental approaches described here also promise to shed light on the roles of metabotropic and kainate receptors, which often occur in an extrasynaptic distribution, and are therefore positioned to sense glutamate escaping from the synaptic cleft.

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Kidd, Fleur L., and John T. R. Isaac. "Kinetics and Activation of Postsynaptic Kainate Receptors at Thalamocortical Synapses: Role of Glutamate Clearance." Journal of Neurophysiology 86, no. 3 (September 1, 2001): 1139–48. http://dx.doi.org/10.1152/jn.2001.86.3.1139.

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Kainate (KA) receptor-mediated excitatory postsynaptic currents (EPSCs) exhibit slow kinetics at the great majority of synapses. However, native or heterologously expressed KA receptors exhibit rapid kinetics in response to agonist application. One possibility to explain this discrepancy is that KA receptors are extrasynaptic and sense glutamate diffusing from the synaptic cleft. We investigated this by studying the effect of three manipulations that change glutamate clearance on evoked KA EPSCs at thalamocortical synapses. First, we used high-frequency stimulation to increase extrasynaptic glutamate levels. This caused an apparent increase in the relative contribution of the KA EPSC to transmission and slowed the decay kinetics. However, scaling and summing the EPSC evoked at low frequency reproduced this, demonstrating that the effect was due to postsynaptic summation of KA EPSCs. Second, we applied inhibitors of high-affinity glutamate transport. This caused a depression in both AMPA and KA EPSC amplitude due to the activation of a presynaptic glutamatergic autoreceptor. However, transport inhibitors had no selective effect on the amplitude or kinetics of the KA EPSC. Third, to increase glutamate clearance, we raised temperature during recordings. This shortened the decay of both the AMPA and KA components and increased their amplitudes, but this effect was the same for both. Therefore these data provide evidence against glutamate diffusion out of the synaptic cleft as the mechanism for the slow kinetics of KA EPSCs. Other possibilities such as interactions of KA receptors with other proteins or novel properties of native synaptic heteromeric receptors are required to explain the slow kinetics.

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Bernabeu, Ramon, and Frank R. Sharp. "NMDA and AMPA/Kainate Glutamate Receptors Modulate Dentate Neurogenesis and CA3 Synapsin-I in Normal and Ischemic Hippocampus." Journal of Cerebral Blood Flow & Metabolism 20, no. 12 (December 2000): 1669–80. http://dx.doi.org/10.1097/00004647-200012000-00006.

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The effect of N-methyl-d-aspartate (NMDA) and 2-(aminomethyl)phenylacetic acid/kainate (AMPA/kainate) glutamate receptors on dentate cell proliferation and hippocampal synapsin-I induction was examined after global ischemia. Cell proliferation was assessed using BrdU labeling, and synaptic responses were assessed using synapsin-I expression, Systemic glutamate receptor antagonists (MK-801 and NBQX) increased BrdU-labeled cells in the dentate subgranular zone (SGZ) of control adult gerbils (30% to 90%, P < 0.05). After global ischemia (at 15 days after 10 minutes of ischemia), most CA1 pyramidal neurons died, whereas the numbers of BrdU-labeled cells in the SGZ increased dramatically (>1000%, P < 0,0001). Systemic injections of MK801 or NBQX, as well as intrahippocampal injections of either drug, when given at the time of ischemia completely blocked the birth of cells in the SGZ and the death of CA1 pyramidal neurons at 15 days after ischemia. Glutamate receptor antagonists had little effect on cell birth and death when administered 7 days after ischemia. The induction of synapsin-I protein in stratum moleculare of CA3 at 7 and 15 days after global ischemia was blocked by pretreatment with systemic or intrahippocampal MK-801 or NBQX. It is proposed that decreased dentate glutamate receptor activation—produced by glutamate receptor antagonists in normal animals and by chronic ischemic hippocampal injury—may trigger dentate neurogenesis and synaptogenesis. The synapsin-I induction in mossy fiber terminals most likely represents re-modeling of dentate granule cell neuron presynaptic elements in CA3 in response to the ischemia. The dentate neurogenesis and synaptogenesis that occur after ischemia may contribute to memory recovery after hippocampal injury caused by global ischemia.

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Braga, Maria F. M., Vassiliki Aroniadou-Anderjaska, Jianwu Xie, and He Li. "Bidirectional Modulation of GABA Release by Presynaptic Glutamate Receptor 5 Kainate Receptors in the Basolateral Amygdala." Journal of Neuroscience 23, no. 2 (January 15, 2003): 442–52. http://dx.doi.org/10.1523/jneurosci.23-02-00442.2003.

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