A Presynaptic Kainate Receptor Is Involved in Regulating the Dynamic Properties of Thalamocortical Synapses during Development

Kidd, Fleur L.; Coumis, Urania; Collingridge, Graham L.; Crabtree, John W.; Isaac, John T.R.

doi:10.1016/s0896-6273(02)00699-2

Cited by 71 publications

(64 citation statements)

References 53 publications

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“…Synaptically released glutamate, acting on kainate receptors, has been shown to modulate excitatory transmission in the hippocampus (Contractor et al, 2001;Lauri et al, 2001) and immature neocortex (Kidd and Issac, 2001;Kidd et al, 2002). In the present study we found that bath application of the GluR5 antagonist LY382884 decreased EPSC amplitudes and changed paired-pulse facilitation to paired-pulse depression.…”

Section: Kainate Facilitation Involves Glur5 Subunitssupporting

confidence: 58%

“…Physiologically released glutamate has been shown to modulate excitatory transmission in the hippocampus (Contractor et al, 2001;Lauri et al, 2001) and immature neocortex (Kidd and Issac, 2001;Kidd et al, 2002). To test whether synaptically released glutamate could affect EPSCs in layer II/III pyramidal cells, we examined responses to paired pulse stimulation before and after bath application of the GluR5 antagonist LY382884.…”

Section: Facilitation Of Spontaneous Epscs By Kainatementioning

confidence: 99%

“…This view has recently been undergoing revision since ionotropic kainate receptors are known to be located presynaptically in several brain regions including amygdala , cerebellum (Delaney and Jahr, 2002), hippocampus (Vignes et al, 1998;Schmitz et al, 2001) and substantia nigra pars compacta (Nakamura et al, 2003) where they can either facilitate or depress synaptic transmission. In developing neocortex, high frequency stimulation or application of kainate receptor agonists produces a significant EPSC depression via presynaptic kainate receptors (Kidd et al, 2002). Glutamate release from isolated cerebral cortex nerve terminals (synaptosomes), evoked by 4-aminopyridine, is enhanced by presynaptic kainate receptors (Perkinton and Sihra, 1999), indicating that facilitatory autoreceptors are also present in neocortex.…”

Section: Introductionmentioning

confidence: 99%

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Pre- and postsynaptic effects of kainate on layer II/III pyramidal cells in rat neocortex

2007

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Kainate receptors mediate both direct excitatory and indirect modulatory actions in the CNS. We report here that kainate has both pre-and postsynaptic actions in layer II/III pyramidal neurons of rat prefrontal cortex. Application of low concentration of kainate (50-500 nM) increased the amplitude of evoked excitatory postsynaptic currents (EPSCs) whereas higher concentrations (3 μM) caused a decrease. The frequency of spontaneous and miniature (action potential-independent) EPSCs was increased by low concentrations of kainate without affecting their amplitudes, suggesting a presynaptic mechanism of action. The facilitatory and inhibitory effects of kainate were mimicked by the GluR5 subunit selective agonist ATPA. In addition to decreasing EPSC amplitudes, high concentrations of kainate and ATPA induced an inward current which was not blocked by AMPAor NMDA-receptor antagonists GYKI52466 and D-APV, respectively. The inward currents were blocked by the AMPA/KA receptor antagonist CNQX, indicating the presence of postsynaptic kainate receptors. Single shock stimulation in the presence of GYKI52466 and D-APV evoked an EPSC which was blocked by CNQX. The GluR5 antagonist LY382884 changed paired-pulse facilitation to paired pulse depression, indicating that synaptically released glutamate can activate presynaptic kainate receptors. These results suggest that kainate receptors containing GluR5 subunits play a major role in glutamatergic transmission in rat neocortex, having both presynaptic modulatory and direct postsynaptic excitatory actions.

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Section: Kainate Facilitation Involves Glur5 Subunitssupporting

confidence: 58%

Section: Facilitation Of Spontaneous Epscs By Kainatementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pre- and postsynaptic effects of kainate on layer II/III pyramidal cells in rat neocortex

2007

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“…A large number of genes, potentially involved in synaptic plasticity and axon growth, have been found to be transiently expressed in the ventrobasal thalamic nuclei, with a time course that could match the time course of this form of TCA plasticity because they are maximal during the first postnatal week, with a rapid decrease of expression after P10. Among these genes, the kainate receptors (Kidd et al, 2002), adenylate cyclase 1 (Nicol et al, 2005), the serotonin transporter, and the 5-HT 1B receptor (for review, see Gaspar et al, 2003) could potentially be important for permitting this developmental remodeling of thalamocortical axons to occur.…”

Section: Discussionmentioning

confidence: 99%

Dissociating Barrel Development and Lesion-Induced Plasticity in the Mouse Somatosensory Cortex

Rebsam

Seif²,

Gaspar³

2005

J. Neurosci.

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In the mouse somatosensory cortex, thalamocortical axons (TCAs) corresponding to individual whiskers cluster into restricted barrel domains during the first days of life. If whiskers are lesioned before that time, the cortical space devoted to the afferents from the damaged whisker shrinks and becomes occupied by thalamocortical afferents from neighboring unlesioned whiskers. This plasticity ends by postnatal day 3 (P3) to P4 when barrels emerge. To test whether TCA development and lesion-induced plasticity are linked, we used monoamine oxidase A knock-out (MAOA-KO) mice in which normal TCA development is halted by an excess of serotonin. Normal TCA development can be restored when serotonin levels are lowered by parachlorophenylalanine (PCPA). By varying the time of PCPA administration, we found that barrel development can be reinitiated until P11, although the emergence of TCA clusters becomes gradually slower and less complete. In mice in which barrels emerge 3 d later than the normal schedule, at P6 instead of P3, we examined lesion-induced plasticity. We find a progressive decline of the lesion-induced plasticity and a closure at P3, similar to normal mice, showing that this plasticity is not influenced by an excess of serotonin levels. Thus, in MAOA-KO mice, the emergence of barrel patterning can be delayed without a concomitant delay in lesion-induced plasticity, and the cortical space devoted to one whisker representation cannot be modified by the periphery once patterning is imprinted in the subcortical relays. We conclude that the closure of the lesioninduced plasticity period in the barrelfield is probably not determined at the cortical level.

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“…This developmental decrease closely matches the developmental loss of the ability to induce LTP at these synapses (Crair and Malenka, 1995) supporting the idea that unsilencing is an important mechanism for TC LTP. Subsequent evidence for the presence of silent TC synapses has come in the form of differing short-term plasticity of AMPA and NMDA receptor-mediated synaptic currents (Yanagisawa et al, 2004) although these data appear to contradict finding of other groups at the same synapse (Gil et al, 1997;Gil et al, 1999;Kidd et al, 2002).…”

Section: Long-term Potentiation (Ltp) At Tc Synapsesmentioning

confidence: 97%

Developmental synaptic plasticity at the thalamocortical input to barrel cortex: Mechanisms and roles

Daw

Scott

Isaac

2007

Molecular and Cellular Neuroscience

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The thalamocortical (TC) input to layer IV provides the major pathway for ascending sensory information to the mammalian sensory cortex. During development there is a dramatic refinement of this input that underlies the maturation of the topographical map in layer IV. Over the last ten years our understanding of the mechanisms of the developmental and experience-driven changes in synaptic function at TC synapses has been greatly advanced. Here we describe these studies that point to a key role for NMDA receptor-dependent synaptic plasticity, a role for kainate receptors and for a rapid maturation in GABAergic inhibition. The expression mechanisms of some of the forms of neonatal synaptic plasticity are novel and, in combination with other mechanisms, produce a layer IV circuit that exhibits functional properties necessary for mature sensory processing.

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A Presynaptic Kainate Receptor Is Involved in Regulating the Dynamic Properties of Thalamocortical Synapses during Development

Cited by 71 publications

References 53 publications

Pre- and postsynaptic effects of kainate on layer II/III pyramidal cells in rat neocortex

Pre- and postsynaptic effects of kainate on layer II/III pyramidal cells in rat neocortex

Dissociating Barrel Development and Lesion-Induced Plasticity in the Mouse Somatosensory Cortex

Developmental synaptic plasticity at the thalamocortical input to barrel cortex: Mechanisms and roles

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