Repetition of mGluR-dependent LTD causes slowly developing persistent reduction in synaptic strength accompanied by synapse elimination

Shinoda, Yo; Kamikubo, Yuji; Egashira, Yasuyuki; Tominaga-Yoshino, Keiko; Ogura, Akihiko

doi:10.1016/j.brainres.2005.02.028

Cited by 49 publications

(49 citation statements)

References 26 publications

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“…The predicted sustained long term depression in the cortex will also lead in the long run to the pruning of the affected synapses (Shinoda et al, 2005). The link between synaptic pruning and Schizophrenia has been investigated for nearly 3 decades (Feinberg, 1982;Rapoport et al, 2005;Iglesias and Villa, 2007) and is well established.…”

Section: Discussionmentioning

confidence: 99%

How feedback inhibition shapes spike-timing-dependent plasticity and its implications for recent Schizophrenia models

et al. 2011

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It has been shown that plasticity is not a fixed property but, in fact, changes depending on the location of the synapse on the neuron and/or changes of biophysical parameters. Here we investigate how plasticity is shaped by feedback inhibition in a cortical microcircuit. We use a differential Hebbian learning rule to model spike-timing dependent plasticity and show analytically that the feedback inhibition shortens the time window for LTD during spike-timing dependent plasticity but not for LTP. We then use a realistic GENESIS model to test two hypothesis about interneuron hypofunction and conclude that a reduction in GAD67 is the most likely candidate as the cause for hypofrontality as observed in Schizophrenia.

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Section: Discussionmentioning

confidence: 99%

How feedback inhibition shapes spike-timing-dependent plasticity and its implications for recent Schizophrenia models

et al. 2011

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“…It is therefore tempting to speculate that impaired synaptic plasticity may underlie specific cognitive deficits incurred during induction of chronic epilepsy. An additional, particularly intriguing issue is suggested by a previous study in which repeated induction of mGluR LTD caused elimination of glutamatergic synapses (Shinoda et al, 2005). Thus, a loss of mGluR LTD may cause an impaired capacity to eliminate synapses in the epileptic brain.…”

Section: Functional Consequences Of Impaired Mglur Ltdmentioning

confidence: 97%

Loss of Metabotropic Glutamate Receptor-Dependent Long-Term Depression via Downregulation of mGluR5 after Status Epilepticus

Kirschstein

Bauer²,

Müller³

et al. 2007

J. Neurosci.

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“…mGluRdependent LTD has been implicated in synaptic remodeling during development, especially at synapses in which such LTD is age dependent (Li et al, 2002). For instance, mGluR I/II-LTD of glutamate synapses is accompanied by synaptic elimination at CA3-CA1 synapses in hippocampus (Shinoda et al, 2005), and mGluR I-LTD contributes to synaptic elimination of climbing fiber synapses on cerebellar Purkinje neurons (Ichise et al, 2000). In the auditory system, LTD at inhibitory synapses may contribute to synaptogenesis and synaptic refinement Kotak et al, 2001).…”

Section: Functional Implicationsmentioning

confidence: 99%

Activation of Synaptic Group II Metabotropic Glutamate Receptors Induces Long-Term Depression at GABAergic Synapses in CNS Neurons

et al. 2013

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Metabotropic glutamate receptor (mGluR)-dependent homosynaptic long-term depression (LTD) has been studied extensively at glutamatergic synapses in the CNS. However, much less is known about heterosynaptic long-term plasticity induced by mGluRs at inhibitory synapses. Here we report that pharmacological or synaptic activation of group II mGluRs (mGluR II) induces LTD at GABAergic synapses without affecting the excitatory glutamatergic transmission in neurons of the chicken cochlear nucleus. Coefficient of variation and failure rate analysis suggested that the LTD was expressed presynaptically. The LTD requires presynaptic spike activity, but does not require the activation of NMDA receptors. The classic cAMP-dependent protein kinase A signaling is involved in the transduction pathway. Remarkably, blocking mGluR II increased spontaneous GABA release, indicating the presence of tonic activation of mGluR II by ambient glutamate. Furthermore, synaptically released glutamate induced by electrical stimulations that concurrently activated both the glutamatergic and GABAergic pathways resulted in significant and constant suppression of GABA release at various stimulus frequencies (3.3, 100, and 300 Hz). Strikingly, low-frequency stimulation (1 Hz, 15 min) of the glutamatergic synapses induced heterosynaptic LTD of GABAergic transmission, and the LTD was blocked by mGluR II antagonist, indicating that synaptic activation of mGluR II induced the LTD. This novel form of long-term plasticity in the avian auditory brainstem may play a role in the development as well as in temporal processing in the sound localization circuit.

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Repetition of mGluR-dependent LTD causes slowly developing persistent reduction in synaptic strength accompanied by synapse elimination

Cited by 49 publications

References 26 publications

How feedback inhibition shapes spike-timing-dependent plasticity and its implications for recent Schizophrenia models

How feedback inhibition shapes spike-timing-dependent plasticity and its implications for recent Schizophrenia models

Loss of Metabotropic Glutamate Receptor-Dependent Long-Term Depression via Downregulation of mGluR5 after Status Epilepticus

Activation of Synaptic Group II Metabotropic Glutamate Receptors Induces Long-Term Depression at GABAergic Synapses in CNS Neurons

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