A simple exploratory algorithm for the accurate and fast detection of spontaneous synaptic events

Kudoh, Suguru N.; Taguchi, Takahisa

doi:10.1016/s0956-5663(02)00053-2

Cited by 51 publications

(53 citation statements)

References 17 publications

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“…1); its role in physiological conditions, however, remains to be determined. Differential mechanisms of Ca 2ϩ signaling at GrC and mf synapses need to be further studied in relation with plasticity (Kelly et al, 2009;Robberechts et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Granule Cell Ascending Axon Excitatory Synapses onto Golgi Cells Implement a Potent Feedback Circuit in the Cerebellar Granular Layer

Cesana

Pietrajtis

Bidoret

et al. 2013

Journal of Neuroscience

113

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The function of inhibitory interneurons within brain microcircuits depends critically on the nature and properties of their excitatory synaptic drive. Golgi cells (GoCs) of the cerebellum inhibit cerebellar granule cells (GrCs) and are driven both by feedforward mossy fiber (mf) and feedback GrC excitation. Here, we have characterized GrC inputs to GoCs in rats and mice. We show that, during sustained mf discharge, synapses from local GrCs contribute equivalent charge to GoCs as mf synapses, arguing for the importance of the feedback inhibition. Previous studies predicted that GrC-GoC synapses occur predominantly between parallel fibers (pfs) and apical GoC dendrites in the molecular layer (ML). By combining EM and Ca 2ϩ imaging, we now demonstrate the presence of functional synaptic contacts between ascending axons (aa) of GrCs and basolateral dendrites of GoCs in the granular layer (GL). Immunohistochemical quantification estimates these contacts to be ϳ400 per GoC. Using Ca 2ϩ imaging to identify synaptic inputs, we show that EPSCs from aa and mf contacts in basolateral dendrites display similarly fast kinetics, whereas pf inputs in the ML exhibit markedly slower kinetics as they undergo strong filtering by apical dendrites. We estimate that approximately half of the local GrC contacts generate fast EPSCs, indicating their basolateral location in the GL. We conclude that GrCs, through their aa contacts onto proximal GoC dendrites, define a powerful feedback inhibitory circuit in the GL.

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Section: Discussionmentioning

confidence: 99%

Granule Cell Ascending Axon Excitatory Synapses onto Golgi Cells Implement a Potent Feedback Circuit in the Cerebellar Granular Layer

Cesana

Pietrajtis

Bidoret

et al. 2013

Journal of Neuroscience

113

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“…Data were analyzed using IGOR Pro (Wavemetrics) together with Neuromatic (Jason Rothman). Events were detected using amplitude threshold crossing (15), with the threshold (typically ϳ7-8 pA) set according to the baseline current variance. For amplitude and kinetic analyses, only events with monotonic fast rise (Ͻ1 ms) and uncontaminated decay were included.…”

Section: Methodsmentioning

confidence: 99%

Novel Regulation of the Synthesis of α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptor Subunit GluA1 by Carnitine Palmitoyltransferase 1C (CPT1C) in the Hippocampus

Fadó

Soto

Miñano-Molina

et al. 2015

Journal of Biological Chemistry

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Background:One interacting partner of the AMPA receptor (AMPAR) complex in the endoplasmic reticulum is carnitine palmitoyltransferase 1C (CPT1C). Results: CPT1C regulates synaptic AMPAR levels and synaptic transmission by post-transcriptional regulation of GluA1 protein synthesis. Conclusion: CPT1C is a new regulator of AMPAR translation efficiency. Significance: CPT1C modulation could be a new tool to prevent AMPAR decline and learning deficits.

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“…Miniature IPSCs were detected using custom-written functions in IgorPro (Wavemetrics), which implemented the algorithm described by Kudoh and Taguchi (2002). Event rates for control conditions were calculated in a 1 min window before the addition of drug.…”

Section: Methodsmentioning

confidence: 99%

Recurrent Dendrodendritic Inhibition of Accessory Olfactory Bulb Mitral Cells Requires Activation of Group I Metabotropic Glutamate Receptors

Castro¹,

Hovis²,

Urban³

2007

J. Neurosci.

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Metabotropic glutamate receptors (mGluRs) modulate neural excitability and network tone in many brain regions. Expression of mGluRs is particularly high in the accessory olfactory bulb (AOB), a CNS structure critical for detecting chemicals that identify kin and conspecifics. Because of its relative simplicity and its direct projection to the hypothalamus, the AOB provides a model system for studying how mGluRs affect the flow of encoded sensory information to downstream areas. We investigated the role of group I mGluRs in synaptic processing in AOB slices and found that under control conditions, recurrent inhibition of principal neurons (mitral cells) was completely eliminated by the mGluR1 antagonist LY367385 [(S)-(ϩ)-␣-amino-4-carboxy-2 methylbenzeneacetic acid]. In addition, the group I mGluR agonist DHPG [(S)-3,5-dihydroxyphenylglycine; 20 M] induced a dramatic increase in the rate of spontaneous IPSCs. This increase was dependent on voltage-gated calcium channels but persisted even after blockade of ionotropic glutamatergic transmission and sodium channels. Together, these results indicate that mGluR1 plays a critical role in controlling information flow through the AOB and suggest that mGluR1 may be an important locus for experience-dependent changes in synaptic function.

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A simple exploratory algorithm for the accurate and fast detection of spontaneous synaptic events

Cited by 51 publications

References 17 publications

Granule Cell Ascending Axon Excitatory Synapses onto Golgi Cells Implement a Potent Feedback Circuit in the Cerebellar Granular Layer

Granule Cell Ascending Axon Excitatory Synapses onto Golgi Cells Implement a Potent Feedback Circuit in the Cerebellar Granular Layer

Novel Regulation of the Synthesis of α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptor Subunit GluA1 by Carnitine Palmitoyltransferase 1C (CPT1C) in the Hippocampus

Recurrent Dendrodendritic Inhibition of Accessory Olfactory Bulb Mitral Cells Requires Activation of Group I Metabotropic Glutamate Receptors

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