Transient oxytocin signaling primes the development and function of excitatory hippocampal neurons

Ripamonti, Silvia; Ambrozkiewicz, Mateusz C.; Guzzi, Francesco; Gravati, Marta; Biella, Gerardo; Bormuth, Ingo; Hammer, Markus; Tuffy, Liam P.; Sigler, Albrecht; Kawabe, Hiroshi; Nishimori, Katsuhiko; Toselli, Mauro; Brose, Nils; Parenti, Marco; Rhee, Jeong−Seop

doi:10.7554/elife.22466

Cited by 68 publications

(57 citation statements)

References 87 publications

(116 reference statements)

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“…Exposure of perinatal hippocampal neurons to Oxt reduces both the number and strength of excitatory synapses while GABAergic synapses are unaffected. Slices prepared from both Oxtr wildtype and deficient mice indicate that loss of Oxtr signaling increases dendritic complexity of both CA3 and CA1 pyramidal neurons and is paralleled with increases in sEPSCs . Thus, early developmental Oxt signaling in the hippocampus plays a critical neuroprotective role and shapes circuit development in young offspring.…”

Section: Neurophysiological Mechanisms Of Oxytocin and Vasopressin Inmentioning

confidence: 99%

Oxytocin and vasopressin in the rodent hippocampus

Cilz

Cymerblit‐Sabba

Young

2018

Genes Brain and Behavior

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The role of the hippocampus in social memory and behavior is under intense investigation. Oxytocin (Oxt) and vasopressin (Avp) are two neuropeptides with many central actions related to social cognition. Oxt‐ and Avp‐expressing fibers are abundant in the hippocampus and receptors for both peptides are seen throughout the different subfields, suggesting that Oxt and Avp modulate hippocampal‐dependent processes. In this review, we first focus on the anatomical sources of Oxt and Avp input to the hippocampus and consider the distribution of their corresponding receptors in different hippocampal subfields and neuronal populations. We next discuss the behavioral outcomes related to social memory seen with perturbation of hippocampal Oxt and Avp signaling. Finally, we review Oxt and Avp modulatory mechanisms in the hippocampus that may underlie the behavioral roles for both peptides.

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Section: Neurophysiological Mechanisms Of Oxytocin and Vasopressin Inmentioning

confidence: 99%

Oxytocin and vasopressin in the rodent hippocampus

Cilz

Cymerblit‐Sabba

Young

2018

Genes Brain and Behavior

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“…6A and 6B). Notably, bath application of 100 nM KA (Ripamonti et al, 2017) (Table S1Y). (D and E) Quantification of the frequency (D;…”

Section: Ube3b Cko Mice Show Altered Local Network Activity In the Himentioning

confidence: 99%

“…Briefly, autaptic cultured neurons (9-14DIV) were whole-cell voltage-clamped at −70 mV with the amplifier EPSC10 (HEKA) under the control of the Patchmaster 2 program (HEKA) (Ripamonti et al, 2017). All acquired traces were analyzed using AxoGraph X (AxoGraph Scientific inserted into CA3 pyramidal cell layer, and extracellular field potential were recorded for more than 20 minutes before the addition of 50 nM or 100 nM kainate.…”

Section: Autaptic Neuronsmentioning

confidence: 99%

The Kaufman oculocerebrofacial syndrome protein Ube3b regulates synapse number by ubiquitinating Ppp3cc

Ambrozkiewicz

Ripamonti

Борисова

et al. 2019

Preprint

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Kaufman oculocerebrofacial syndrome (KOS) is a severe autosomal recessive disorder characterized by intellectual disability, developmental delays, microcephaly and characteristic dysmorphisms. Biallelic mutations of UBE3B, encoding for a ubiquitin ligase E3B are causative for KOS. In this report, we characterize neuronal functions of its murine ortholog Ube3b. We show that Ube3b regulates dendritic branching in a cell-autonomous manner.Moreover, Ube3b knockout (KO) neurons exhibit increased density and aberrant morphology of dendritic spines, altered synaptic physiology and changes in hippocampal circuit activity. Dorsal forebrain-specific Ube3b KO animals show impaired spatial learning and alterations in social interactions. We further demonstrate that Ube3b ubiquitinates the catalytic γ-subunit of calcineurin (Ppp3cc), the overexpression of which phenocopies the loss of Ube3b with regard to dendritic spine density. This work provides insights into the molecular pathologies underlying intellectual disability-like phenotypes in a genetic mouse model for KOS.

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“…Recordings of LFPs from acute hippocampal slices and the induction of oscillations were performed as previously described (Ripamonti et al, 2017). The frequency at maximum…”

Section: In Vitro Recording Of γ-Oscillationsmentioning

confidence: 99%

Physiological and pathophysiological homeostasis of astroglial channel proteins by Nedd4-2

Altas

Solis

et al. 2019

Preprint

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ORCID for Hiroshi Kawbae; https://orcid.org/0000-0001-5650-8696 CONDENSED TITLE:Ubiquitination of Astrocytic Channels by Nedd4-2 SUMMARY:Ubiquitination is a key regulatory machinery for protein expression. Our present work provides evidence that astrocytic ion channel proteostasis coordinated by an E3 ubiquitin ligase Nedd4-2 is of particular importance for the maintenance of neuronal network activity. ABSTRACTNedd4-2 is an E3 ubiquitin ligase, missense mutation of which is related to familial epilepsy, indicating its critical role in regulating neuronal network activity. However, Nedd4-2 substrates involved in neuronal network function have yet to be identified. Using mouse lines lacking Nedd4-1 and Nedd4-2, we identified astrocytic channel proteins inwardly rectifying K + channel 4.1 (Kir4.1) and Connexin43 as Nedd4-2 substrates. We found that the expression of Kir4.1 and Connexin43 is increased upon conditional deletion of Nedd4-2 in astrocytes, leading to an elevation of astrocytic membrane ion permeability and gap junction activity, with a consequent reduction of γ-oscillatory neuronal network activity. Interestingly, our biochemical data demonstrate that missense mutations found in familial epileptic patients produce gain-of-function of Nedd4-2 gene product. Our data reveal a process of coordinated astrocytic ion channel proteostasis that controls astrocyte function and astrocyte-dependent neuronal network activity, and elucidate a potential mechanism by which aberrant Nedd4-2 function leads to epilepsy.

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Transient oxytocin signaling primes the development and function of excitatory hippocampal neurons

Cited by 68 publications

References 87 publications

Oxytocin and vasopressin in the rodent hippocampus

Oxytocin and vasopressin in the rodent hippocampus

The Kaufman oculocerebrofacial syndrome protein Ube3b regulates synapse number by ubiquitinating Ppp3cc

Physiological and pathophysiological homeostasis of astroglial channel proteins by Nedd4-2

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