Does extracellular proteolysis control mammalian cognition?

Tamura, Hideki; Ishikawa, Yasuyuki; Shiosaka, Sadao

doi:10.1515/revneuro-2013-0007

Cited by 17 publications

(12 citation statements)

References 77 publications

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“…10 Because the activation of synaptic proteolysis largely depends on neural activity, extracellular proteases have distinct effects on activity-dependent neural events that underlie cognitive function. 11, 12, 13 Indeed, recent studies showed that extracellular proteolysis has a critical role in dynamic synaptic remodeling, long-term potentiation, synaptic plasticity, memory formation and epileptogenesis.…”

Section: Introductionmentioning

confidence: 99%

Ablation of neuropsin–neuregulin 1 signaling imbalances ErbB4 inhibitory networks and disrupts hippocampal gamma oscillation

et al. 2017

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Parvalbumin-expressing interneurons are pivotal for the processing of information in healthy brain, whereas the coordination of these functions is seriously disrupted in diseased brain. How these interneurons in the hippocampus participate in pathological functions remains unclear. We previously reported that neuregulin 1 (NRG1)–ErbB4 signaling, which is actuated by neuropsin, is important for coordinating brain plasticity. Neuropsin cleaves mature NRG1 (bound to extracellular glycosaminoglycans) in response to long-term potentiation or depression, liberating a soluble ligand that activates its receptor, ErbB4. Here, we show in mice that kainate-induced status epilepticus transiently elevates the proteolytic activity of neuropsin and stimulates cFos expression with a time course suggesting that activation of ErbB4- and parvalbumin-expressing interneurons follows the excitation and subsequent silencing of pyramidal neurons. In neuropsin-deficient mice, kainate administration impaired signaling and disrupted the neuronal excitation–inhibition balance (E/I balance) in hippocampal networks, by decreasing the activity of parvalbumin-positive interneurons while increasing that of pyramidal neurons, resulting in the progression of status epilepticus. Slow, but not fast, gamma oscillations in neuropsin-deficient mice showed reduced power. Intracerebroventricular infusion of the soluble NRG1 ligand moiety restored the E/I balance, status epilepticus and gamma oscillations to normal levels. These results suggest that the neuropsin–NRG1 signaling system has a role in pathological processes underlying temporal lobe epilepsy by regulating the activity of parvalbumin-expressing interneurons, and that neuropsin regulates E/I balance and gamma oscillations through NRG1–ErbB4 signaling toward parvalbumin-expressing interneurons. This neuronal system may be a useful target of pharmacological therapies against cognitive disorders.

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Section: Introductionmentioning

confidence: 99%

Ablation of neuropsin–neuregulin 1 signaling imbalances ErbB4 inhibitory networks and disrupts hippocampal gamma oscillation

et al. 2017

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“…In fact, Tsien [92] has proposed that such a cleavage may relieve the synapses/dendritic spines from local environmental constraints limiting their growth, any by this virtue allowing them to undergo plastic changes supporting learning and memory. It should be noted that disruption of ECM may indeed affect synaptic plasticity [93][94][95][96]. Although, possible role of MMP-9 in ECM remodeling has been suggested by studies on the cerebellum, no clear MMP-9 substrate has emerged, and in fact we have failed to demonstrate that MMP-9 cleaves suspected substrate, tenascin-C [97,98].…”

Section: Synaptic Cell Adhesion Molecules As Major Neuronal Mmp-9 Tarmentioning

confidence: 71%

Od c-Fos do MMP-9 w kontroli plastyczności synaptycznej zdrowego i chorego umysłu, spojrzenie osobiste

Kaczmarek¹

2018

Postepy Biochem

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c-Fos jest składnikiem czynnika transkrypcyjnego AP-1. Trzy linie dowodów wspierają kluczową rolę c-Fos w uczeniu się i pamięci: (i) uczenie się pobudza jego ekspresję; (ii) blokowanie c-Fos upośledza, podczas gdy optogenetyczna aktywacja neuronów wyrażających c-Fos wspomaga uczenie się i pamięć; (iii) docelowe geny dla c-Fos/AP-1 w pobudzonych neuronach, kodują tkankowy inhibitor metaloproteaz-1 (TIMP-1) oraz metaloproteazę macierzową 9 (MMP-9), które to białka odgrywają kluczową rolę w plastyczności synaptycznej, leżącej u podstaw uczenia się i pamięci. TIMP-1 i MMP-9 tworzą działający zewnątrzkomórkowo układ enzymatyczny, aktywny miejscowo wokół synaps pobudzających i modulujący ich morfologię, skład biochemiczny oraz efektywność. Badania na zwierzętach sugerują zaangażowanie MMP-9 w różnych stanach neuropsychicznych, np. rozwoju padaczki, zaburzeniach ze spektrum autyzmu, rozwoju uzależnienia i depresji. U ludzi MMP-9 przyczynia się do padaczki, uzależnienia od alkoholu i kokainy, zespołu łamliwego chromosomu X, schizofrenii i zaburzeń afektywnych dwubiegunowych. Łącznie wszystkie te sytuacje można uznać za przykładowe dla zdrowego lub chorego umysłu.

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“…Focalized proteolysis of synaptic ECMs and CAMs by serine proteases and MMPs might participate in a mechanical and signaling conversion system during neural plasticity (Yoshida and Shiosaka, 1999;Shiosaka, 2004;Shiosaka and Ishikawa, 2011). The advantage of this system is the quick and local activation of extracellular zymogen, fine-tuning of cellular responses by altering protease/inhibitor balance, and, in some cases, simultaneous induction of multiple signals (Tamura et al, 2013). Actually, pre-and postsynaptic sides get in direct contact with each other via CAMs that can regulate synaptic efficacy, by recruiting scaffolding proteins, neurotransmitter receptors, and synaptic vesicles in response to the binding of counter-receptors across the synaptic cleft.…”

Section: The Main Functional Characteristics Of the Ecm And Of The Ecsmentioning

confidence: 99%

On the role of the extracellular space on the holistic behavior of the brain

Marcoli¹,

Agnati²,

Benedetti

et al. 2015

Reviews in the Neurosciences

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AbstractMultiple players are involved in the brain integrative action besides the classical neuronal and astrocyte networks. In the past, the concept of complex cellular networks has been introduced to indicate that all the cell types in the brain can play roles in its integrative action. Intercellular communication in the complex cellular networks depends not only on well-delimited communication channels (wiring transmission) but also on diffusion of signals in physically poorly delimited extracellular space pathways (volume transmission). Thus, the extracellular space and the extracellular matrix are the main players in the intercellular communication modes in the brain. Hence, the extracellular matrix is an ‘intelligent glue’ that fills the brain and, together with the extracellular space, contributes to the building-up of the complex cellular networks. In addition, the extracellular matrix is part of what has been defined as the global molecular network enmeshing the entire central nervous system, and plays important roles in synaptic contact homeostasis and plasticity. From these premises, a concept is introduced that the global molecular network, by enmeshing the central nervous system, contributes to the brain holistic behavior. Furthermore, it is suggested that plastic ‘brain compartments’ can be detected in the central nervous system based on the astrocyte three-dimensional tiling of the brain volume and on the existence of local differences in cell types and extracellular space fluid and extracellular matrix composition. The relevance of the present view for neuropsychiatry is discussed. A glossary box with terms and definitions is provided.

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Does extracellular proteolysis control mammalian cognition?

Cited by 17 publications

References 77 publications

Ablation of neuropsin–neuregulin 1 signaling imbalances ErbB4 inhibitory networks and disrupts hippocampal gamma oscillation

Ablation of neuropsin–neuregulin 1 signaling imbalances ErbB4 inhibitory networks and disrupts hippocampal gamma oscillation

Od c-Fos do MMP-9 w kontroli plastyczności synaptycznej zdrowego i chorego umysłu, spojrzenie osobiste

On the role of the extracellular space on the holistic behavior of the brain

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