scholarly journals Collagen-derived matricryptins promote inhibitory nerve terminal formation in the developing neocortex

2016 ◽  
Vol 212 (6) ◽  
pp. 721-736 ◽  
Author(s):  
Jianmin Su ◽  
Jiang Chen ◽  
Kumiko Lippold ◽  
Aboozar Monavarfeshani ◽  
Gabriela Lizana Carrillo ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Nerve Terminal ◽  
Inhibitory Synapses ◽  
Mammalian Brain ◽  
Nerve Terminals ◽  
Brain Disorders ◽  
Integrin Receptors ◽  
Developing Neocortex ◽  
Cortical Circuit ◽  
Circuit Formation

Inhibitory synapses comprise only ∼20% of the total synapses in the mammalian brain but play essential roles in controlling neuronal activity. In fact, perturbing inhibitory synapses is associated with complex brain disorders, such as schizophrenia and epilepsy. Although many types of inhibitory synapses exist, these disorders have been strongly linked to defects in inhibitory synapses formed by Parvalbumin-expressing interneurons. Here, we discovered a novel role for an unconventional collagen—collagen XIX—in the formation of Parvalbumin+ inhibitory synapses. Loss of this collagen results not only in decreased inhibitory synapse number, but also in the acquisition of schizophrenia-related behaviors. Mechanistically, these studies reveal that a proteolytically released fragment of this collagen, termed a matricryptin, promotes the assembly of inhibitory nerve terminals through integrin receptors. Collectively, these studies not only identify roles for collagen-derived matricryptins in cortical circuit formation, but they also reveal a novel paracrine mechanism that regulates the assembly of these synapses.

Effects of high calcium solutions on glutamate sensitivity of crayfish muscle fibres

1980 ◽  
Vol 209 (1176) ◽  
pp. 415-429 ◽  
Keyword(s):  
Nerve Terminal ◽  
Aminobutyric Acid ◽  
Inhibitory Synapses ◽  
Muscle Fibres ◽  
Nerve Terminals ◽  
Direct Stimulation ◽  
Calcium Spikes ◽  
Crayfish Muscle ◽  
High Calcium ◽  
Denervated Muscles

Crayfish neuromuscular preparations were studied after 18-36 h exposure to high calcium solutions. As previously reported for frog neuromuscular preparations the treatment damaged the nerve terminals and decreased junctional potentials. The resting potentials and input resistances of the muscle fibres were not affected; but their sensitivity to glutamate was significantly decreased when compared to that of control muscles. After exposure to high calcium, the sensitivity to γ-aminobutyric acid, the putative transmitter at inhibitory synapses, was increased. Apparently normal twitches were elicited by direct stimulation, and calcium spikes could still be observed in the fibres. A decreased sensitivity to glutamate was also noted in experiments carried out on denervated muscles 8 months after section of the motor axons. Possible relations between nerve terminal damage and the decrease in sensitivity to glutamate are discussed.

scholarly journals Active presynaptic ribosomes in mammalian brain nerve terminals, and increased transmitter release after protein synthesis inhibition

2018 ◽  
Author(s):  
Matthew S. Scarnati ◽  
Rahul Kataria ◽  
Mohana Biswas ◽  
Kenneth G. Paradiso
Keyword(s):  
Protein Synthesis ◽  
Nerve Terminal ◽  
Brain Slices ◽  
Mammalian Brain ◽  
Nerve Terminals ◽  
Local Translation ◽  
Vesicle Recycling ◽  
Presynaptic Vesicle ◽  
Presynaptic Nerve Terminals ◽  
Presynaptic Protein

AbstractPresynaptic neuronal activity requires the localization of thousands of proteins that are typically synthesized in the soma and transported to nerve terminals. Local translation for some dendritic proteins occurs, but local translation in mammalian presynaptic nerve terminals is difficult to demonstrate. Here, we present evidence for local presynaptic protein synthesis in the mammalian brain at a glutamatergic nerve terminal. We show an essential ribosomal component, 5.8s rRNA, in terminals. We also show active translation in nerve terminals, in situ, in brain slices demonstrating ongoing presynaptic protein synthesis. After inhibiting translation for ~1 hour, the presynaptic terminal exhibits increased spontaneous release, and increased evoked release with an increase in vesicle recycling during stimulation trains. Postsynaptic response, shape and amplitude were not affected. We conclude that ongoing protein synthesis limits vesicle release at the nerve terminal which reduces the need for presynaptic vesicle replenishment, thus conserving energy required for maintaining synaptic transmission.

Atlas of 99mTc-HMPAO SPECT brain perfusion in pediatric brain disorders

2021 ◽  
Vol 2 (2) ◽  
Author(s):  
Saleh A Othman ◽  
Keyword(s):  
Blood Flow ◽  
Neuronal Activity ◽  
Pediatric Patients ◽  
Brain Perfusion ◽  
Brain Disorders ◽  
Hmpao Spect ◽  
Perfusion Scan ◽  
Pediatric Brain ◽  
The Brain ◽  
99Mtc Hmpao

Background: Blood flow to the brain is in parallel with brain metabolism in almost all brain disorders except in brain tumors and therefore regional cerebral blood flow can be used as a marker of metabolic brain activity and hence it is closely linked to neuronal activity, the activity distribution is presumed to reflect neuronal activity levels in different areas of the brain. Purpose: The aim of this work is to demonstrate to pediatrician in general and pediatric neurologist in particular the variations in cerebral perfusion during normal development which should be taken into consideration at the time of interpreting SPECT brain perfusion scan in different pediatric brain disorders. Method: Brain SPECT was performed 10 minutes after an intravenous injection of 11.1 MBq/kg (0.3 mCi/kg), and the minimum dose is 185 MBq (5 mCi) of 99mTc-HMPAO (4). Results: This was a retrospective analysis of SPECT brain perfusion scan of pediatric patients performed between October 2015 and December 2019 at our institution. We selected normal and abnormal studies in pediatric population with age range (5 months - 14 years). Conclusion: Although anatomic cross sectional imaging give details of neurological structural changes, SPECT perfusion mirrors indirectly both metabolic and neuronal activity changes. Therefore, accurate interpretation of SPECT perfusion will consolidate its role as part of the diagnostic protocol and used when the findings of other imaging modalities do not explain the symptoms or fail partially or completely in determining the etiology of brain disorders in pediatric patients.

Developmental shift in bidirectional functions of taurine-sensitive chloride channels during cortical circuit formation in postnatal mouse brain

2004 ◽  
Vol 60 (2) ◽  
pp. 166-175 ◽  
Author(s):  
Mika Yoshida ◽  
Satoshi Fukuda ◽  
Yusuke Tozuka ◽  
Yusei Miyamoto ◽  
Tatsuhiro Hisatsune
Keyword(s):  
Mouse Brain ◽  
Chloride Channels ◽  
Developmental Shift ◽  
Cortical Circuit ◽  
Circuit Formation

scholarly journals Cytoplasmic accumulation of FUS triggers early behavioral alterations linked to cortical neuronal hyperactivity and defects in inhibitory synapses

2020 ◽  
Author(s):  
Jelena Scekic-Zahirovic ◽  
Inmaculada Sanjuan-Ruiz ◽  
Vanessa Kan ◽  
Salim Megat ◽  
Pierre De Rossi ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Rna Binding ◽  
Gene Mutations ◽  
Neuronal Loss ◽  
Inhibitory Neurons ◽  
Inhibitory Synapses ◽  
Behavioral Alterations ◽  
Behavioral Abnormalities ◽  
Cytoplasmic Accumulation

AbstractGene mutations causing cytoplasmic mislocalization of the RNA-binding protein FUS, lead to severe forms of amyotrophic lateral sclerosis (ALS). Cytoplasmic accumulation of FUS is also observed in other diseases, with unknown consequences. Here, we show that cytoplasmic mislocalization of FUS drives behavioral abnormalities in knock-in mice, including locomotor hyperactivity and alterations in social interactions, in the absence of widespread neuronal loss. Mechanistically, we identified a profound increase in neuronal activity in the frontal cortex of Fus knock-in mice in vivo. Importantly, RNAseq analysis suggested involvement of defects in inhibitory neurons, that was confirmed by ultrastructural and morphological defects of inhibitory synapses and increased synaptosomal levels of mRNAs involved in inhibitory neurotransmission. Thus, cytoplasmic FUS triggers inhibitory synaptic deficits, leading to increased neuronal activity and behavioral phenotypes. FUS mislocalization may trigger deleterious phenotypes beyond motor neuron impairment in ALS, but also in other neurodegenerative diseases with FUS mislocalization.

The Dogfish Neuromuscular Junction: Dual Innervation of Vertebrate Striated Muscle Fibres?

1972 ◽  
Vol 10 (3) ◽  
pp. 657-665
Author(s):  
Q. BONE
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Striated Muscle ◽  
Dense Core ◽  
The Other ◽  
Muscle Fibres ◽  
Nerve Terminals ◽  
Nerve Fibres ◽  
Different Types ◽  
Motor End Plate

In the myotomal muscles of the dogfish, Scyliorhinu canicula, there are 2 major types of fibre. The red fibres at the periphery of the myotome receive a distributed en grappe pattern of innervation. There are subjunctional folds at these endings, and the nerve terminals contain vesicles around 50 nm in diameter. In contrast to this, the white twitch fibres of the myotome are innervated focally, by 2 nerve fibres passing to the same motor end-plate. These 2 fibres contain vesicles of different types. One type of nerve terminal contains vesicles around 50 nm in diameter; these terminals resemble those upon the red fibres. The other contains vesicles up to 100 nm in diameter, frequently possessing a dense core. It is suggested that the white twitch fibres of dogfish are innervated by 2 separate axons, possibly containing different transmitter substances.

scholarly journals Simulating Reversibility of Dense Core Vesicles Capture in En Passant Boutons: Using Mathematical Modeling to Understand the Fate of Dense Core Vesicles in En Passant Boutons

2018 ◽  
Vol 140 (5) ◽  
Author(s):  
I. A. Kuznetsov ◽  
A. V. Kuznetsov
Keyword(s):  
Mathematical Modeling ◽  
Steady State ◽  
Nerve Terminal ◽  
Dense Core ◽  
Reasonable Assumption ◽  
Nerve Terminals ◽  
Dense Core Vesicles ◽  
Type Iii ◽  
Capture And Release ◽  
Kinetics Of

The goal of this paper is to use mathematical modeling to investigate the fate of dense core vesicles (DCVs) captured in en passant boutons located in nerve terminals. One possibility is that all DCVs captured in boutons are destroyed, another possibility is that captured DCVs can escape and reenter the pool of transiting DCVs that move through the boutons, and a third possibility is that some DCVs are destroyed in boutons, while some reenter the transiting pool. We developed a model by applying the conservation of DCVs in various compartments composing the terminal, to predict different scenarios that emerge from the above assumptions about the fate of DCVs captured in boutons. We simulated DCV transport in type Ib and type III terminals. The simulations demonstrate that, if no DCV destruction in boutons is assumed and all captured DCVs reenter the transiting pool, the DCV fluxes evolve to a uniform circulation in a type Ib terminal at steady-state and the DCV flux remains constant from bouton to bouton. Because at steady-state the amount of captured DCVs is equal to the amount of DCVs that reenter the transiting pool, no decay of DCV fluxes occurs. In a type III terminal at steady-state, the anterograde DCV fluxes decay from bouton to bouton, while retrograde fluxes increase. This is explained by a larger capture efficiency of anterogradely moving DCVs than of retrogradely moving DCVs in type III boutons, while the captured DCVs that reenter the transiting pool are assumed to be equally split between anterogradely and retrogradely moving components. At steady-state, the physiologically reasonable assumption of no DCV destruction in boutons results in the same number of DCVs entering and leaving a nerve terminal. Because published experimental results indicate no DCV circulation in type III terminals, modeling results suggest that DCV transport in these type III terminals may not be at steady-state. To better understand the kinetics of DCV capture and release, future experiments in type III terminals at different times after DCV release (molting) may be proposed.

scholarly journals Neuronal Activity-Dependent Control of Postnatal Neurogenesis and Gliogenesis

2018 ◽  
Vol 41 (1) ◽  
pp. 139-161 ◽  
Author(s):  
Ragnhildur T. Káradóttir ◽  
Chay T. Kuo
Keyword(s):  
Nervous System ◽  
Neuronal Activity ◽  
Molecular Mechanisms ◽  
Driving Forces ◽  
Nervous System Development ◽  
Current Evidence ◽  
Mammalian Brain ◽  
Postnatal Neurogenesis ◽  
Proliferation And Differentiation ◽  
Activity Dependent

The addition of new neurons and oligodendroglia in the postnatal and adult mammalian brain presents distinct forms of gray and white matter plasticity. Substantial effort has been devoted to understanding the cellular and molecular mechanisms controlling postnatal neurogenesis and gliogenesis, revealing important parallels to principles governing the embryonic stages. While during central nervous system development, scripted temporal and spatial patterns of neural and glial progenitor proliferation and differentiation are necessary to create the nervous system architecture, it remains unclear what driving forces maintain and sustain postnatal neural stem cell (NSC) and oligodendrocyte progenitor cell (OPC) production of new neurons and glia. In recent years, neuronal activity has been identified as an important modulator of these processes. Using the distinct properties of neurotransmitter ionotropic and metabotropic channels to signal downstream cellular events, NSCs and OPCs share common features in their readout of neuronal activity patterns. Here we review the current evidence for neuronal activity-dependent control of NSC/OPC proliferation and differentiation in the postnatal brain, highlight some potential mechanisms used by the two progenitor populations, and discuss future studies that might advance these research areas further.

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