The extracellular matrix molecule brevican is an integral component of the machinery mediating fast synaptic transmission at the calyx of Held

Blosa, Maren; Sonntag, Mandy; Jäger, Carsten; Weigel, Solveig; Seeger, Johannes; Frischknecht, Renato; Seidenbecher, Constanze I.; Matthews, Russell T.; Arendt, Thomas; Rübsamen, Rudolf; Morawski, Markus

doi:10.1113/jp270849

Cited by 63 publications

(77 citation statements)

References 82 publications

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“…In recordings from brain slices in which PNNs were degraded by chondroitinase (by breaking down GAGs of chondroitin sulfate proteoglycans), it was found that there was no change in passive membrane properties in these neurons, or in their ability to fire rapid short-duration action potentials, but that there was reduced and delayed spiking (Balmer 2016). Similar results were obtained in brevican knock-out mice (Blosa et al, 2015). Thus, it appears that PNNs increase the excitability of the ensheathed neurons in response to synaptic inputs.…”

Section: Discussionsupporting

confidence: 86%

Perineuronal nets labeled by monoclonal antibody VC1.1 ensheath interneurons expressing parvalbumin and calbindin in the rat amygdala

2017

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Perineuronal nets (PNNs) are specialized condensations of extracellular matrix that ensheath particular neuronal subpopulations in the brain and spinal cord. PNNs regulate synaptic plasticity, including the encoding of fear memories by the amygdala. The present immunohistochemical investigation studied PNN structure and distribution, as well as the neurochemistry of their ensheathed neurons, in the rat amygdala using monoclonal antibody VC1.1, which recognizes a glucuronic acid 3-sulfate glycan associated with PNNs in the cerebral cortex. VC1.1+ PNNs surrounded the cell bodies and dendrites of a subset of nonpyramidal neurons in cortex-like portions of the amygdala (basolateral amygdalar complex, cortical nuclei, nucleus of the lateral olfactory tract, and amygdalohippocampal region). There was also significant neuropilar VC1.1 immunoreactivity whose density varied in different amygdalar nuclei. Cell counts in the basolateral nucleus revealed that virtually all neurons ensheathed by VC1.1+ PNNs were parvalbumin-positive (PV+) interneurons, and these VC1.1+/PV+ cells constituted 60% of all PV+ interneurons, including all of the larger PV+ neurons. Approximately 70% of VC1.1+ neurons were calbindin-positive (CB+), and these VC1.1+/CB+ cells constituted about 40% of all CB+ neurons. Colocalization of VC1.1 with Vicia villosa agglutinin (VVA) binding, which stains terminal N-acetylgalactosamines, revealed that VC1.1+ PNNs were largely a subset of VVA+ PNNs. This investigation provides baseline data regarding PNNs in the rat which should be useful for future studies of their function in this species.

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Section: Discussionsupporting

confidence: 86%

Perineuronal nets labeled by monoclonal antibody VC1.1 ensheath interneurons expressing parvalbumin and calbindin in the rat amygdala

2017

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“…However, because most research on the calyx of Held had been performed in mice or rats but not in ITD-using animals like gerbils (47) or guinea pigs (48), one can only speculate how constant synaptic delays are achieved in the subpopulation described above. A recent study even points to the importance of extracellular matrix, which can be found in the auditory brainstem and midbrain, for rapid synaptic release in the MNTB (49,50). In any case, a multicausal explanation seems likely.…”

Section: Discussionmentioning

confidence: 99%

Input timing for spatial processing is precisely tuned via constant synaptic delays and myelination patterns in the auditory brainstem

Stange-Marten¹,

Nabel²,

Sinclair³

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Precise timing of synaptic inputs is a fundamental principle of neural circuit processing. The temporal precision of postsynaptic input integration is known to vary with the computational requirements of a circuit, yet how the timing of action potentials is tuned presynaptically to match these processing demands is not well understood. In particular, action potential timing is shaped by the axonal conduction velocity and the duration of synaptic transmission delays within a pathway. However, it is not known to what extent these factors are adapted to the functional constraints of the respective circuit. Here, we report the finding of activity-invariant synaptic transmission delays as a functional adaptation for input timing adjustment in a brainstem sound localization circuit. We compared axonal and synaptic properties of the same pathway between two species with dissimilar timing requirements (gerbil and mouse): In gerbils (like humans), neuronal processing of sound source location requires exceptionally high input precision in the range of microseconds, but not in mice. Activityinvariant synaptic transmission and conduction delays were present exclusively in fast conducting axons of gerbils that also exhibited unusual structural adaptations in axon myelination for increased conduction velocity. In contrast, synaptic transmission delays in mice varied depending on activity levels, and axonal myelination and conduction velocity exhibited no adaptations. Thus, the specializations in gerbils and their absence in mice suggest an optimization of axonal and synaptic properties to the specific demands of sound localization. These findings significantly advance our understanding of structural and functional adaptations for circuit processing. myelination | synaptic transmission delay | sound localization | circuit processing | input timing T emporal integration of bioelectrical signals via chemical synapses is fundamental to neuronal computations. During circuit processing, neuronal information transfer via action potentials is controlled by exact differences in the occurrence between excitatory and inhibitory inputs (1-5). The arrival time of inputs within circuits in turn is largely shaped by the conduction delay of action potentials along the axons and during synaptic transmission. During ongoing activity, the transmission delays of chemical synapses generally increase in the range of hundreds of microseconds due to short-term adaptations (6-9). However, because temporal integration on postsynaptic neurons usually operates on time scales in the range of milliseconds or even longer (10, 11), sluggishness arising from synaptic mechanisms and axonal conductance is negligible for most of these computations. There are, however, some essential neuronal processing tasks that challenge the temporal precision of our nervous system. For instance, weakly electric fish detect miniature changes in the frequency of a constant electrical field. The neuronal circuits in these animals use electrical instead of chemical synapses in t...

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“…The electrophysiological changes were not due to changes in synapse diameter, cell densities or cell death, suggesting that CSPGs, at least the four removed in this study, were required for synaptic maturation in mixed neuronal and astrocyte cultures (Geissler et al, ). Furthermore, brevican is individually required in vivo for maintaining key aspects of synaptic transmission at primary synapses of the auditory circuitry in mice (Table ) (Blosa et al, ).…”

Section: Glycosaminoglycans In Synapse Formation and Functionmentioning

confidence: 99%

Diverse roles for glycosaminoglycans in neural patterning

Saied-Santiago

Bülow

2017

Developmental Dynamics

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The nervous system coordinates the functions of most multicellular organisms and their response to the surrounding environment. Its development involves concerted cellular interactions, including migration, axon guidance, and synapse formation. These processes depend on the molecular constituents and structure of the extracellular matrices (ECM). An essential component of ECMs are proteoglycans, i.e., proteins containing unbranched glycan chains known as glycosaminoglycans (GAGs). A defining characteristic of GAGs is their enormous molecular diversity, created by extensive modifications of the glycans during their biosynthesis. GAGs are widely expressed, and their loss can lead to catastrophic neuronal defects. Despite their importance, we are just beginning to understand the function and mechanisms of GAGs in neuronal development. In this review, we discuss recent evidence suggesting GAGs have specific roles in neuronal patterning and synaptogenesis. We examine the function played by the complex modifications present on GAG glycans and their roles in regulating different aspects of neuronal patterning. Moreover, the review considers the function of proteoglycan core proteins in these processes, stressing their likely role as co-receptors of different signaling pathways in a redundant and context-dependent manner. We conclude by discussing challenges and future directions toward a better understanding of these fascinating molecules during neuronal development.

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The extracellular matrix molecule brevican is an integral component of the machinery mediating fast synaptic transmission at the calyx of Held

Cited by 63 publications

References 82 publications

Perineuronal nets labeled by monoclonal antibody VC1.1 ensheath interneurons expressing parvalbumin and calbindin in the rat amygdala

Perineuronal nets labeled by monoclonal antibody VC1.1 ensheath interneurons expressing parvalbumin and calbindin in the rat amygdala

Input timing for spatial processing is precisely tuned via constant synaptic delays and myelination patterns in the auditory brainstem

Diverse roles for glycosaminoglycans in neural patterning

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