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Synaptic-like transmission between neural axons and arterial smooth muscle cells drives cerebral neurovascular coupling

ABSTRACT: Synaptic-like transmission between neural axons and arterial smooth muscle cells drives cerebral neurovascular coupling

PROVIDER: PRJNA878800 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21504079.fastq.gz	Fastqsanger.gz
	SRR21504080.fastq.gz	Fastqsanger.gz
	SRR21504081.fastq.gz	Fastqsanger.gz
	SRR21504082.fastq.gz	Fastqsanger.gz
	SRR21504083.fastq.gz	Fastqsanger.gz

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Synaptic-like transmission between neural axons and arterial smooth muscle cells drives cerebral neurovascular coupling

Project description:Normally functioning brains depend on neurovascular coupling (NVC) and its dysfunction underlies many neuropathologies. Although cell-type specificity has been implicated in NVC, how active neural information is specifically conveyed to the targeted arterioles in the brain remains poorly understood. Here, using two-photon focal optogenetics in the mouse cerebral cortex, we demonstrated that single glutamatergic axons dilate their innervating arterioles via synaptic-like transmission between neural-arteriolar smooth muscle cells junction (NsMJ). The presynaptic parental-daughter bouton makes dual innervations on postsynaptic dendrites and on arteriolar smooth muscles cells (aSMCs), which expressed many types of neuromediator receptors, including glutamate NMDA receptor subunit 1 (Grin1). Disruption of NsMJ transmission, by aSMC specific knockout of GluN1, diminished the optogenetic and whisker stimulation-caused functional hyperemia. Notably, the absence of GluN1 subunit in aSMCs protected the brain atrophy from cerebral ischemia by preventing Ca2+ overload in aSMCs during arteriolar constriction caused by the ischemia-induced spreading depolarization. Our findings reveal that NsMJ transmission drives neurovascular coupling and also open up a new avenue for studying stroke.

2023-10-05 | GSE213026 | GEO

Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39

Project description:Microglia tightly interact with brain capillaries and regulate blood brain barrel permeability in pathological conditions. However, it is still unknown whether and how microglia regulate CBF in homeostatic condition. Here we show microglia directly regulate cerebral blood flow (CBF) and neurovascular coupling. Conditional knockout of microglial CD39 resulted in CBF hyper perfusion, reduced ATP induced CBF increase, impaired neurovascular coupling by whisker stimulation and reduced whisker stimulation induced adenosine increase in barrel cortex. Out data suggest that microglia is an important player for CBF regulation.

2023-07-01 | GSE223314 | GEO

Endothelial-neuronal coupling revealed in a decoupled neurovascular unit based Organ-on-Chip approach.

Project description:This data set is for the article: Endothelial-neuronal coupling revealed in a decoupled neurovascular unit based Organ-on-Chip approach.

2017-08-24 | MSV000081480 | MassIVE

Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39

Project description:Microglia regulate basal cerebral blood flow and neurovascular coupling through ectonucleotidase CD39

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Ectopic vesicular neurotransmitter release along sensory axons mediates neurovascular coupling via glial calcium signaling.

Project description:Neurotransmitter release generally is considered to occur at active zones of synapses, and ectopic release of neurotransmitters has been demonstrated in a few instances. However, the mechanism of ectopic neurotransmitter release is poorly understood. We took advantage of the intimate morphological and functional proximity of olfactory receptor axons and specialized glial cells, olfactory ensheathing cells (OECs), to study ectopic neurotransmitter release. Axonal stimulation evoked purinergic and glutamatergic Ca(2+) responses in OECs, indicating ATP and glutamate release. In axons expressing synapto-pHluorin, stimulation evoked an increase in synapto-pHluorin fluorescence, indicative of vesicle fusion. Transmitter release was dependent on Ca(2+) and could be inhibited by bafilomycin A1 and botulinum toxin A. Ca(2+) transients in OECs evoked by ATP, axonal stimulation, and laser photolysis of NP-EGTA resulted in constriction of adjacent blood vessels. Our results indicate that ATP and glutamate are released ectopically by vesicles along axons and mediate neurovascular coupling via glial Ca(2+) signaling.

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Caveolin1 Deficiency: A Type I Endothelial Interferonopathy Associated with Pulmonary Arterial Hypertension

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2021-02-24 | GSE138991 | GEO

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Project description:We previously identified that the RNA binding protein Nucleolin is localized to axons of DRG sensory neurons by interaction with the molecular motor Kinesin-1 (Kif5A) and subsequently localizes importin beta1 mRNA there (Perry et al., 2016). To further identify additional RNAs that are localized to axons in a similar mechanism, we immunopercipitated Kif5A from dorsal roots (centrally projecting axons) or Sciatic nerves (peripherally projecting axons), isolated the bound RNA and sequnced it.

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Receptor-specific interactome as a hub for rapid cue-induced selective translation in axons

Project description:During neuronal wiring, extrinsic cues trigger the local translation of specific mRNAs in axons via cell surface receptors. The coupling of ribosomes to receptors has been proposed as a mechanism linking signals to local translation but it is not known how broadly this mechanism operates, nor whether it can selectively regulate mRNA translation. We report that receptor-ribosome coupling is employed by multiple guidance cue receptors and this interaction is mRNA-dependent. We find that different receptors bind to distinct sets of mRNAs and RNA-binding proteins. Cue stimulation induces rapid dissociation of ribosomes from receptors and the selective translation of receptor-specific mRNAs in retinal axon growth cones. Further, we show that receptor-ribosome dissociation and cue-induced selective translation are inhibited by simultaneous exposure to translation-repressive cues, suggesting a novel mode of signal integration. Our findings reveal receptor-specific interactomes and provide a general model for the rapid, localized and selective control of cue-induced translation.

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The endfeetome, a astroglial translatome of the neurovascular unit

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