Synaptotagmin: Is 2 Better than 1?: Table 1.

Leitzell, Katherine

doi:10.1523/jneurosci.0668-07.2007

Cited by 7 publications

(3 citation statements)

References 7 publications

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“…We observed that SDF-1-mRFP1-containing vesicles situated in close proximity to CXCR4-EGFP-expressing cells in the SGZ frequently stained with antibodies against synaptotagmin-1, synaptoporin, or SV2, which are all known to be associated with transmittercontaining synaptic vesicles (Jinno and Kosaka, 2003;Khanna et al, 2007;Leitzell, 2007) (Fig. 4).…”

Section: Resultsmentioning

confidence: 95%

The Chemokine Stromal Cell-Derived Factor-1 Regulates GABAergic Inputs to Neural Progenitors in the Postnatal Dentate Gyrus

Bhattacharyya¹,

Banisadr²,

Jung³

et al. 2008

Journal of Neuroscience

132

140

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Stromal cell-derived factor-1 (SDF-1) and its receptor CXC chemokine receptor 4 (CXCR4) are important regulators of the development of the dentate gyrus (DG). Both SDF-1 and CXCR4 are also highly expressed in the adult DG. We observed that CXCR4 receptors were expressed by dividing neural progenitor cells located in the subgranular zone (SGZ) as well as their derivatives including doublecortinexpressing neuroblasts and immature granule cells. SDF-1 was located in DG neurons and in endothelial cells associated with DG blood vessels. SDF-1-expressing neurons included parvalbumin-containing GABAergic interneurons known as basket cells. Using transgenic mice expressing an SDF-1-mRFP1 (monomeric red fluorescence protein 1) fusion protein we observed that SDF-1 was localized in synaptic vesicles in the terminals of basket cells together with GABA-containing vesicles. These terminals were often observed to be in close proximity to dividing nestin-expressing neural progenitors in the SGZ. Electrophysiological recordings from slices of the DG demonstrated that neural progenitors received both tonic and phasic GABAergic inputs and that SDF-1 enhanced GABAergic transmission, probably by a postsynaptic mechanism. We also demonstrated that, like GABA, SDF-1 was tonically released in the DG and that GABAergic transmission was partially dependent on coreleased SDF-1. These data demonstrate that SDF-1 plays a novel role as a neurotransmitter in the DG and regulates the strength of GABAergic inputs to the pool of dividing neural progenitors. Hence, SDF-1/ CXCR4 signaling is likely to be an important regulator of adult neurogenesis in the DG.

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Section: Resultsmentioning

confidence: 95%

The Chemokine Stromal Cell-Derived Factor-1 Regulates GABAergic Inputs to Neural Progenitors in the Postnatal Dentate Gyrus

Bhattacharyya¹,

Banisadr²,

Jung³

et al. 2008

Journal of Neuroscience

132

140

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“…8a ). Of note, the SYT1 protein level, which is the homolog of SYT2 and the most studied member of the synaptotagmin family 46 , 48 , 49 , remained unchanged (Fig. 8a ).…”

Section: Resultsmentioning

confidence: 98%

ATR regulates neuronal activity by modulating presynaptic firing

et al. 2021

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Ataxia Telangiectasia and Rad3-related (ATR) protein, as a key DNA damage response (DDR) regulator, plays an essential function in response to replication stress and controls cell viability. Hypomorphic mutations of ATR cause the human ATR-Seckel syndrome, characterized by microcephaly and intellectual disability, which however suggests a yet unknown role for ATR in non-dividing cells. Here we show that ATR deletion in postmitotic neurons does not compromise brain development and formation; rather it enhances intrinsic neuronal activity resulting in aberrant firing and an increased epileptiform activity, which increases the susceptibility of ataxia and epilepsy in mice. ATR deleted neurons exhibit hyper-excitability, associated with changes in action potential conformation and presynaptic vesicle accumulation, independent of DDR signaling. Mechanistically, ATR interacts with synaptotagmin 2 (SYT2) and, without ATR, SYT2 is highly upregulated and aberrantly translocated to excitatory neurons in the hippocampus, thereby conferring a hyper-excitability. This study identifies a physiological function of ATR, beyond its DDR role, in regulating neuronal activity.

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“…4). Synaptotagmin1 is a multifunctional substrate that acts as calcium sensor in the Ca 2+ ‐dependent release of neurotransmitter vesicles (Leitzell, 2007) and in the regulation of synaptic vesicle docking and recycling (Fukuda et al, 2000; Llinas et al, 2004). Because synaptotagmin1 is an abundant synaptic vesicle protein and is expressed throughout the brain, it has also been used as a marker to estimate the number of synapse boutons in the CNS.…”

Section: Discussionmentioning

confidence: 99%

Spinal anterior horn has the capacity to self‐regenerate in amyotrophic lateral sclerosis model mice

Miyazaki

Nagai

Morimoto

et al. 2009

J of Neuroscience Research

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The exact host environment necessary for neural regeneration in amyotrophic lateral sclerosis (ALS) has not yet been fully elucidated. We first focused on the extracellular matrix proteins in ALS model mice during development of the disease and then attempted to examine whether regeneration occurs in the ALS spinal cord under regenerative conditions. A progressive increase in gamma1 laminin (a promoter of regeneration) and a progressive decrease in semaphorin3A (Sema3A; an inhibitor of regeneration) were observed, mainly in the neuropil of the spinal anterior horn from 15 to 18 weeks, when astrocytes began to express both gamma1 laminin and Sema3A. On the other hand, a progressive increase in growth-associated protein 43 (GAP43; synaptic regeneration site) and a progressive decrease in synaptotagmin1 (actual synaptic bouton) were observed in the same areas of the spinal anterior horn from 15 to 18 weeks. Thus, the present data suggest that, although the spinal anterior horn in ALS models loses motor neurons, it initially possesses the capacity to self-regenerate but displays a progressive loss of ability to regenerate new effective synapses.

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Synaptotagmin: Is 2 Better than 1?: Table 1.

Cited by 7 publications

References 7 publications

The Chemokine Stromal Cell-Derived Factor-1 Regulates GABAergic Inputs to Neural Progenitors in the Postnatal Dentate Gyrus

The Chemokine Stromal Cell-Derived Factor-1 Regulates GABAergic Inputs to Neural Progenitors in the Postnatal Dentate Gyrus

ATR regulates neuronal activity by modulating presynaptic firing

Spinal anterior horn has the capacity to self‐regenerate in amyotrophic lateral sclerosis model mice

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