Dynamics of peptidergic secretory granule transport are regulated by neuronal stimulation

Sobota, Jacqueline A.; Mohler, William A.; Cowan, Ann E.; Eipper, Betty A.; Mains, Richard E.

doi:10.1186/1471-2202-11-32

Cited by 12 publications

(8 citation statements)

References 43 publications

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“…Electrical stimulation (ES) evokes vesicular release of glutamate (Glu) along DRG axons, at least in cocultures with oligodendrocytes (Wake et al, 2011 ). Observations demonstrating exocytosis of large dense core vesicles by chemically depolarized axons of trigeminal ganglion neurons further support the concept of activity-induced extrasynaptic axonal secretion (Sobota et al, 2010 ).…”

Section: Detection Of Axonal Activity By Scssupporting

confidence: 55%

Neuronal activity in the hub of extrasynaptic Schwann cell-axon interactions

Samara¹,

Poirot²,

Domènech-Estévez³

et al. 2013

Front. Cell. Neurosci.

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The integrity and function of neurons depend on their continuous interactions with glial cells. In the peripheral nervous system glial functions are exerted by Schwann cells (SCs). SCs sense synaptic and extrasynaptic manifestations of action potential propagation and adapt their physiology to support neuronal activity. We review here existing literature data on extrasynaptic bidirectional axon-SC communication, focusing particularly on neuronal activity implications. To shed light on underlying mechanisms, we conduct a thorough analysis of microarray data from SC-rich mouse sciatic nerve at different developmental stages and in neuropathic models. We identify molecules that are potentially involved in SC detection of neuronal activity signals inducing subsequent glial responses. We further suggest that alterations in the activity-dependent axon-SC crosstalk impact on peripheral neuropathies. Together with previously reported data, these observations open new perspectives for deciphering glial mechanisms of neuronal function support.

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Section: Detection Of Axonal Activity By Scssupporting

confidence: 55%

Neuronal activity in the hub of extrasynaptic Schwann cell-axon interactions

Samara¹,

Poirot²,

Domènech-Estévez³

et al. 2013

Front. Cell. Neurosci.

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“…Interestingly, large DCV transport in axons has been shown to be activity-dependent. Stimulation of cultured trigeminal neurons with KCl (to depolarize them) increased the fraction of DCVs moving in an anterograde direction, though it also decreased their instantaneous velocity (Sobota et al 2010). Additional studies will be necessary to determine whether estradiol regulates the factors that control DCV maturation and/or their movements within axons.…”

Section: Discussionmentioning

confidence: 99%

Estradiol regulates large dense core vesicles in the hippocampus of adult female rats

et al. 2013

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Previous work has shown that the steroid hormone estradiol facilitates the release of anticonvulsant neuropeptides from inhibitory neurons in the hippocampus to suppress seizures. Because neuropeptides are packaged in large dense core vesicles, estradiol may facilitate neuropeptide release through regulation of dense core vesicles. In the current study, we used serial section electron microscopy in the hippocampal CA1 region of adult female rats to test three hypotheses about estradiol regulation of dense core vesicles: (1) Estradiol increases the number of dense core vesicles in axonal boutons, (2) Estradiol increases the size of dense core vesicles in axonal boutons, (3) Estradiol shifts the location of dense core vesicles toward the periphery of axonal boutons, potentially lowering the threshold for neuropeptide release during seizures. We found that estradiol increases the number and size of dense core vesicles in inhibitory axonal boutons, consistent with increased neuropeptide content, but does not shift the location of dense core vesicles closer to the bouton periphery. These effects were specific to large dense core vesicles (>80 nm) in inhibitory boutons. Estradiol had no effects on small dense core vesicles or dense core vesicles in excitatory boutons. Our results indicate that estradiol suppresses seizures at least in part by increasing the potentially releasable pool of neuropeptides in the hippocampus, and that estradiol facilitation of neuropeptide release involves a mechanism other than mobilization of dense core vesicles toward sites of release.

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“…In order to further investigate this effect during early development, we used early life MS, which has been commonly used to study G × E interaction on anxiety and depression in mice 50 , 51 and has been shown to impact anxiety-like behaviors in rodents via the 5-HT system 52 , 53 . Exposure of wildtype mice, on a mixed c57BL6/J–129S6/Sv background, to MS significantly decreased distance travelled and time spent in the center of the OFT, while MS had no effect in Tph2 KI mice 54 .…”

Section: Discussionmentioning

confidence: 99%

Serotonin deficiency induced after brain maturation rescues consequences of early life adversity

Aboagye

Weber

Merdian

et al. 2021

Sci Rep

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Brain serotonin (5-HT) system dysfunction is implicated in depressive disorders and acute depletion of 5-HT precursor tryptophan has frequently been used to model the influence of 5-HT deficiency on emotion regulation. Tamoxifen (TAM)-induced Cre/loxP-mediated inactivation of the tryptophan hydroxylase-2 gene (Tph2) was used to investigate the effects of provoked 5-HT deficiency in adult mice (Tph2 icKO) previously subjected to maternal separation (MS). The efficiency of Tph2 inactivation was validated by immunohistochemistry and HPLC. The impact of Tph2 icKO in interaction with MS stress (Tph2 icKO × MS) on physiological parameters, emotional behavior and expression of 5-HT system-related marker genes were assessed. Tph2 icKO mice displayed a significant reduction in 5-HT immunoreactive cells and 5-HT concentrations in the rostral raphe region within four weeks following TAM treatment. Tph2 icKO and MS differentially affected food and water intake, locomotor activity as well as panic-like escape behavior. Tph2 icKO prevented the adverse effects of MS stress and altered the expression of the genes previously linked to stress and emotionality. In conclusion, an experimental model was established to study the behavioral and neurobiological consequences of 5-HT deficiency in adulthood in interaction with early-life adversity potentially affecting brain development and the pathogenesis of depressive disorders.

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Dynamics of peptidergic secretory granule transport are regulated by neuronal stimulation

Cited by 12 publications

References 43 publications

Neuronal activity in the hub of extrasynaptic Schwann cell-axon interactions

Neuronal activity in the hub of extrasynaptic Schwann cell-axon interactions

Estradiol regulates large dense core vesicles in the hippocampus of adult female rats

Serotonin deficiency induced after brain maturation rescues consequences of early life adversity

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