ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Neurohormone secretion persists after post-afterdischarge membrane depolarization and cytosolic calcium elevation in peptidergic neurons in intact nervous tissue.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 30 citations in OpenAlex.
- Hydrogen Peroxide Gates a Voltage-Dependent Cation Current inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- A Closely Associated Phospholipase C Regulates Cation Channel Function through Phosphoinositide Hydrolysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Protein Kinase C Enhances Electrical Synaptic Transmission by Acting on Junctional and Postsynaptic CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Diacylglycerol-mediated regulation of Aplysia bag cell neuron excitability requires protein kinase C.The Journal of physiology · 2016Article
- Nicotine inhibits potassium currents in Aplysia bag cell neurons.Journal of neurophysiology · 2016Article
- Ca2+ removal by the plasma membrane Ca2+-ATPase influences the contribution of mitochondria to activity-dependent Ca2+ dynamics in Aplysia neuroendocrine cells.Journal of neurophysiology · 2016Article
- PKC enhances the capacity for secretion by rapidly recruiting covert voltage-gated Ca2+ channels to the membrane.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Separate Ca2+ sources are buffered by distinct Ca2+ handling systems in aplysia neuroendocrine cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- A store-operated Ca(2+) influx pathway in the bag cell neurons of Aplysia.Journal of neurophysiology · 2006Article
- Regulation of activity-dependent dendritic vasopressin release from rat supraoptic neurones.The Journal of physiology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The purpose of this work was to test the hypothesis that an electrical afterdischarge (AD) causes prolonged elevation in cytosolic calcium levels that is associated with prolonged secretion of egg-laying hormone (ELH) from peptidergic neurons in intact nervous tissue of Aplysia. Using a combination of radioimmunoassay measurement of ELH secretion, electrophysiological measurement of membrane potential, and optical imaging of the concentration of intracellular free calcium ions ([Ca2+]i), we verified that there was persistent secretion of ELH after the end of the AD; this was accompanied by prolonged post-AD membrane depolarization and prolonged post-AD elevation in [Ca2+]i. Extracellular treatment with the calcium chelator EGTA had no effect on the pattern or magnitude of ELH secretion or on the post-AD membrane potential (V(m)) and post-AD Ca2+ signal, ruling out a role for extracellular calcium in the post-AD elevation of [Ca2+]i. Both V(m) and [Ca2+]i returned to baseline well before ELH secretion, such that neither prolonged membrane depolarization nor prolonged Ca2+ signaling can fully account for the extent of the persistent secretion of ELH. These findings suggest a unique relationship between membrane excitability, Ca2+ signaling, and prolonged neuropeptide secretion.
Indexed as
Identifiers
12388613PMC6757704W2139408067What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.