ArticleAmerican journal of physiology. Cell physiology2008
Hypotonicity and peptide discharge from a single vesicle.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- Secretion and Function of Pituitary Prolactin in Evolutionary Perspective.Frontiers in neuroscience · 2020Review
- Ketamine Inhibits ATP-Evoked Exocytotic Release of Brain-Derived Neurotrophic Factor from Vesicles in Cultured Rat Astrocytes.Molecular neurobiology · 2016Article
- Hyperpolarization-activated cyclic nucleotide-gated channels and cAMP-dependent modulation of exocytosis in cultured rat lactotrophs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- High-resolution membrane capacitance measurements for the study of exocytosis and endocytosis.Nature protocols · 2013Article
- cAMP-mediated stabilization of fusion pores in cultured rat pituitary lactotrophs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Comparison of unitary exocytic events in pituitary lactotrophs and in astrocytes: modeling the discrete open fusion-pore states.Frontiers in cellular neuroscience · 2013Article
- Munc18-1, exocytotic fusion pore regulation and local membrane anisotropy.Communicative & integrative biology · 2012Article
- Munc18-1 tuning of vesicle merger and fusion pore properties.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Neuroendocrine secretory vesicles discharge their cargo in response to a stimulus, but the nature of this event is poorly understood. We studied the release of the pituitary hormone prolactin by hypotonicity, because this hormone also contributes to osmoregulation. In perfused rat lactotrophs, hypotonicity resulted in a transient increase followed by a sustained depression of prolactin release, as monitored by radioimmunoassay. In single cells imaged by confocal microscopy, hypotonicity elicited discharge of the fluorescently labeled atrial natriuretic peptide cargo from approximately 2% of vesicles/cell. In contrast, KCl-induced depolarization resulted in a response of approximately 10% of vesicles/cell, with different unloading/loading time course of the two fluorescent probes. In cell-attached studies, discrete changes in membrane capacitance were recorded in both unstimulated and stimulated conditions, reflecting single vesicle fusion/fissions with the plasma membrane. In stimulated cells, the probability of occurrence of full fusion events was low and unchanged, whereas over 95% of fusion events were transient, with the open fusion pore probability, the average pore dwell-time, the frequency of occurrence, and the fusion pore conductance increased. Hypotonicity only rarely elicited new fusion events in silent membrane patches. The results indicate that, in hypotonicity-stimulated lactotrophs, transient vesicle fusion mediates hormone release.
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