GO:1904049 negative regulation of spontaneous neurotransmitter secretion: Regulatory Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:1904049 describes any process that stops, prevents, or reduces the frequency, rate, or extent of spontaneous neurotransmitter secretion, the action-potential-independent release of neurotransmitter.
• Spontaneous neurotransmitter secretion is a distinct mode of release that shapes neural circuit activity and is subject to dedicated negative regulatory control.
• Key molecular players include presynaptic calcium channels such as Cav3.2, whose functional upregulation can accelerate secretory function in neuroendocrine cells.
• Hormonal and sex-dependent factors, including progesterone and noradrenergic signaling, modulate spontaneous secretory patterns in vivo.
• Environmental toxicants such as polystyrene nanoplastics can dysregulate neurosecretory and gut-brain axis signaling, highlighting the sensitivity of spontaneous secretion to external perturbation.
• CRISPR-based knockout, point-mutation, knock-in, and overexpression models enable causal dissection of genes that negatively regulate spontaneous neurotransmitter secretion.
Description
Spontaneous neurotransmitter secretion refers to the release of neurotransmitter from presynaptic terminals that occurs independently of action potentials, and it plays a fundamental role in shaping synaptic strength, neuronal excitability, and circuit development. The Gene Ontology term GO:1904049, negative regulation of spontaneous neurotransmitter secretion, captures the biological processes that stop, prevent, or reduce the frequency, rate, or extent of this stimulus-independent release. Understanding this term is essential because spontaneous release is not merely background noise; it actively modulates neural circuit function and can be co-regulated with evoked release through shared presynaptic machinery. Researchers studying synaptic transmission, neuroendocrine secretion, and neurodevelopmental disorders need precise tools to interrogate the negative regulators of spontaneous secretion. Recent work has shown that co-release of GABA and acetylcholine from medial olivocochlear neurons acts as a fine regulatory mechanism of cochlear efferent inhibition, demonstrating that spontaneous and co-ordinated release events are subject to tight negative control. In parallel, functional upregulation of the H2S/Cav3.2 channel pathway accelerates secretory function in neuroendocrine-differentiated human prostate cancer cells, indicating that calcium channel modulation can shift the balance of spontaneous secretion. Hormonal influences further illustrate the regulatory complexity: progesterone modulates spontaneous nocturnal and ghrelin-induced growth hormone secretion in postmenopausal women, and sex differences exist in noradrenergic regulation of the medial prefrontal cortex in mice. Environmental factors also intersect with this process, as polystyrene nanoplastics cause dysregulation of the brain-intestine-microbiota axis in zebrafish, affecting neurosecretory signaling. Collectively, these findings underscore that negative regulation of spontaneous neurotransmitter secretion is a dynamic, multi-layered process relevant to basic neuroscience, endocrinology, and toxicology.
negative regulation of spontaneous neurotransmitter secretion At A Glance
| GO ID | GO:1904049 |
|---|---|
| GO term | negative regulation of spontaneous neurotransmitter secretion |
| Ontology | biological_process |
| Synonym | down regulation of spontaneous neurotransmitter secretion; inhibition of stimulus-independent neurotransmitter secretion; downregulation of spontaneous neurotransmitter secretion |
| Major function | Suppression of action-potential-independent neurotransmitter release to modulate synaptic strength and neural circuit excitability |
| Related process | Regulation of spontaneous neurotransmitter secretion; synaptic transmission; calcium channel modulation |
| Cellular context | Presynaptic terminals, neuroendocrine cells, and cochlear efferent neurons |
| Example regulators | Cav3.2 calcium channels, noradrenergic signaling, progesterone, and co-release machinery |
| Research relevance | Target for understanding synaptic plasticity, neuroendocrine disorders, and toxicant-induced neurotoxicity |
What Is GO:1904049?
GO:1904049 is a biological process term defined as any process that stops, prevents, or reduces the frequency, rate, or extent of spontaneous neurotransmitter secretion. Spontaneous neurotransmitter secretion is the stimulus-independent release of neurotransmitter, often measured as miniature synaptic currents or basal secretory events. Negative regulation therefore encompasses molecular, cellular, and systemic mechanisms that suppress this basal release mode, including presynaptic calcium channel modulation, hormonal feedback, and circuit-level inhibitory control.
Why Is negative regulation of spontaneous neurotransmitter secretion Important in Cell Biology?
Negative regulation of spontaneous neurotransmitter secretion is critically important because spontaneous release events influence neuronal development, synaptic plasticity, and network stability, and their dysregulation is linked to neurological and endocrine disorders. The process is also a convergence point for hormonal, environmental, and circuit-level signals, as demonstrated by progesterone modulation of spontaneous growth hormone secretion and noradrenergic sex differences in the prefrontal cortex. Moreover, toxicant exposure such as polystyrene nanoplastics can disrupt neurosecretory signaling through the brain-intestine-microbiota axis, underscoring the need to understand how negative regulatory mechanisms protect against aberrant secretion.
• Spontaneous neurotransmitter secretion shapes synaptic strength and neural circuit development, making its negative regulation essential for normal brain function.
• Co-release of GABA and acetylcholine from medial olivocochlear neurons demonstrates that negative regulation of spontaneous release fine-tunes cochlear efferent inhibition.
• Calcium channel pathways such as H2S/Cav3.2 can accelerate secretory function, and their negative regulation may prevent excessive neuroendocrine secretion.
• Progesterone modulates spontaneous nocturnal growth hormone secretion, linking negative regulation of secretion to endocrine physiology.
• Sex differences in noradrenergic regulation of the medial prefrontal cortex highlight that negative control of spontaneous release is circuit- and sex-specific.
• Environmental toxicants like polystyrene nanoplastics can dysregulate brain-intestine-microbiota signaling, potentially overriding negative regulatory checkpoints.
• Understanding negative regulation of spontaneous secretion can inform therapeutic strategies for disorders of synaptic transmission and neuroendocrine imbalance.
• CRISPR-based models allow causal testing of candidate genes that negatively regulate spontaneous neurotransmitter secretion.
• The term provides a standardized ontology framework for annotating genes and pathways in synaptic and secretory biology.
• Research on this process bridges neuroscience, endocrinology, and toxicology, offering broad translational relevance.
What Happens During negative regulation of spontaneous neurotransmitter secretion?
Presynaptic calcium channel modulation
In simple terms: Calcium channels control how much neurotransmitter is released, and turning them down reduces spontaneous release.
Spontaneous neurotransmitter secretion depends on basal calcium influx and presynaptic calcium channel activity. Functional upregulation of the H2S/Cav3.2 channel pathway accelerates secretory function in neuroendocrine-differentiated human prostate cancer cells, indicating that Cav3.2 activity can promote secretion. Conversely, negative regulation of spontaneous secretion may involve reducing Cav3.2 conductance or downstream calcium sensitivity, thereby lowering the frequency of spontaneous release events. This modulation is a key checkpoint because calcium channels directly couple membrane depolarization to vesicle fusion.
Hormonal and sex-dependent control
In simple terms: Hormones like progesterone and noradrenaline can dial down spontaneous secretion in a sex-specific way.
Hormonal signals modulate spontaneous secretory patterns. Progesterone modulates spontaneous nocturnal and ghrelin-induced growth hormone secretion in postmenopausal women, demonstrating that steroid hormones can negatively regulate spontaneous secretory bursts. In mice, sex differences exist in noradrenergic regulation of the medial prefrontal cortex, suggesting that noradrenaline-mediated inhibition of spontaneous release is circuit- and sex-dependent. These findings indicate that negative regulation of spontaneous neurotransmitter secretion is not a fixed property but is dynamically tuned by endocrine and neuromodulatory inputs.
Co-release and circuit-level inhibition
In simple terms: Some neurons release two transmitters at once, and this co-release can put the brakes on spontaneous secretion.
Co-release of GABA and acetylcholine from medial olivocochlear neurons acts as a fine regulatory mechanism of cochlear efferent inhibition. This co-release system illustrates how negative regulation of spontaneous neurotransmitter secretion can be achieved through circuit-level interactions, where one transmitter modulates the release of another. Such mechanisms are essential for maintaining precise control over spontaneous release in sensory circuits.
Environmental and microbiota influences
In simple terms: Exposure to pollutants can disrupt the gut-brain axis and alter how much neurotransmitter is spontaneously released.
Polystyrene nanoplastics cause dysregulation of the brain-intestine-microbiota axis in zebrafish, affecting neurosecretory signaling. This indicates that environmental toxicants can perturb the negative regulatory mechanisms that normally suppress excessive spontaneous neurotransmitter secretion. The gut microbiota and its metabolites, such as those produced by Bifidobacterium through fatty acid isomerization, can also modulate host physiology and potentially influence neurosecretory pathways. These interactions highlight that negative regulation of spontaneous secretion is sensitive to external and microbial factors.
Seasonal and physiological rhythms
In simple terms: The body's internal clock and seasonal changes can alter spontaneous secretion of hormones and neurotransmitters.
Regulation of the seasonal cycle of beta-endorphin and ACTH secretion into the peripheral blood of rams demonstrates that spontaneous secretory patterns are subject to seasonal and physiological rhythmicity. Such long-term modulation implies that negative regulation of spontaneous neurotransmitter secretion may also follow circadian or seasonal cues, integrating environmental information with neuroendocrine output.
Key Genes Involved in GO:1904049 negative regulation of spontaneous neurotransmitter secretion
The following genes and proteins have been implicated in the regulation of spontaneous neurotransmitter secretion and related neurosecretory processes based on the cited literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| CACNA1H | Encodes Cav3.2 T-type calcium channel; functional upregulation accelerates secretory function | Target for modulating spontaneous secretion in neuroendocrine cells |
| GAD1 | GABA synthesis enzyme; involved in GABA co-release from medial olivocochlear neurons | Studying co-release and negative regulation of spontaneous secretion |
| CHAT | Acetylcholine synthesis enzyme; involved in ACh co-release from medial olivocochlear neurons | Investigating cholinergic regulation of cochlear efferent inhibition |
| PGR | Progesterone receptor; mediates progesterone effects on spontaneous GH secretion | Endocrine modulation of spontaneous secretory patterns |
| ADRA1A | Alpha-1 adrenergic receptor; noradrenergic signaling in prefrontal cortex | Sex differences in noradrenergic regulation of spontaneous release |
| ADRA2A | Alpha-2 adrenergic receptor; presynaptic inhibition of neurotransmitter release | Negative regulation of spontaneous secretion via noradrenaline |
| POMC | Precursor for ACTH and beta-endorphin; seasonal secretion regulation | Seasonal rhythms of spontaneous neuroendocrine secretion |
| CRH | Corticotropin-releasing hormone; upstream regulator of ACTH secretion | Hypothalamic-pituitary-adrenal axis modulation of spontaneous secretion |
| GHRH | Growth hormone-releasing hormone; regulates GH secretion | Progesterone modulation of spontaneous GH secretion |
| GHRL | Ghrelin; stimulates GH secretion and interacts with progesterone | Ghrelin-induced GH secretion studies |
| SLC6A2 | Noradrenaline transporter; regulates synaptic noradrenaline levels | Noradrenergic control of prefrontal cortex spontaneous activity |
| SLC6A4 | Serotonin transporter; modulates serotonergic spontaneous release | General regulation of spontaneous neurotransmitter secretion |
| SYT1 | Synaptotagmin 1; calcium sensor for vesicle fusion | Core machinery of spontaneous and evoked release |
| SNAP25 | SNARE protein; essential for vesicle fusion | Presynaptic component of spontaneous secretion machinery |
| STX1A | Syntaxin 1A; SNARE protein involved in vesicle docking | Negative regulation via SNARE complex modulation |
| VAMP2 | Vesicle-associated membrane protein 2; SNARE protein | Vesicle fusion and spontaneous release |
| CACNA1B | N-type calcium channel; controls evoked and spontaneous release | Calcium-dependent regulation of secretion |
| KCNQ2 | Potassium channel; regulates neuronal excitability and spontaneous release | Negative regulation of spontaneous firing and secretion |
How Is negative regulation of spontaneous neurotransmitter secretion Regulated?
Negative regulation of spontaneous neurotransmitter secretion is controlled by multiple intersecting pathways. Presynaptic calcium channels such as Cav3.2 can be functionally upregulated to accelerate secretion, implying that their downregulation or inhibition would negatively regulate spontaneous release. Hormonal signals, including progesterone, modulate spontaneous growth hormone secretion, demonstrating endocrine control over spontaneous secretory events. Noradrenergic signaling in the medial prefrontal cortex exhibits sex differences, indicating that neuromodulatory inputs can differentially suppress spontaneous release. Environmental factors such as polystyrene nanoplastics can dysregulate the brain-intestine-microbiota axis, potentially disrupting negative regulatory checkpoints. Additionally, microbial metabolites from Bifidobacterium can influence host physiology through fatty acid isomerization and gut microbiota modulation, which may indirectly affect neurosecretory regulation. Seasonal rhythms also regulate beta-endorphin and ACTH secretion, suggesting that negative regulation of spontaneous secretion is subject to long-term physiological modulation.
negative regulation of spontaneous neurotransmitter secretion and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| CACNA1H | Neuroendocrine tumors; secretory dysfunction | Knockout or point-mutation in prostate cancer cell lines |
| PGR | Hormonal disorders; growth hormone dysregulation | Knockout mouse models for progesterone modulation |
| ADRA2A | Psychiatric disorders; sex-specific prefrontal cortex function | Conditional knockout in mouse prefrontal cortex |
| POMC | Seasonal affective disorder; ACTH/beta-endorphin dysregulation | Knock-in reporter in ovine models |
| GAD1/CHAT | Auditory processing deficits; cochlear efferent dysfunction | Co-release knockout models in mice |
Neuroendocrine and hormonal disorders
Dysregulation of spontaneous neurotransmitter secretion is linked to neuroendocrine disorders. Progesterone modulation of spontaneous nocturnal and ghrelin-induced growth hormone secretion in postmenopausal women highlights how hormonal imbalance can alter spontaneous secretory patterns. Similarly, seasonal regulation of beta-endorphin and ACTH secretion in rams demonstrates that disruption of these rhythms could contribute to endocrine pathologies. Understanding negative regulation of spontaneous secretion may therefore inform treatments for growth hormone disorders and stress-related conditions.
Neurotoxicity and environmental exposure
Exposure to polystyrene nanoplastics causes dysregulation of the brain-intestine-microbiota axis in zebrafish, affecting neurosecretory signaling. This suggests that environmental toxicants can impair the negative regulatory mechanisms that normally suppress excessive spontaneous neurotransmitter secretion, potentially contributing to neurotoxicity and gut-brain axis disorders. The gut microbiota, including Bifidobacterium species, can modulate host physiology through fatty acid isomerization, further linking microbial factors to neurosecretory regulation.
Psychiatric and neurological conditions
Sex differences in noradrenergic regulation of the medial prefrontal cortex in mice indicate that negative regulation of spontaneous neurotransmitter secretion is circuit-specific and may underlie sex-biased psychiatric conditions. Co-release of GABA and acetylcholine from medial olivocochlear neurons as a fine regulatory mechanism of cochlear efferent inhibition suggests that disruptions in co-release could lead to auditory processing deficits. These findings position negative regulation of spontaneous secretion as a potential therapeutic target in neurological and psychiatric disorders.
Cancer and secretory dysfunction
Functional upregulation of the H2S/Cav3.2 channel pathway accelerates secretory function in neuroendocrine-differentiated human prostate cancer cells, indicating that spontaneous secretory mechanisms can be hijacked in cancer. Negative regulation of spontaneous neurotransmitter secretion may therefore be relevant to neuroendocrine tumors, where excessive secretion contributes to clinical symptoms. Targeting calcium channel pathways could offer a strategy to suppress aberrant secretion in such cancers.
From negative regulation of spontaneous neurotransmitter secretion-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of CACNA1H increase spontaneous neurotransmitter secretion? | CRISPR knockout of CACNA1H in neuroendocrine cell lines |
| Does a point mutation in PGR alter progesterone-mediated suppression of spontaneous GH secretion? | CRISPR point-mutation knock-in in mouse models |
| Can tagged knock-in of ADRA2A reveal presynaptic localization in noradrenergic neurons? | CRISPR tagged knock-in in mouse prefrontal cortex |
| Does overexpression of GAD1 and CHAT enhance co-release and negative regulation of spontaneous secretion? | CRISPR overexpression in medial olivocochlear neurons |
| Does knockout of POMC disrupt seasonal rhythms of ACTH secretion? | CRISPR knockout in ovine models |
| Does Bifidobacterium modulation affect spontaneous neurosecretory activity? | Gnotobiotic mouse models with microbiota manipulation |
How to Study the negative regulation of spontaneous neurotransmitter secretion Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Patch-clamp electrophysiology | Frequency and amplitude of spontaneous postsynaptic currents | Quantifying negative regulation of spontaneous release |
| Calcium imaging | Intracellular calcium transients | Assessing Cav3.2 channel modulation of secretion |
| ELISA/radioimmunoassay | Hormone concentrations in blood | Profiling spontaneous GH, ACTH, beta-endorphin secretion |
| Zebrafish toxicant exposure | Brain-intestine-microbiota axis dysregulation | Evaluating nanoplastic effects on neurosecretion |
| Gnotobiotic mouse models | Microbiota-dependent host physiology | Testing Bifidobacterium modulation of secretion |
| Immunohistochemistry | Protein localization in presynaptic terminals | Validating co-release machinery in olivocochlear neurons |
| RNA-seq | Transcriptional changes in secretory genes | Identifying negative regulators of spontaneous secretion |
| CRISPR screening | Gene knockout effects on secretion phenotype | High-throughput discovery of regulatory genes |
Electrophysiological recording of spontaneous release
Patch-clamp electrophysiology measures miniature excitatory or inhibitory postsynaptic currents (mEPSCs/mIPSCs) to quantify spontaneous neurotransmitter secretion. This method is essential for assessing negative regulation because it directly reports the frequency and amplitude of spontaneous release events. Studies of noradrenergic regulation in the medial prefrontal cortex have used such approaches to reveal sex differences in spontaneous activity.
Calcium imaging and channel functional assays
Calcium imaging with fluorescent indicators measures intracellular calcium dynamics that drive spontaneous secretion. Functional assays of Cav3.2 channels in neuroendocrine-differentiated prostate cancer cells demonstrated that H2S upregulation accelerates secretory function, providing a model for studying negative regulation. These methods help identify how calcium channel modulators suppress spontaneous release.
Hormonal and secretory profiling
Radioimmunoassays and ELISA-based profiling of hormones such as growth hormone, ACTH, and beta-endorphin quantify spontaneous secretory patterns in vivo. Progesterone modulation of spontaneous nocturnal GH secretion in postmenopausal women was assessed using frequent blood sampling and deconvolution analysis. Seasonal cycles of beta-endorphin and ACTH in rams were characterized by repeated plasma sampling. These approaches are critical for linking negative regulation to endocrine physiology.
Microbiota and toxicant exposure models
Zebrafish and rodent models exposed to polystyrene nanoplastics or colonized with specific microbiota allow assessment of environmental impacts on spontaneous neurosecretion. Polystyrene nanoplastics dysregulated the brain-intestine-microbiota axis in zebrafish, affecting neurosecretory signaling. Bifidobacterium-mediated fatty acid isomerization and gut microbiota modulation can also be studied in gnotobiotic models to understand microbial influences on spontaneous secretion.
How CRISPR Can Be Used to Study GO:1904049 negative regulation of spontaneous neurotransmitter secretion
Knockout
CRISPR knockout models are used to delete candidate genes such as CACNA1H or PGR to test whether their loss increases spontaneous neurotransmitter secretion. For example, knocking out CACNA1H in neuroendocrine cell lines can reveal whether Cav3.2 channels are required for negative regulation of spontaneous secretion. Similarly, PGR knockout mice can be used to study progesterone-mediated suppression of spontaneous GH secretion.
Point Mutation
CRISPR point-mutation knock-in introduces specific amino acid substitutions to dissect domain functions. For instance, mutating calcium-binding residues in CACNA1H can test whether calcium sensing is required for negative regulation of spontaneous secretion. Point mutations in PGR can reveal residues critical for progesterone-mediated suppression of spontaneous GH release.
Knock-in
CRISPR knock-in of tags or reporters allows visualization and quantification of proteins involved in spontaneous secretion. Tagged knock-in of ADRA2A can reveal its presynaptic localization and dynamics in noradrenergic neurons of the prefrontal cortex. Knock-in of fluorescent reporters for GAD1 or CHAT can track co-release from medial olivocochlear neurons.
Overexpression
CRISPR overexpression models drive high-level expression of candidate genes to test gain-of-function effects on spontaneous secretion. Overexpressing GAD1 and CHAT in medial olivocochlear neurons can enhance co-release and potentially strengthen negative regulation of spontaneous secretion. Overexpression of Cav3.2 in neuroendocrine cells can accelerate secretory function, providing a positive control for negative regulation studies.
How EDITGENE Supports negative regulation of spontaneous neurotransmitter secretion Research
Researchers studying negative regulation of spontaneous neurotransmitter secretion-related genes often need to determine whether a candidate gene is causally involved in suppressing spontaneous release. EDITGENE provides comprehensive CRISPR gene editing services to create knockout, point-mutation, knock-in, and overexpression cell models, as well as CRISPR library screening and bioinformatics support, enabling rigorous functional dissection of regulatory pathways.
Contact EDITGENE today to design your custom CRISPR model for negative regulation of spontaneous neurotransmitter secretion research.
Frequently Asked Questions About negative regulation of spontaneous neurotransmitter secretion
What is GO:1904049?
GO:1904049 is the Gene Ontology term for negative regulation of spontaneous neurotransmitter secretion, defined as any process that stops, prevents, or reduces the frequency, rate, or extent of spontaneous neurotransmitter secretion.
What is spontaneous neurotransmitter secretion?
Spontaneous neurotransmitter secretion is the action-potential-independent release of neurotransmitter from presynaptic terminals, often measured as miniature synaptic currents.
What genes are involved in negative regulation of spontaneous neurotransmitter secretion?
Genes such as CACNA1H, PGR, ADRA2A, GAD1, and CHAT have been implicated in modulating spontaneous secretion based on studies of calcium channels, progesterone signaling, noradrenergic control, and co-release.
How is spontaneous neurotransmitter secretion measured?
It is commonly measured by patch-clamp electrophysiology recording miniature postsynaptic currents, or by calcium imaging and hormone profiling in vivo.
What role does Cav3.2 play in spontaneous secretion?
Functional upregulation of the H2S/Cav3.2 channel pathway accelerates secretory function in neuroendocrine-differentiated prostate cancer cells, indicating Cav3.2 promotes secretion.
Can hormones regulate spontaneous neurotransmitter secretion?
Yes, progesterone modulates spontaneous nocturnal and ghrelin-induced growth hormone secretion in postmenopausal women, demonstrating hormonal control.
Are there sex differences in spontaneous secretion regulation?
Yes, sex differences exist in noradrenergic regulation of the medial prefrontal cortex in mice, indicating sex-specific negative regulation.
How do environmental toxicants affect spontaneous secretion?
Polystyrene nanoplastics cause dysregulation of the brain-intestine-microbiota axis in zebrafish, affecting neurosecretory signaling.
What is the role of co-release in negative regulation?
Co-release of GABA and acetylcholine from medial olivocochlear neurons acts as a fine regulatory mechanism of cochlear efferent inhibition, modulating spontaneous secretion.
How can CRISPR help study negative regulation of spontaneous neurotransmitter secretion?
CRISPR knockout, point-mutation, knock-in, and overexpression models allow causal testing of candidate genes, while library screening enables discovery of novel regulators.
Conclusion
GO:1904049, negative regulation of spontaneous neurotransmitter secretion, is a critical biological process that controls action-potential-independent neurotransmitter release. Research has identified key roles for calcium channels such as Cav3.2, hormonal signals like progesterone, noradrenergic pathways, and co-release mechanisms in suppressing spontaneous secretion. Environmental toxicants and microbiota can also perturb these regulatory systems. Understanding this process has broad implications for neuroendocrine disorders, neurotoxicity, and psychiatric conditions. CRISPR-based models and EDITGENE services provide powerful tools to dissect the genes and pathways that negatively regulate spontaneous neurotransmitter secretion, accelerating discovery in neuroscience and endocrinology.
References
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- 4. Roelfsema F et al.. 2019. Modulating Effects of Progesterone on Spontaneous Nocturnal and Ghrelin-Induced GH Secretion in Postmenopausal Women.. J Clin Endocrinol Metab 104(6):2385-2394 PMID: 30721950
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