ArticleRegulatory peptides2010
Cellular distribution of chromogranin A in excitatory, inhibitory, aminergic and peptidergic neurons of the rodent central nervous system.
Article in Regulatory peptides, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
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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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Pineal parenchymal tumor of intermediate differentiation: a systematic review and contemporary management of 389 cases reported during the last two decades.Neurosurgical review · 2022Pooled it
- Chromogranin A deficiency attenuates tauopathy by altering epinephrine-alpha-adrenergic receptor signaling in PS19 mice.Nature communications · 2025Article
- Pangenome reconstruction in rats enhances genotype-phenotype mapping and variant discovery.iScience · 2025Article
- Pangenome reconstruction in rats enhances genotype-phenotype mapping and novel variant discovery.bioRxiv : the preprint server for biology · 2024Article
- Immunohistochemical field parcellation of the human hippocampus along its antero-posterior axis.Brain structure & function · 2024Article
- Brain-Biomarker Changes in Body Fluids of Patients with Parkinson's Disease.International journal of molecular sciences · 2023Review
- Protein Expression of the Microglial Marker Tmem119 Decreases in Association With Morphological Changes and Location in a Mouse Model of Traumatic Brain Injury.Frontiers in cellular neuroscience · 2022Article
- An increase in VGF expression through a rapid, transcription-independent, autofeedback mechanism improves cognitive function.Translational psychiatry · 2021Article
- Stathmin-2 Mediates Glucagon Secretion From Pancreatic α-Cells.Frontiers in endocrinology · 2020Article
- Chromogranin A and its fragments in cardiovascular, immunometabolic, and cancer regulation.Annals of the New York Academy of Sciences · 2019Review
- Pituitary Adenylate Cyclase-Activating Peptide (PACAP)-Glutamate Co-transmission Drives Circadian Phase-Advancing Responses to Intrinsically Photosensitive Retinal Ganglion Cell Projections by Suprachiasmatic Nucleus.Frontiers in neuroscience · 2019Article
- ATM and ATR play complementary roles in the behavior of excitatory and inhibitory vesicle populations.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Activation of the HPA axis and depression of feeding behavior induced by restraint stress are separately regulated by PACAPergic neurotransmission in the mouse.Stress (Amsterdam, Netherlands) · 2016Article
- The extended granin family: structure, function, and biomedical implications.Endocrine reviews · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Immunoreactivity for both processed and unprocessed forms of chromogranin A (CGA) was examined, using an antibody recognizing the WE14 epitope, among terminal fields and cell bodies of anatomically defined GABAergic, glutamatergic, cholinergic, catecholaminergic, and peptidergic cell groups in the rodent central nervous system. CGA is ubiquitous within neuronal cell bodies, with no obvious anatomical or chemically-coded subdivision of the nervous system in which CGA is not expressed in most neurons. CGA expression is essentially absent from catecholaminergic terminal fields in the CNS, suggesting a relative paucity of large dense-core vesicles in CNS compared to peripheral catecholaminergic neurons. Extensive synaptic co-localization with classical transmitter markers is not observed even in areas such as amygdala, where CGA fibers are numerous, suggesting preferential segregation of CGA to peptidergic terminals in CNS. Localization of CGA in dendrites in some areas of CNS may indicate its involvement in regulation of dendritic release mechanisms. Finally, the ubiquitous presence of CGA in neuronal cell somata, especially pronounced in GABAergic neurons, suggests a second non-secretory vesicle-associated function for CGA in CNS. We propose that CGA may function in the CNS as a prohormone and granulogenic factor in some terminal fields, but also possesses as-yet unknown unique cellular functions within neuronal somata and dendrites.
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What 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.