ArticleThe Journal of physiology2005
Alpha-1 adrenergic input to solitary nucleus neurones: calcium oscillations, excitation and gastric reflex control.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Thrombin action on astrocytes in the hindbrain of the rat disrupts glycemic and respiratory control.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Evidence that hindbrain astrocytes in the rat detect low glucose with a glucose transporter 2-phospholipase C-calcium release mechanism.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Activation of alpha-1 adrenergic receptors increases cytosolic calcium in neurones of the paraventricular nucleus of the hypothalamus.Journal of neuroendocrinology · 2019Article
- Hindbrain astrocytes and glucose counter-regulation.Physiology & behavior · 2019Review
- Response of catecholaminergic neurons in the mouse hindbrain to glucoprivic stimuli is astrocyte dependent.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Bidirectional brain-gut interactions: Involvement of noradrenergic transmission within the ventral part of the bed nucleus of the stria terminalis.Neuropsychopharmacology reports · 2018Article
- Differential activation of chemically identified neurons in the caudal nucleus of the solitary tract in non-entrained rats after intake of satiating vs. non-satiating meals.Physiology & behavior · 2014Article
- Adrenoreceptor modulation of oromotor pathways in the rat medulla.Journal of neurophysiology · 2014Article
- Activation of opioid μ-receptors, but not δ- or κ-receptors, switches pulmonary C-fiber-mediated rapid shallow breathing into an apnea in anesthetized rats.Respiratory physiology & neurobiology · 2012Article
- Satiation and stress-induced hypophagia: examining the role of hindbrain neurons expressing prolactin-releasing Peptide or glucagon-like Peptide 1.Frontiers in neuroscience · 2012Article
- Vagal afferent stimulation activates astrocytes in the nucleus of the solitary tract via AMPA receptors: evidence of an atypical neural-glial interaction in the brainstem.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- The role of the central noradrenergic system in behavioral inhibition.Brain research reviews · 2011Review
- Leptin amplifies the action of thyrotropin-releasing hormone in the solitary nucleus: an in vitro calcium imaging study.Brain research · 2011Article
- Hindbrain noradrenergic A2 neurons: diverse roles in autonomic, endocrine, cognitive, and behavioral functions.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Review
- Co-localization of TRHR1 and LepRb receptors on neurons in the hindbrain of the rat.Brain research · 2010Article
- Leptin "gates" thermogenic action of thyrotropin-releasing hormone in the hindbrain.Brain research · 2009Article
- Marked behavioral activation from inhibitory stimulation of locus coeruleus alpha1-adrenoceptors by a full agonist.Brain research · 2009Article
- Local circuit input to the medullary reticular formation from the rostral nucleus of the solitary tract.American journal of physiology. Regulatory, integrative and comparative physiology · 2008Article
- CXCR4 receptors in the dorsal medulla: implications for autonomic dysfunction.The European journal of neuroscience · 2008Article
- TNFalpha: a trigger of autonomic dysfunction.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2008Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The nucleus of the solitary tract (NST) processes substantial visceral afferent input and sends divergent projections to a wide array of CNS targets. The NST is essential to the maintenance of behavioural and autonomic homeostasis and is the source, as well as the recipient, of considerable noradrenergic (NE) projections. The significance of NE projections from the NST to other CNS regions has long been appreciated, but the nature of NE action on NST neurones themselves, especially on the alpha-1 receptor subtype, is controversial. We used a combination of methodologies to establish, systematically, the effects and cellular basis of action of the alpha-1 agonist, phenylephrine (PHE), to control NST neurones responsible for vago-vagal reflex regulation of the stomach. Immunocytochemical and retrograde tracing studies verified that the area postrema, A2, A5, ventrolateral medulla and locus coeruleus regions are sources of catecholaminergic input to the NST. In vivo electrophysiological recordings showed that PHE activates physiologically identified, second-order gastric sensory NST neurones. In vivo microinjection of PHE onto NST neurones caused a significant reduction in gastric tone. Finally, in vitro calcium imaging studies revealed that PHE caused dramatic cytosolic calcium oscillations in NST neurones. These oscillations are probably the result of an interplay between agonist-induced and inositol 1,4,5-trisphosphate (IP(3))-mediated intracellular calcium release and Ca(2+)-ATPase control of intracellular calcium storage pumps. The oscillations persisted even in perfusions of zero calcium-EGTA Krebs solution suggesting that the calcium oscillation is mediated principally by intracellular calcium release-reuptake mechanisms. Cyclical activation of the NST may function to increase the responsiveness of these neurones to incoming afferent input (i.e., elevate the "gain"). An increase in gain of afferent input may cause an amplification of the response part of the reflex and help explain the powerful effects that alpha-1 agonists have in suppressing gastric motility and producing anorexia.
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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.