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Pathophysiological Significance of α-Synuclein in Sympathetic Nerves: In Vivo Observations.
Neurology
February 2025
From the Autonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD.
Background And Objectives: Lewy body diseases (LBDs) such as Parkinson disease (PD) feature increased deposition of α-synuclein (α-syn) in cutaneous sympathetic noradrenergic nerves. The pathophysiologic significance of sympathetic intraneuronal α-syn is unclear. We reviewed data about immunoreactive α-syn, tyrosine hydroxylase (TH, a marker of catecholaminergic fibers), and the sympathetic neurotransmitter norepinephrine (NE) in skin biopsies from control participants and patients with PD, the related LBD pure autonomic failure (PAF), the non-LBD synucleinopathy multiple system atrophy (MSA), or neurologic postacute sequelae of severe acute respiratory syndrome coronavirus 2 (neuro-PASC).
View Article and Find Full Text PDFDual calcium-voltage optical mapping of regional voltage and calcium signals in intact murine -R2474S hearts.
J Mol Cell Cardiol Plus
December 2024
Key Laboratory of Medical Electrophysiology of the Ministry of Education, Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan 646000, China.
Unlabelled: Abnormal regional variations in electrical and calcium homeostasis properties have been implicated in catecholaminergic polymorphic ventricular tachycardias (CPVT) attributable to abnormal RyR2-mediated store Ca release, but their underlying mechanism have not been well explored in intact hearts.
Methods: We performed in vivo and ex vivo studies including high throughput mapping of Ca transients (CaT) and transmembrane voltage (V) in murine wild-type (WT) and heterozygous -R2474S/+ hearts, before and during isoprenaline (ISO) challenge.
Results: ISO-challenged -R2474S/+ showed increased incidence of arrhythmia accompanied by abnormal Ca transients compared to WT.
Gain-of-Function and Loss-of-Function Mutations in the RyR2-Expressing Gene Are Responsible for the CPVT1-Related Arrhythmogenic Activities in the Heart.
Curr Issues Mol Biol
November 2024
School of Systems Biology, George Mason University, Fairfax, VA 22030, USA.
Mutations in the ryanodine receptor (RyR2) gene have been linked to arrhythmia and possibly sudden cardiac death (SCD) during acute emotional stress, physical activities, or catecholamine perfusion. The most prevalent disorder is catecholaminergic polymorphic ventricular tachycardia (CPVT1). Four primary mechanisms have been proposed to describe CPVT1 with a RyR2 mutation: (a) gain-of-function, (b) destabilization of binding proteins, (c) store-overload-induced Ca release (SOICR), and (d) loss of function.
View Article and Find Full Text PDFNoradrenaline modulates sensory information in mouse vomeronasal sensory neurons.
iScience
October 2024
Neurobiology Group, SISSA, Scuola Internazionale Superiore di Studi Avanzati, 34136 Trieste, Italy.
Article Synopsis
- The sympathetic nervous system enhances sensory detection and prepares organs for alertness, influencing how we sense our environment.
- The study focused on noradrenaline (NA) and its effect on vomeronasal sensory neurons (VSNs), which are crucial for sensing pheromones and other chemical signals.
- Findings revealed that NA boosts the activity of VSNs through alpha 1 adrenergic receptors, indicating a significant role of NA in regulating sensory processing and the connection between the sympathetic system and chemosensation.
Management of Pheochromocytomas and Paragangliomas.
Surg Clin North Am
August 2024
Department of Surgery, University of Pennsylvania Health System, 3400 Spruce Street, 4th Floor, Maloney Building, Philadelphia, PA 19104, USA; Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Pheochromocytomas and paragangliomas are distinctive neuroendocrine tumors which frequently produce excess catecholamines with resultant cardiovascular morbidity. These tumors have a strong genetic component, with up to 40% linked to hereditary pathogenic variants; therefore, germline genetic testing is recommended for all patients. Surgical resection offers the only potential cure in the case of localized disease.
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