The active principle of suprenal extract that produces its pressor effects was isolated by the joint research of John Abel in 1899 and Jokichi Takamine in 1901. Within three years Elliott, working in Langley's laboratory, suggested that this active principle, referred to by British physiologists as "adrenaline" and named "Adrenalin" by Takamine, was released from sympathetic nerve terminals to act on smooth muscle cells. However, it was not until 1946 that von Euler showed that demythelated adrenaline (noradrenaline) rather than adrenaline is a sympathetic transmitter. The possibility that this sympathetic transmitter could also act on nerve terminals was not developed until 1971. Research on autoreceptors culminated in the identification of adrenergic receptors on nerve terminals different to those on muscle cells. This paper assesses the contributions that established the idea of the adrenergic autoreceptor, 100 years after the discovery of adrenaline.
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http://dx.doi.org/10.1007/BF02281628 | DOI Listing |
Sci Rep
January 2025
Key Laboratory for Stem Cells and Tissue Engineering Ministry of Education, Guangdong Provincial Key Laboratory of Brain Function and Disease, Institute of Spinal Cord Injury, Department of Histology and Embryology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Neuromuscular diseases usually manifest as abnormalities involving motor neurons, neuromuscular junctions, and skeletal muscle (SkM) in postnatal stage. Present in vitro models of neuromuscular interactions require a long time and lack neuroglia involvement. Our study aimed to construct rodent bioengineered spinal cord neural network-skeletal muscle (NN-SkM) assembloids to elucidate the interactions between spinal cord neural stem cells (SC-NSCs) and SkM cells and their biological effects on the development and maturation of postnatal spinal cord motor neural circuits.
View Article and Find Full Text PDFJ Pain Res
January 2025
Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.
Bone is a common site of advanced cancer metastasis, second only to the lungs and liver. Cancer-induced bone pain (CIBP) is a persistent and intense pain that is caused by a combination of inflammatory and neuropathic factors. As CIBP progresses, the degree of pain intensifies.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Institute of Biomedicine of Seville (IBiS), Virgen del Rocío University Hospital/CSIC/University of Seville, 41013 Seville, Spain.
The ubiquitin proteasome system (UPS) is implicated in protein homeostasis. One of the proteins involved in this system is HERC1 E3 ubiquitin ligase, which was associated with several processes including the normal development and neurotransmission at the neuromuscular junction (NMJ), autophagy in projection neurons, myelination of the peripheral nervous system, among others. The tambaleante (tbl) mouse model carries the spontaneous mutation Gly483Glu substitution in the HERC1 E3 protein.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Azriele Faculty of Medicine in the Galilee, Bar-Ilan University, Safed 1311502, Israel.
Provoked vulvodynia (PV) is the leading cause of vulvar pain and dyspareunia. The etiology of PV is multifactorial and remains poorly understood. PV is associated with a history of repeated vulvar inflammation and is often accompanied by sensory neuromodulation as a result of activation of the metabotropic glutamate receptor 5 (mGluR5) in the sensory nerve terminals.
View Article and Find Full Text PDFJ Neurochem
January 2025
Centre for Discovery Brain Sciences, Hugh Robson Building, George Square, University of Edinburgh, Edinburgh, Scotland, UK.
Synaptic vesicle protein 2A (SV2A) is an abundant synaptic vesicle cargo with an as yet unconfirmed role in presynaptic function. It is also heavily implicated in epilepsy, firstly being the target of the leading anti-seizure medication levetiracetam and secondly with loss of function mutations culminating in human disease. A range of potential presynaptic functions have been proposed for SV2A; however its interaction with the calcium sensor for synchronous neurotransmitter release, synaptotagmin-1 (Syt1), has received particular attention over the past decade.
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