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Muscarinic acetylcholine type 1 receptor antagonism activates TRPM3 to augment mitochondrial function and drive axonal repair in adult sensory neurons.

Mol Metab

December 2024

Division of Neurodegenerative Disorders, St. Boniface Hospital Albrechtsen Research Centre, University of Manitoba, Winnipeg, Canada; Department of Pharmacology and Therapeutics, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. Electronic address:

Objective: Antagonism of the muscarinic acetylcholine type 1 receptor (MR) promotes sensory axon repair and is protective in peripheral neuropathy, however, the mechanism remains elusive. We investigated the role of the heat-sensing transient receptor potential melastatin-3 (TRPM3) cation channel in MR antagonism-mediated nerve regeneration and explored the potential of TRPM3 activation to facilitate axonal plasticity.

Methods: Dorsal root ganglion (DRG) neurons from adult control or diabetic rats were cultured and treated with TRPM3 agonists (CIM0216, pregnenolone sulfate) and MR antagonists pirenzepine (PZ) or muscarinic toxin 7 (MT7).

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Gravity may exert species-specific effects on quadrupedal vasoreactivity, reflecting variations in the vertical displacement of the cardiocranial axis from the dorsal plane. Deer show markedly displaced cardiocranial axes compared to their closest phylogenetic relatives, but their relative cerebrovascular responses remain unelucidated. Accordingly, we investigated the responses to noradrenaline (NA), acetylcholine (ACh), 5-hydroxytryptamine (5-HT), histamine, angiotensin (Ang) II, and bradykinin (BK) in cervine basilar arterial rings.

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Drug repurposing for hard-to-treat human alveolar echinococcosis: pyronaridine and beyond.

Parasitology

November 2024

State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.

Article Synopsis
  • Human alveolar echinococcosis is a challenging parasitic disease that is hard to treat and often untreated, leading to high healthcare costs.
  • Current treatment relies on albendazole, which isn't fully effective and can have serious side effects, highlighting the need for better options.
  • Pyronaridine, an antimalarial drug, has shown promising results in mouse models for treating the disease, significantly reducing parasite size and counts compared to albendazole, and could serve as an alternative therapy, while another compound, pirenzepine, also shows potential for further research.
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Article Synopsis
  • Memory updating helps integrate new info into existing memories but can lead to issues in PTSD when fear memories spread to neutral situations.
  • A study in rats showed that reactivating a fear memory in a familiar context before introducing a neutral context allowed fear memories to transfer, but this only worked if the reactivation was recent.
  • Blocking M1 muscarinic acetylcholine receptors in the dorsal hippocampus stopped this memory transfer, indicating that memory reactivation and disruption are necessary for updating fear memories, which could guide new PTSD treatments.
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Lower levels of kainate receptors, but not AMPA or NMDA receptors, in Brodmann's area (BA) 9, but not BA 10, from a subgroup of people with schizophrenia who have a marked deficit in cortical muscarinic M1 receptors.

Schizophr Res

December 2024

The Molecular Psychiatry Laboratory, The Florey, Parkville, Victoria, Australia; The Florey Department of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia. Electronic address:

Article Synopsis
  • The study investigates the differences in receptor binding in the brains of people with schizophrenia, specifically focusing on the Muscarinic Receptor Deficit subgroup (MRDS), which shows reduced binding to the M1 receptor.
  • Researchers confirmed MRDS by measuring [H]pirenzepine binding and then examined the binding of other glutamate receptors ([H]kainate, [H]AMPA, [H]NMDA) in Brodmann's areas 9 and 10 to see if there were subgroup-specific differences.
  • Results showed that while M1 and kainate receptor binding was lower in BA 9 and BA 10 for MRDS individuals, other glutamate receptors (AMPA and NMDA) did not
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