Electrophysiological effects of BDNF and TrkB signaling at type-identified diaphragm neuromuscular junctions.

Previous studies show that synaptic quantal release decreases during repetitive stimulation, i.e., synaptic depression.

Bicarbonate ion transport by the electrogenic Na /HCO cotransporter, NBCe1, is required for normal electrical slow-wave activity in mouse small intestine.

Background: Normal gastrointestinal motility depends on electrical slow-wave activity generated by interstitial cells of Cajal (ICC) in the tunica muscularis of the gastrointestinal tract. A requirement for HCO in extracellular solutions used to record slow waves indicates a role for HCO transport in ICC pacemaking. The Slc4a4 gene transcript encoding the electrogenic Na /HCO cotransporter, NBCe1, is enriched in mouse small intestinal myenteric region ICC (ICC-MY) that generate slow waves.

Antioxidant power as biochemical endpoint in bread for screening and early managing quality and toxicant-related safety anomalies in food production.

Flaxseeds are both a food ingredient and a natural source of antioxidants (e.g. lignans, PUFAs) and pro-oxidant contaminants (e.

Ageing and neurotrophic signalling effects on diaphragm neuromuscular function.

The age-related mechanisms underlying sarcopenia are largely unknown. We hypothesize that age-related neuromuscular changes depend on brain-derived neurotrophic factor (BDNF) acting through the tropomyosin-related kinase receptor B (TrkB). Maximal specific force and neuromuscular transmission failure were assessed at 6, 18 and 24 months following control, BDNF or phosphoprotein phosphatase 1 derivative (1NMPP1) treatment in male TrkB(F616A) mice.

TrkB kinase activity maintains synaptic function and structural integrity at adult neuromuscular junctions.

Activation of the tropomyosin-related kinase receptor B (TrkB) by brain-derived neurotrophic factor acutely regulates synaptic transmission at adult neuromuscular junctions (NMJs). The role of TrkB kinase activity in the maintenance of NMJ function and structure at diaphragm muscle NMJs was explored using a chemical-genetic approach that permits reversible inactivation of TrkB kinase activity in TrkB(F616A) mice by 1NMPP1. Inhibiting TrkB kinase activity for 7 days resulted in significant, yet reversible, impairments in neuromuscular transmission at diaphragm NMJs.