Abstract
Gastrointestinal motility relies on the release of acetylcholine (ACh), purines and tachykinins (e.g. substance P) from excitatory enteric neurons. Tachykinins acting via NK1 and NK3 receptors facilitate cholinergic neurotransmission in the enteric nervous system. Recently, we showed that muscarinic M3 receptors facilitate ACh release indirectly by increasing adenosine outflow from stimulated myenteric neurons leading to the activation of excitatory A2A receptors [1]. It is well established that adenosine A2A receptors play a widespread role in synaptic plasticity via a sophisticated interaction with receptors for other neurotransmitters/neuromodulators. In the myenteric plexus, endogenous adenosine may arise from the catabolism of released ATP through the ectonucleotidase pathway together with the release of the nucleoside per se via the equilibrative transport system [2]. Preliminary accounts from our lab, suggest that CAP-sensitive tachykinergic neurons are an important source of purines in the rat myenteric plexus. These findings prompted us to investigate the cross talk between facilitatory A2A, M3 and NK1 receptors in rat longitudinal muscle-myenteric plexus preparations, focusing our attention on the role of tachykinergic nerve fibres which can be selectively eliminated (>95%) by neonatal capsaicin administration (CAP, 50 mg/kg, SC).
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call