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Endogenous peptidergic modulation of perisynaptic Schwann cells at the frog neuromuscular junction

1 Although peptides are important modulators of synapses, their action on synapse‐glia interactions remain unclear. The amphibian neuromuscular junction (NMJ) was used to examine the effects of substance P (SP) on perisynaptic Schwann cells (PSCs), glial cells at the frog NMJ, by monitoring changes in intracellular Ca2+. 2 SP induced Ca2+ responses that were mimicked by the neurokinin 1 receptor (NK‐1) agonist septide and with a shorter delay by the SP fragment, SP(6–11). SP and SP(6–11) responses were blocked by NK‐1 antagonists SR140333 and LY303870. 3 Ca2+ responses remained unchanged when extracellular Ca2+ was removed but were blocked after pertussis toxin (PTX) treatment, indicating that the receptors were linked to internal stores of Ca2+ via a PTX‐sensitive G‐protein. 4 The slowly hydrolysable NK‐1 agonist [Sar9, Met(O2)11]‐SP only induced Ca2+ responses when applied for a long period of time and not during brief, local applications, suggesting the involvement of SP hydrolysis. Acetylcholinesterase (AChE) may not be involved in SP degradation since Ca2+ responses evoked by SP were unchanged in the presence of the cholinesterase inhibitor neostigmine. 5 Ca2+ responses induced by muscarine and nerve stimulations were almost abolished when preceded by SP applications, while those induced by ATP were significantly reduced. The rundown of the nerve‐evoked Ca2+ responses in PSCs was attenuated in the presence of SR140333. 6 These results indicate that endogenous SP is involved in the regulation of PSC activity and that SP is an important modulator of glial cell Ca2+ signalling and synapse‐glia communication.