| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4343869 | Neuroscience Letters | 2014 | 5 Pages |
•Serine kinases and trkB receptor cooperate in neurotransmitter release.•PKC can potentiate ACh release without the involvement of the trkB.•trkB needs an operative PKC pathway if it is to potentiate ACh release.•To actively stimulate PKA the operativity of trkB is a necessary condition.•A consequence of trkB activity can be PKA stimulation.
We conducted an electrophysiological study of the functional link between the tropomyosin-related kinase B (trkB) receptor signaling mechanism and serine-threonine kinases, both protein kinase C (PKC) and protein kinase A (PKA). We describe their coordinated role in transmitter release at the neuromuscular junction (NMJ) of the Levator auris longus muscle of the adult mouse. The trkB receptor normally seems to be coupled to stimulate ACh release because inhibiting the trkB receptor with K-252a results in a significant reduction in the size of EPPs. We found that the intracellular PKC pathway can operate as in basal conditions (to potentiate ACh release) without the involvement of the trkB receptor function, although the trkB pathway needs an operative PKC pathway if it is to couple to the release mechanism and potentiate it. To actively stimulate PKA (which also results in ACh release potentiation), the operativity of trkB is a necessary condition, and one effect of trkB may be PKA stimulation.
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