Abstract
Cranial visceral afferents contained within the solitary tract (ST) contact second-order neurons in the nucleus of the solitary tract (NTS) and release the excitatory amino acid glutamate via three distinct exocytosis pathways; synchronous, asynchronous, and spontaneous release. The presence of TRPV1 in the central terminals of a majority of ST afferents conveys activity-dependent asynchronous glutamate release and provides a temperature sensitive calcium conductance which largely determines the rate of spontaneous vesicle fusion. TRPV1 is present in unmyelinated C-fiber afferents and these facilitated forms of glutamate release may underlie the relative strength of C-fibers in activating autonomic reflex pathways. However, pharmacological blockade of TRPV1 signaling eliminates only ~50% of the asynchronous profile and attenuates the temperature sensitivity of spontaneous release indicating additional thermosensitive calcium influx pathways may exist which mediate these forms of vesicle release. In the present study we isolate the contribution of TRPV1 independent forms of glutamate release at ST-NTS synapses. We found ST afferent innervation at NTS neurons and synchronous vesicle release from TRPV1 KO mice was not different to control animals; however, only half of TRPV1 KO ST afferents completely lacked asynchronous glutamate release. Further, temperature driven spontaneous rates of vesicle release were not different from 33 to 37°C between control and TRPV1 KO afferents. These findings suggest additional temperature dependent mechanisms controlling asynchronous and thermosensitive spontaneous release at physiological temperatures, possibly mediated by additional thermosensitive TRP channels in primary afferent terminals.
Highlights
Primary vagal afferent neurons provide a direct neural pathway through which the ongoing status of visceral organ systems is conveyed to the brain (Loewy, 1990)
We found that the amplitude of solitary tract evoked excitatory postsynaptic currents (EPSCs) (ST-EPSCs) from single ST afferent contacts were not statistically different between control and TRPV1 KO animals (Figure 1)
The latency to event onset is an approximate measure of conduction velocity and was not different between groups (Figure 1B); indicating the afferent fibers activated have the same degree of myelination
Summary
Primary vagal afferent neurons provide a direct neural pathway through which the ongoing status of visceral organ systems (including the heart, lungs, and gastrointestinal tract) is conveyed to the brain (Loewy, 1990). As a result information transfer must be at one time reliable and precise while maintaining plasticity to match autonomic function to the physiological state. Vagal afferents release the fast excitatory neurotransmitter glutamate via three distinct pathways: synchronous, asynchronous, and spontaneous (Andresen et al, 2012b). Synchronous glutamate release is a tightly regulated process by which an action potential evokes a coordinated release of multiple glutamate vesicles into the synaptic cleft to ensure highfidelity signaling between neurons. We predict that the interplay between multiple complementary vesicle release pathways allows for robust/precise information transfer which is adaptable and plastic to changing physiological states
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