ArticlePloS one2015
Temperature differentially facilitates spontaneous but not evoked glutamate release from cranial visceral primary afferents.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- TRPM3 expression and control of glutamate release from primary vagal afferent neurons.Journal of neurophysiology · 2021Article
- 5-HTBrain research · 2019Article
- Dynasore blocks evoked release while augmenting spontaneous synaptic transmission from primary visceral afferents.PloS one · 2017Article
- Distinct Calcium Sources Support Multiple Modes of Synaptic Release from Cranial Sensory Afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Excitatory amino acid transporters tonically restrain nTS synaptic and neuronal activity to modulate cardiorespiratory function.Journal of neurophysiology · 2016Article
- Vanilloids selectively sensitize thermal glutamate release from TRPV1 expressing solitary tract afferents.Neuropharmacology · 2016Article
- Central control of body temperature.F1000Research · 2016Review
- Spinal cord thermosensitivity: An afferent phenomenon?Temperature (Austin, Tex.)Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Temperature is fundamentally important to all biological functions including synaptic glutamate release. Vagal afferents from the solitary tract (ST) synapse on second order neurons in the nucleus of the solitary tract, and glutamate release at this first central synapse controls autonomic reflex function. Expression of the temperature-sensitive Transient Receptor Potential Vanilloid Type 1 receptor separates ST afferents into C-fibers (TRPV1+) and A-fibers (TRPV1-). Action potential-evoked glutamate release is similar between C- and A-fiber afferents, but TRPV1 expression facilitates a second form of synaptic glutamate release in C-fibers by promoting substantially more spontaneous glutamate release. The influence of temperature on different forms of glutamate release is not well understood. Here we tested how temperature impacts the generation of evoked and spontaneous release of glutamate and its relation to TRPV1 expression. In horizontal brainstem slices of rats, activation of ST primary afferents generated synchronous evoked glutamate release (ST-eEPSCs) at constant latency whose amplitude reflects the probability of evoked glutamate release. The frequency of spontaneous EPSCs in these same neurons measured the probability of spontaneous glutamate release. We measured both forms of glutamate from each neuron during ramp changes in bath temperature of 4-5 °C. Spontaneous glutamate release from TRPV1+ closely tracked with these thermal changes indicating changes in the probability of spontaneous glutamate release. In the same neurons, temperature changed axon conduction registered as latency shifts but ST-eEPSC amplitudes were constant and independent of TRPV1 expression. These data indicate that TRPV1-operated glutamate release is independent of action potential-evoked glutamate release in the same neurons. Together, these support the hypothesis that evoked and spontaneous glutamate release originate from two pools of vesicles that are independently modulated and are distinct processes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.