Article ; Online: Slow NMDA-Mediated Excitation Accelerates Offset-Response Latencies Generated via a Post-Inhibitory Rebound Mechanism.
2019 Volume 6, Issue 3
Abstract: In neural circuits, action potentials (spikes) are conventionally caused by excitatory inputs whereas inhibitory inputs reduce or modulate neuronal excitability. We previously showed that neurons in the superior paraolivary nucleus (SPN) require solely ... ...
Abstract | In neural circuits, action potentials (spikes) are conventionally caused by excitatory inputs whereas inhibitory inputs reduce or modulate neuronal excitability. We previously showed that neurons in the superior paraolivary nucleus (SPN) require solely synaptic inhibition to generate their hallmark offset response, a burst of spikes at the end of a sound stimulus, via a post-inhibitory rebound mechanism. In addition SPN neurons receive excitatory inputs, but their functional significance is not yet known. Here we used mice of both sexes to demonstrate that in SPN neurons, the classical roles for excitation and inhibition are switched, with inhibitory inputs driving spike firing and excitatory inputs modulating this response. Hodgkin-Huxley modeling suggests that a slow, NMDA receptor (NMDAR)-mediated excitation would accelerate the offset response. We find corroborating evidence from |
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MeSH term(s) | Acoustic Stimulation ; Action Potentials/physiology ; Animals ; Auditory Perception/physiology ; Excitatory Postsynaptic Potentials ; Female ; Inhibitory Postsynaptic Potentials ; Male ; Mice, Inbred C57BL ; Neurons/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Superior Olivary Complex/physiology |
Chemical Substances | Receptors, N-Methyl-D-Aspartate |
Language | English |
Publishing date | 2019-06-18 |
Publishing country | United States |
Document type | Journal Article ; Research Support, Non-U.S. Gov't |
ZDB-ID | 2800598-3 |
ISSN | 2373-2822 ; 2373-2822 |
ISSN (online) | 2373-2822 |
ISSN | 2373-2822 |
DOI | 10.1523/ENEURO.0106-19.2019 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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