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Text
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URL Address
<a href="http://doi.org/10.1016/j.heares.2017.01.011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.heares.2017.01.011</a>
Pages
14–24
Volume
346
Dublin Core
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Title
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Metabotropic glutamate and GABA receptors modulate cellular excitability and glutamatergic transmission in chicken cochlear nucleus angularis neurons.
Publisher
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Hearing research
Date
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2017
2017-03
Subject
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*Cellular excitability; *GABA(B)R; *mGluR; *Neuromodulation; *Nucleus angularis; *Synaptic transmission; Action Potentials/drug effects; Animals; Chick Embryo; Cochlear Nucleus/cytology/*physiology; Excitatory Postsynaptic Potentials/drug effects; GABA-B Receptor Agonists/pharmacology; GABA-B/*physiology; Glutamic Acid/*physiology; Metabotropic Glutamate/agonists/classification/*physiology; Neurons/drug effects/physiology; Patch-Clamp Techniques; Receptors; Synaptic Transmission/drug effects
Creator
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Shi Wei; Lu Yong
Description
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Neurons in the avian cochlear nucleus angularis (NA) receive glutamatergic input from the auditory nerve, and GABAergic input from the superior olivary nucleus. Physiologically heterogeneous, NA neurons perform multiple functions including encoding sound intensity information. Using in vitro whole-cell patch recordings from acute brain slices and immunohistochemistry staining, we investigated neuromodulation mediated by metabotropic glutamate and GABA receptors (mGluRs and GABABRs) in NA neurons. Based on their intrinsic firing patterns in response to somatic current injections, NA neurons were classified into onset, damped, and tonic cells. Pharmacological activation of group II mGluRs, group III mGluRs, and GABABRs, by their respective agonists, suppressed the cellular excitability of non-onset firing NA neurons. Each of these agonists inhibited the glutamatergic transmission in NA neurons, in a cell type-independent manner. The frequency but not the amplitude of spontaneous release of glutamate was reduced by each of these agonists, suggesting that the modulation of the glutamatergic transmission was via presynaptic actions. Interestingly, activation of group I mGluRs increased cellular excitability and suppressed glutamatergic transmission in non-onset neurons. These results elaborate that auditory processing in NA neurons is subject to neuromodulation mediated by metabotropic receptors activated by native neurotransmitters released at NA.
Identifier
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<a href="http://doi.org/10.1016/j.heares.2017.01.011" target="_blank" rel="noreferrer noopener">10.1016/j.heares.2017.01.011</a>
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*Cellular excitability
*GABA(B)R
*mGluR
*Neuromodulation
*Nucleus angularis
*Synaptic Transmission
2017
Action Potentials/drug effects
Animals
Chick Embryo
Cochlear Nucleus/cytology/*physiology
Department of Anatomy & Neurobiology
Excitatory Postsynaptic Potentials/drug effects
GABA-B Receptor Agonists/pharmacology
GABA-B/*physiology
Glutamic Acid/*physiology
Hearing research
Lu Yong
Metabotropic Glutamate/agonists/classification/*physiology
NEOMED College of Medicine
Neurons/drug effects/physiology
Patch-Clamp Techniques
Receptors
Shi Wei
Synaptic Transmission/drug effects