TY - JOUR
T1 - Factors Influencing Short-term Synaptic Plasticity in the Avian Cochlear Nucleus Magnocellularis
AU - Sanchez, Jason Tait
AU - Quinones, Karla
AU - Otto-Meyer, Sebastian
N1 - Publisher Copyright:
© the authors, publisher and licensee Libertas Academica Limited.
Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 2015
Y1 - 2015
N2 - Defined as reduced neural responses during high rates of activity, synaptic depression is a form of short-term plasticity important for the temporal filtering of sound. In the avian cochlear nucleus magnocellularis (NM), an auditory brainstem structure, mechanisms regulating short-term synaptic depression include pre-, post-, and extrasynaptic factors. Using varied paired-pulse stimulus intervals, we found that the time course of synaptic depression lasts up to four seconds at late-developing NM synapses. Synaptic depression was largely reliant on exogenous Ca2+-dependent probability of presynaptic neurotransmitter release, and to a lesser extent, on the desensitization of postsynaptic a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptor (AMPA-R). Interestingly, although extrasynaptic glutamate clearance did not play a significant role in regulating synaptic depression, blocking glutamate clearance at early-developing synapses altered synaptic dynamics, changing responses from depression to facilitation. These results suggest a developmental shift in the relative reliance on pre-, post-, and extrasynaptic factors in regulating short-term synaptic plasticity in NM.
AB - Defined as reduced neural responses during high rates of activity, synaptic depression is a form of short-term plasticity important for the temporal filtering of sound. In the avian cochlear nucleus magnocellularis (NM), an auditory brainstem structure, mechanisms regulating short-term synaptic depression include pre-, post-, and extrasynaptic factors. Using varied paired-pulse stimulus intervals, we found that the time course of synaptic depression lasts up to four seconds at late-developing NM synapses. Synaptic depression was largely reliant on exogenous Ca2+-dependent probability of presynaptic neurotransmitter release, and to a lesser extent, on the desensitization of postsynaptic a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptor (AMPA-R). Interestingly, although extrasynaptic glutamate clearance did not play a significant role in regulating synaptic depression, blocking glutamate clearance at early-developing synapses altered synaptic dynamics, changing responses from depression to facilitation. These results suggest a developmental shift in the relative reliance on pre-, post-, and extrasynaptic factors in regulating short-term synaptic plasticity in NM.
KW - AMPA receptors
KW - Desensitization
KW - Development
KW - Glutamate transporters
KW - Nucleus magnocellularis
KW - short-term synaptic depression
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U2 - 10.4137/JEn.s25472
DO - 10.4137/JEn.s25472
M3 - Article
AN - SCOPUS:84950993483
VL - 2015
SP - 11
EP - 24
JO - Journal of Experimental Neuroscience
JF - Journal of Experimental Neuroscience
SN - 1179-0695
ER -