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ZFIN ID: ZDB-PUB-100702-16
Synaptic scaling and the development of a motor network
Knogler, L.D., Liao, M., and Drapeau, P.
Date: 2010
Source: The Journal of neuroscience : the official journal of the Society for Neuroscience   30(26): 8871-8881 (Journal)
Registered Authors: Drapeau, Pierre
Keywords: none
MeSH Terms:
  • Action Potentials/drug effects
  • Animals
  • Glutamic Acid/metabolism
  • Motor Neurons/drug effects
  • Motor Neurons/physiology*
  • Muscle, Skeletal/drug effects
  • Muscle, Skeletal/embryology
  • Muscle, Skeletal/physiology
  • Neural Pathways/drug effects
  • Neural Pathways/embryology
  • Neural Pathways/physiology
  • Neuronal Plasticity/drug effects
  • Neuronal Plasticity/physiology
  • Receptors, AMPA/metabolism
  • Swimming/physiology*
  • Synapses/drug effects
  • Synapses/physiology*
  • Synaptic Potentials/drug effects
  • Synaptic Transmission/drug effects
  • Tumor Necrosis Factor-alpha/metabolism
  • Zebrafish
PubMed: 20592209 Full text @ J. Neurosci.
Neurons respond homeostatically to chronic changes in network activity with compensatory changes such as a uniform alteration in the size of miniature postsynaptic current (mPSC) amplitudes termed synaptic scaling. However, little is known about the impact of synaptic scaling on the function of neural networks in vivo. We used the embryonic zebrafish to address the effect of synaptic scaling on the neural network underlying locomotion. Activity was decreased during development by TTX injection to block action potentials or CNQX injection to block glutamatergic transmission. Alternatively TNFalpha was chronically applied. Recordings from spinal neurons showed that glutamatergic mPSCs scaled up approximately 25% after activity reduction and fortuitously scaled down approximately 20% after TNFalpha treatment, and were unchanged following blockade of neuromuscular activity alone with alpha-bungarotoxin. Regardless of the direction of scaling, immediately following reversal of treatment no chronic effect was distinguishable in motoneuron activity patterns or in swimming behavior. We also acutely induced a similar increase of glutamatergic mPSC amplitudes using cyclothiazide to reduce AMPA receptor desensitization or decrease of glutamatergic mPSC amplitudes using a low concentration of CNQX to partially block AMPA receptors. Though the strength of the motor output was altered, neither chronic nor acute treatments disrupted the patterning of synaptic activity or swimming. Our results show, for the first time, that scaling of glutamatergic synapses can be induced in vivo in the zebrafish and that synaptic patterning is less plastic than synaptic strength during development.