Homeostatic plasticity in the developing nervous system View Full Text


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Article Info

DATE

2004-02

AUTHORS

Gina G. Turrigiano, Sacha B. Nelson

ABSTRACT

Key PointsNeuronal activity often leads to changes in synaptic efficacy. However, such plasticity must be accompanied by homeostatic mechanisms that prevent neural activity from being driven towards runaway activity or quiescence. One potential homeostatic mechanism is the adjustment of synaptic excitability so that firing rates remain relatively constant.At the neuromuscular junction, genetic alterations in synaptic transmission lead to compensatory changes. For example, a decrease in the number of synapses leads to a compensatory increase in quantal amplitude. Such mechanisms might normally adjust neuromuscular transmission during development to allow for changes in muscle growth or synaptic drive.Similar phenomena have been seen in cultured networks of central neurons. Blocking spontaneous activity in cortical cultures results in hyperactivity when the block is lifted. One mechanism for such adjustment is the global regulation of excitatory synapses within a given neuron.Synaptic strength can be measured by analysing miniature excitatory postsynaptic currents (mEPSCs), which result from spontaneous release of quanta of transmitter from individual vesicles. Chronic alterations in activity can increase or decrease the amplitude of mEPSCs. The amplitude seems to be scaled so that each synaptic strength is multiplied or divided by the same factor. Such multiplicative scaling should preserve the relative strengths of synapses.Synaptic strength could be regulated through changes in postsynaptic receptor numbers, presynaptic transmitter release or reuptake, or the number of functional synapses. Evidence in favour of a change in receptor number includes the increase in mEPSC amplitude and in the response to glutamate application. It is unclear whether the homeostatic regulation of receptor numbers shares a signalling pathway with the insertion of receptors into the membrane by long-term potentiation (LTP).Presynaptic changes in transmission are involved in homeostatic plasticity at the neuromuscular junction, but it is less clear whether they are involved in homeostasis in central neurons. In some circumstances, such as developing hippocampal cultures, changes in activity cause changes in the frequency of mEPSCs, as well as in their amplitude, indicating presynaptic alterations.It is unclear how homeostatic plasticity is induced. Important questions include: whether homeostatic plasticity is cell-autonomous; how changes in activity are integrated and read out; and what intracellular signalling cascades generate global changes in synaptic strength.The functioning of cortical networks requires a balance between excitatory and inhibitory inputs onto neurons. Homeostasis in recurrent networks seems to involve adjustments in the relative strengths of excitatory and inhibitory feedback. It seems that excitatory and inhibitory synapses are adjusted independently to maintain activity in the face of changes in drive.Evidence that these mechanisms are important in vivo comes from the developing visual system. For example, during development, there is an inverse relationship between mEPSC frequency and amplitude, indicating that as synaptic drive increases, synaptic strength is reduced. More... »

PAGES

97-107

References to SciGraph publications

  • 2003-11. The other side of the engram: experience-driven changes in neuronal intrinsic excitability in NATURE REVIEWS NEUROSCIENCE
  • 1998-02. Activity-dependent scaling of quantal amplitude in neocortical neurons in NATURE
  • 2003-04. Conservation of total synaptic weight through balanced synaptic depression and potentiation in NATURE
  • 1973-06. Self-organization of orientation sensitive cells in the striate cortex in KYBERNETIK
  • 1999-01. Regulation of morphological postsynaptic silent synapses in developing hippocampal neurons in NATURE NEUROSCIENCE
  • 1996-04. Role of intercellular interactions in heterosynaptic long-term depression in NATURE
  • 2001-03. Activity-dependent modification of inhibitory synapses in models of rhythmic neural networks in NATURE NEUROSCIENCE
  • 1982-11. Simplified neuron model as a principal component analyzer in JOURNAL OF MATHEMATICAL BIOLOGY
  • 1990-01. Development in the absence of spontaneous bioelectric activity results in increased stereotyped burst firing in cultures of dissociated cerebral cortex in EXPERIMENTAL BRAIN RESEARCH
  • 1989-09. NMDA and non-NMDA receptors are co-localized at individual excitatory synapses in cultured rat hippocampus in NATURE
  • 2003-02-10. Activity level controls postsynaptic composition and signaling via the ubiquitin-proteasome system in NATURE NEUROSCIENCE
  • 2000-11. Synaptic plasticity: taming the beast in NATURE NEUROSCIENCE
  • 2002-11. Multiple forms of synaptic plasticity triggered by selective suppression of activity in individual neurons in NATURE
  • 2002-06-24. Critical periods for experience-dependent synaptic scaling in visual cortex in NATURE NEUROSCIENCE
  • 1999-05. Synaptic calcium transients in single spines indicate that NMDA receptors are not saturated in NATURE
  • 1995-06. Properties of synaptic transmission at single hippocampal synaptic boutons in NATURE
  • 2003-07-28. Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation in NATURE NEUROSCIENCE
  • 1986-04. Reduction in number of immunostained GABAergic neurones in deprived-eye dominance columns of monkey area 17 in NATURE
  • 2002-06-10. Facilitation at single synapses probed with optical quantal analysis in NATURE NEUROSCIENCE
  • 1998-03. Synapse-specific control of synaptic efficacy at the terminals of a single neuron in NATURE
  • Identifiers

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    http://scigraph.springernature.com/pub.10.1038/nrn1327

    DOI

    http://dx.doi.org/10.1038/nrn1327

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1005770975

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/14735113


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