推荐：神经系统在发育过程中稳定性维持

转引自生物谷：http://www.bioon.com/Article_Show.asp?ArticleID=8350

这篇是最新发表在Nature Reviews Neuroscience上的文章，很值得一读

Activity has an important role in refining synaptic connectivity during development, in part through 'Hebbian' mechanisms such as long-term potentiation and long-term depression. However, Hebbian plasticity is probably insufficient to explain activity-dependent development because it tends to destabilize the activity of neural circuits. How can complex circuits maintain stable activity states in the face of such destabilizing forces? An idea that is emerging from recent work is that average neuronal activity levels are maintained by a set of homeostatic plasticity mechanisms that dynamically adjust synaptic strengths in the correct direction to promote stability. Here we discuss evidence from a number of systems that homeostatic synaptic plasticity is crucial for processes ranging from memory storage to activity-dependent development.

Summary

Neuronal 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.
Original article:

Homeostatic plasticity in the developing nervous system
G. G. TURRIGIANO AND S. B. NELSON Nature Reviews Neuroscience 5, 97; February 2004

我一定要去看看

哪位英文好些，把上面这段话翻译一下呀？这样看着挺累的，理解上也怕不统一。

请各位在发贴时能否把英文翻译过来，毕尽多数人对英文的理解还是不太足的啊

这个关于突触自平衡调节（可塑性）的说法，可能对本论坛的另一帖“疑惑，神经元阀值的问题？”讨论有一定意义。不过，这种自平衡调节，不应该是突触水平的，应该是细胞功能调节的一种短期表面现象吧。如果突触的动用量和强度总是成反比，那神经细胞的功能就意味着不可变化的了。