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synapses with normal ultrastructure but displayed little spontaneous synaptic activity and high
failure rates in evoked synaptic transmission unless cocultured with neuroglia [Pfrieger and
Barres, 1997]. Moreover, the efficacy of adult synapses may also depend on their intimate
partnership with glial cells [Pfrieger and Barres, 1996]. A subsequent report from this group
demonstrated that the total number of synapses on a neuron is not an intrinsic property of that
neuron, but can be regulated by extrinsic signals [Ullian
et al.,
2001]. In the absence of glia,
retinal ganglion cell neurons had only a limited ability to form synapses. Astrocytes markedly
increased the number of mature, functional synapses and were required for synaptic
maintenance in vitro [Ullian
et al.,
2001] (Fig. 3).
Figure 3. Astrocytes increase the number of synapses per neuron. (A and B) Electron micrographs of
synapses between retinal ganglion cell neurons cultured in the absence of glia (A, left and right) and
glia (B, left and right). No difference is noted in synaptic ultrastructure. Bar, 200 nm. (C) The number
of synapses detected by electron microscopy increased 7-fold in the presence of glia (
p
=0.013,
Student't
t
-test). (D) No differences in the total number of vesicles without glia or docked vesicles
without glia, per synapse. [Reproduced from
Science, 291(657),
E.M. Ullian, S.K. Sapperstein, K.S.
Christopherson and B.A. Barres, Control of synapse number by glia, 657-661 (Fig. 4), Copyright
(2001), with permission from the American Association for the Advancement of Science].
Moreover, most synapses were generated concurrently with the development of glia in
vivo, raising the possibility that glia may actively participate in synaptic plasticity [Ullian
et