For lack of a better understanding, the astrocytes that constitute nearly half the cells in the brain have been ascribed a janitorial role in neuron-to-neuron communication. While they do clean up stray ions and neurotransmitter molecules in the synaptic cleft, recent evidence has suggested they could play a more active role. In the current study, Barres's group first studied retinal ganglion cells (RGCs) in culture, either with or without astrocytes in the medium. With astrocytes present, the RCGs form seven times as many mature, functional synapses (with their target tectal neurons) as they do without astrocytes. There were suggestions that one reason for this is that astrocytes contribute to the aggregation of synaptic proteins, which otherwise are spread throughout the soma or dendrites. Glial cells are also necessary for the maintenance of synapses, for when glia are removed, synapses quickly disappear.

The researchers further found that the presence of astrocytes significantly enhanced synaptic transmission, by both presynaptic and postsynaptic mechanisms. The astrocytes were shown to enhance presynaptic function in part by increasing calcium influx, though other mechanisms also seemed to be at work. Finally, a compelling in vivo correlation to the in vitro data was presented. The researchers showed that, although RGC axons reach their tectal targets around embryonic day 16, substantial numbers of synapses only appear at the end of the first postnatal week, corresponding with the proliferation of astrocytes.

Said Barres, "These findings raise a number of questions for future research. First, do glial cells within the brain have similar functions. Second, do glial cells normally play a role in synaptic plasticity involved in learning. Third, does the glial increase, termed gliosis, found in brain injury and neurodegenerative disease play any role in the pathophysiology of these diseases. In particular, it seems possible that gliosis might trigger an increase in the number of synapses on nearby neurons that might overstimulate these neurons leading to epilepsy and/or excitotoxicity that could produce death of neurons."-Hakon Heimer.

Reference:Ullian EM, Sapperstein SK, Christopherson KS, Barres BA. Control of synapse number by glia. Science 2001 Jan 26;291:657-61. Abstract