Glial amplification of synaptic signals.

Transmitter released from presynaptic neurons has been considered to be the sole generator of postsynaptic excitatory signals. However, astrocytes of the glial cell population have also been shown to release transmitter that can react on postsynaptic receptors. Therefore, we investigated whether astrocytes take part in generation of at least a part of the synaptic current. In this study, mice cerebellar acute slices were prepared and whole cell patch clamp recordings were performed. We found that Bergmann glial cells (BGs), a type of astrocyte in the cerebellum, reacts to a glutamate transporter substrate, d-aspartate (d-Asp) and an anion conductance is generated and glutamate is released from the BGs. Glutamate release was attenuated or augmented by modulating the state of BGs with activation of light-sensitive proteins, archaerhodopsin-T (ArchT) or channelrhodopsin-2 (ChR2) expressed on BGs, respectively. Glutamate release appears to be mediated by anion channels that can be blocked by a volume-regulated anion channel-specific blocker. Synaptic response to a train of parallel fibre stimulation was recorded from Purkinje cells. The latter part of the response was also attenuated or augmented by glial modulation with ArchT or ChR2, respectively. Thus, BGs effectively function as an excitatory signal amplifier, and a part of the 'synaptic' current is actually mediated by glutamate released from BGs. These data show that the state of BGs have potential for having direct and fundamental consequences on the functioning of information processing in the brain.