Astrocytes have been suggested to release gliotransmitters onto neurons, thus regulating their excitability and synaptic strength (Bazargani & Attwell, 2016). We are currently investigating how a previously unstudied G protein coupled receptor on astrocytes mediates this effect (Jolly, Bazargani et al., 2017), and how amine transmitters regulate astrocyte function (Bazargani & Attwell, 2017).
Astrocytes also play a key role in regulating the
excitability of neurons, and preventing excitotoxic damage, by using
transporters to control the extracellular glutamate level. We pioneered the use of patch-clamp techniques to study transporters for
the main excitatory neurotransmitter glutamate (Brew & Attwell, 1987),
investigating in particular the ion movements which drive glutamate transport
(Barbour, Brew & Attwell, 1988, Bouvier et al., 1992; Levy et al., 1998).
We have demonstrated that glutamate transporters can run backwards when ion
gradients run down in conditions like stroke (Szatkowski, Barbour &
Attwell, 1990; Attwell et al., 1993), releasing enough glutamate to activate
receptors in nearby neurons (Billups & Attwell, 1996). Indeed, in the first
10 minutes of a stroke, reversed operation of glutamate transporters is the
main mechanism by which the extracellular glutamate concentration of glutamate
is raised to levels which trigger the death of neurons, leading to mental and
physical impairment (Rossi, Oshima & Attwell, 2000; Szatkowski &