Robinson Laboratory

Unlike most other classical neurotransmitters that are recycled into the presynaptic nerve terminal, most glutamate is cleared into astrocytes. The Robinson Lab was among the first to demonstrate that neurons instruct astrocytes to express the predominant glutamate transporter, called GLT-1 or EAAT2. The lab recently demonstrated that endothelia instruct astrocytes to express GLT-1; this expression is increased during synaptogenesis and is a marker of astrocyte maturation. The laboratory was the first to demonstrate that trafficking of glutamate transporters on and off the plasma membrane provides a mechanism to rapidly regulate glutamate transporter activity. 

In addition, the Robinson Lab was also the first to demonstrate that glutamate transporters co-compartmentalize with and functionally interact with mitochondria in astrocyte processes. Current work in the lab focuses on determining if neurons and endothelia engage distinct signaling pathways and promoter elements to induce expression of GLT-1. In collaboration with Jeffrey Rothstein, MD, PhD, professor of neurology at Johns Hopkins School of Medicine, Baltimore, the Robinson Lab is also determining if subtypes of astrocytes engage different mechanisms to control expression of GLT-1. These studies should help the field determine the signals that contribute to astrocyte maturation.  

In collaboration with researchers Doulas Coulter, PhD, and Hajime Takano, PhD, in the Division of Neurology at Children’s Hospital of Philadelphia, the laboratory is investigating the hypothesis that glutamate uptake activates signals in astrocytes that contribute to the increases in blood flow that accompany increased neuronal activity using two-photon in vivo imaging. Finally, Evelyn Shih, MD, PhD, in the Division of Neurology, and other members of the laboratory are determining how stroke affects astrocytic mitochondria and glutamate transport-dependent neurovascular coupling using photothrombosis to occlude the middle cerebral artery in mice.