Glutamate regulation at the Drosophila larval neuromuscular junction: a model for excitatory synaptic function

The human brain is composed primarily of two cell types – neurons, which extend axons that make contact with other neurons at synapses, and glia, which wrap around neurons, protecting them and regulating their function. An electrical signal is conducted through the axon to the synapse where neurotransmitters are released to electrically excite the next neuron. The termination of this chemical signal is controlled by nearby glia, which remove the neurotransmitter using transporter proteins on their cell surfaces. A malfunction in this activity may lead to excessive levels of neurotransmitter accumulating in the synapse, over-exciting nearby neurons and glia and eventually leading to cell degeneration and death. This type of glial malfunction has been linked to many common neurodegenerative diseases (e.g. stroke, Alzheimer's, multiple sclerosis and muscular dystrophy). Glutamate, the neurotransmitter at most brain synapses, is also present at many synapses of the fruit fly (Drosophila melanogaster). As in humans, fly glia have glutamate transporters that are thought to regulate synaptic communication. Robert Parker is studying glial neurotransmitter transporter function in the fruit fly, altering the amount of glutamate transporter present in glial cells near the Drosophila neuromuscular junction (a synapse between a neuron and a muscle cell) which may cause the over-excitation, degeneration and death of nearby cells. By studying the basic function of glutamate transporters in flies, he hopes to gain a greater understanding of the clinical importance of glutamate transporters in many human neurodegenerative diseases.