Astrocytes play a role in the reuptake of neurotransmitters. They also have a role in providing activity dependent metabolic support to neurons. This is done via the lactate shuttle. When an action potential is fired, some presynaptic neurons release glutamate into the synapse. The glutamate response is eventually terminated by the reuptake of glutamate in astrocytes. Within the astrocyte, the glutamate is converted to glutamine. Then, the glutamine is transported from the astrocyte to the presynaptic cell. In the presynaptic cell, the glutamine is converted back to glutamate, …show more content…
where it can be reused.
While glutamate is being recycled into the presynaptic terminal, lactate shuttling is also taking place.
During the reuptake of glutamate (from the synapse to the astrocyte), glutamate was cotransported into the astrocyte with Na+. This resulted in an increased concentration of Na+ inside the astrocyte. The increased Na+ concentration activated the sodium potassium pumps. This, in turn, activated glycolysis to produce glucose. Glucose was converted into lactate. The lactate was shuttled from the astrocyte to the presynaptic neuron. Within the presynaptic neuron, the lactate was converted back to glucose and glucose was used to produce ATP though the Krebbs cycle and oxidative phosphorylation. In other words, astrocytes provide the metabolic support neurons need via lactate
shuttling.
Astrocytes also maintain ion balance. When axons fire action potentials, K+ concentrations increase in the extracellular fluid. Astrocytes remove excess potassium. Failure to remove potassium can cause the neurons to become hyperexcitable and could result in seizures. The astrocytes wrapped around the synapses take up excess potassium ions and pass them to other astrocytes (to dilute the concentration) via gap junctions.
Under normal conditions, astrocytes are tiled. They are in nonoverlapping, equally spaced domains. They do not proliferate. Also, all of the astrocytes do not express detectable amounts of GFAP. However, deregulation of healthy astrocytes can turn them into reactive astrocytes. Many things can trigger this transformation, including cell damage, ischemia, infection, neurogenerative diseases, and neuronal hyperactivity. Reactive astrocytes have varying degrees of response. In the most severe responses, astrocytes proliferate, individual tile domains are disrupted, and most cells express detectable amounts of GFAP. Reactive astrocytes also form scars that form barriers between healthy CNS cells and unhealthy cells. This limits damage to a certain area. However, astrocyte scars come with their own problems. At these scars, reactive astrocytes release substances that inhibit axonal repair. They may even lead to a secondary response that damages some proximal neurons, which were previously healthy.