More than a sidekick: glia and homeostatic synaptic plasticity.
Homeostatic synaptic plasticity is thought to have a crucial role in stabilizing the activity of neurons and networks, but the mechanisms are poorly understood. In a recent study, Stellwagen and Malenka have shown that synaptic scaling can be induced by activity-dependent changes in release of the cytokine tumor necrosis factor-alpha (TNF-alpha) and, surprisingly, that the source of TNF-alpha is glia rather than neurons. In addition to provide insight into the mechanisms of homeostatic plasticity, these data argue for the first time for an equal partnership between glial cells and neurons in the generation of an important form of synaptic plasticity.
Turrigiano
Gina G
GG
Department of Biology, Brandeis University, Waltham, MA 02454, USA. turrigiano@brandeis.edu
D000818:Animals; D006706:Homeostasis; D051379:Mice; D018345:Mice, Knockout; D008954:Models, Biological; D009457:Neuroglia / Q000737:chemistry / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000737:chemistry / Q000502:physiology; D017470:Receptors, Glutamate / Q000502:physiology; D015398:Signal Transduction; D013569:Synapses / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D017470:Receptors, Glutamate; D014409:Tumor Necrosis Factor-alpha