Glia cells also regulate learning and memory, new Tel Aviv University (TAU) research finds. Glia cells, named for the Greek word for “glue,” hold the brain’s neurons together and protect the cells that determine our thoughts and behaviors, but scientists have long puzzled over their prominence in the activities of the brain dedicated to learning and memory. Now Tel Aviv University researchers say that glia cells are central to the brain’s plasticity — how the brain adapts, learns, and stores information.
According to Ph.D. student Maurizio De Pittà of TAU’s Schools of Physics and Astronomy andElectrical Engineering, glia cells do much more than hold the brain together. A mechanism within the glia cells also sorts information for learning purposes, De Pittà says. “Glia cells are like the brain’s supervisors. By regulating the synapses, they control the transfer of information between neurons, affecting how the brain processes information and learns.”
Researcers has developed the first computer model that incorporates the influence of glia cells on synaptic information transfer. Detailed in the journal PLoS Computational Biology, the model can also be implemented in technologies based on brain networks such as microchips and computer software, Prof. Ben-Jacob says, and aid in research on brain disorders such as Alzheimer’s disease and epilepsy.
Synaptic plasticity is the capacity of a preexisting connection between two neurons to change in strength as a function of neuronal activity. Because it admittedly underlies learning and memory, the elucidation of its constituting mechanisms is of crucial importance in many aspects of normal and pathological brain function. Short-term presynaptic plasticity refers to changes occurring over short time scales (milliseconds to seconds) that are mediated by frequency-dependent modifications of the amount of neurotransmitter released by presynaptic stimulation. Recent experiments have reported that glial cells, especially hippocampal astrocytes, can modulate short-term plasticity, but the mechanism of such modulation is poorly understood. Here, we explore a plausible form of modulation of short-term plasticity by astrocytes using a biophysically realistic computational model. Our analysis indicates that astrocytes could simultaneously affect synaptic release in two ways. First, they either decrease or increase the overall synaptic release of neurotransmitter. Second, for stimuli that are delivered as pairs within short intervals, they systematically increase or decrease the synaptic response to the second one. Hence, our model suggests that astrocytes could transiently trigger switches between paired-pulse depression and facilitation. This property explains several challenging experimental observations and has a deep impact on our understanding of synaptic information transfer.