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Register a new userA tale of two stories: astrocyte regulation of synaptic depression and facilitation
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Short-term presynaptic plasticity designates variations of the amplitude of synaptic information transfer whereby the amount of neurotransmitter released upon presynaptic stimulation changes over seconds as a function of the neuronal firing activity. While a consensus has emerged that changes of the synapse strength are crucial to neuronal computations, their modes of expression in vivo remain unclear. Recent experimental studies have reported that glial cells, particularly astrocytes in the hippocampus, are able to modulate short-term plasticity but the underlying mechanism is poorly understood. Here, we investigate the characteristics of short-term plasticity modulation by astrocytes using a biophysically realistic computational model. Mean-field analysis of the model unravels that astrocytes may mediate counterintuitive effects. Depending on the expressed presynaptic signaling pathways, astrocytes may globally inhibit or potentiate the synapse: the amount of released neurotransmitter in the presence of the astrocyte is transiently smaller or larger than in its absence. But this global effect usually coexists with the opposite local effect on paired pulses: with release-decreasing astrocytes most paired pulses become facilitated, while paired-pulse depression becomes prominent under release-increasing astrocytes. Moreover, we show that the frequency of astrocytic intracellular Ca2+ oscillations controls the effects of the astrocyte on short-term synaptic plasticity. Our model explains several experimental observations yet unsolved, and uncovers astrocytic gliotransmission as a possible transient switch between short-term paired-pulse depression and facilitation. This possibility has deep implications on the processing of neuronal spikes and resulting information transfer at synapses.
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Astrocytes affect neural transmission by a tight control via glutamate transporters on glutamate concentrations in direct vicinity to the synaptic cleft and by extracellular glutamate. Their relevance for information representation has been supported by in-vivo studies in ferret and mouse primary visual cortex. In ferret blocking glutamate transport pharmacologically broadened tuning curves and enhanced the response at preferred orientation. In knock-out mice with reduced expression of glutamate transporters sharpened tuning was observed. It is however unclear how focal and ambient changes in glutamate concentration affect stimulus representation. Here we develop a computational framework, which allows the investigation of synaptic and extrasynaptic effects of glutamate uptake on orientation tuning in recurrently connected network models with pinwheel-domain (ferret) or salt-and-pepper (mouse) organization. This model proposed that glutamate uptake shapes information representation when it affects the contribution of excitatory and inhibitory neurons to the network activity. Namely, strengthening the contribution of excitatory neurons generally broadens tuning and elevates the response. In contrast, strengthening the contribution of inhibitory neurons can have a sharpening effect on tuning. In addition local representational topology also plays a role: In the pinwheel-domain model effects were strongest within domains - regions where neighboring neurons share preferred orientations. Around pinwheels but also within salt-and-pepper networks the effects were less strong. Our model proposes that the pharmacological intervention in ferret increases the contribution of excitatory cells, while the reduced expression in mouse increases the contribution of inhibitory cells to network activity.
In continuous attractor neural networks (CANNs), spatially continuous information such as orientation, head direction, and spatial location is represented by Gaussian-like tuning curves that can be displaced continuously in the space of the preferred stimuli of the neurons. We investigate how short-term synaptic depression (STD) can reshape the intrinsic dynamics of the CANN model and its responses to a single static input. In particular, CANNs with STD can support various complex firing patterns and chaotic behaviors. These chaotic behaviors have the potential to encode various stimuli in the neuronal system.
The Integrated Information is a quantitative measure from information theory how tightly all parts of a system are interconnected in terms of information exchange. In this study we show that astrocyte, playing an important role in regulation of information transmission between neurons, may contribute to a generation of positive Integrated Information in neuronal ensembles. Analytically and numerically we show that the presence of astrocyte may be essential for this information attribute in neuro-astrocytic ensembles. Moreover, the proposed spiking-bursting mechanism of generating positive Integrated Information is shown to be generic and not limited to neuroglial networks, and is given a complete analytic description.
We show that the local Spike Timing-Dependent Plasticity (STDP) rule has the effect of regulating the trans-synaptic weights of loops of any length within a simulated network of neurons. We show that depending on STDPs polarity, functional loops are formed or eliminated in networks driven to normal spiking conditions by random, partially correlated inputs, where functional loops comprise weights that exceed a non-zero threshold. We further prove that STDP is a form of loop-regulating plasticity for the case of a linear network comprising random weights drawn from certain distributions. Thus a notable local synaptic learning rule makes a specific prediction about synapses in the brain in which standard STDP is present: that under normal spiking conditions, they should participate in predominantly feed-forward connections at all scales. Our model implies that any deviations from this prediction would require a substantial modification to the hypothesized role for standard STDP. Given its widespread occurrence in the brain, we predict that STDP could also regulate long range synaptic loops among individual neurons across all brain scales, up to, and including, the scale of global brain network topology.
Protein synthesis-dependent, late long-term potentiation (LTP) and depression (LTD) at glutamatergic hippocampal synapses are well characterized examples of long-term synaptic plasticity. Persistent increased activity of the enzyme protein kinase M (PKM) is thought essential for maintaining LTP. Additional spatial and temporal features that govern LTP and LTD induction are embodied in the synaptic tagging and capture (STC) and cross capture hypotheses. Only synapses that have been tagged by an stimulus sufficient for LTP and learning can capture PKM. A model was developed to simulate the dynamics of key molecules required for LTP and LTD. The model concisely represents relationships between tagging, capture, LTD, and LTP maintenance. The model successfully simulated LTP maintained by persistent synaptic PKM, STC, LTD, and cross capture, and makes testable predictions concerning the dynamics of PKM. The maintenance of LTP, and consequently of at least some forms of long-term memory, is predicted to require continual positive feedback in which PKM enhances its own synthesis only at potentiated synapses. This feedback underlies bistability in the activity of PKM. Second, cross capture requires the induction of LTD to induce dendritic PKM synthesis, although this may require tagging of a nearby synapse for LTP. The model also simulates the effects of PKM inhibition, and makes additional predictions for the dynamics of CaM kinases. Experiments testing the above predictions would significantly advance the understanding of memory maintenance.
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