Influence of synaptic depression on memory storage capacity

Synaptic efficacy between neurons is known to change within a short time scale dynamically. Neurophysiological experiments show that high-frequency presynaptic inputs decrease synaptic efficacy between neurons. This phenomenon is called synaptic depression, a short term synaptic plasticity. Many researchers have investigated how the synaptic depression affects the memory storage capacity. However, the noise has not been taken into consideration in their analysis. By introducing "temperature", which controls the level of the noise, into an update rule of neurons, we investigate the effects of synaptic depression on the memory storage capacity in the presence of the noise. We analytically compute the storage capacity by using a statistical mechanics technique called Self Consistent Signal to Noise Analysis (SCSNA). We find that the synaptic depression decreases the storage capacity in the case of finite temperature in contrast to the case of the low temperature limit, where the storage capacity does not change

ADAR-mediated RNA editing suppresses sleep by acting as a brake on glutamatergic synaptic plasticity.

It has been postulated that synaptic potentiation during waking is offset by a homoeostatic reduction in net synaptic strength during sleep. However, molecular mechanisms to support such a process are lacking. Here we demonstrate that deficiencies in the RNA-editing gene Adar increase sleep due to synaptic dysfunction in glutamatergic neurons in Drosophila. Specifically, the vesicular glutamate transporter is upregulated, leading to over-activation of NMDA receptors, and the reserve pool of glutamatergic synaptic vesicles is selectively expanded in Adar mutants. Collectively these changes lead to sustained neurotransmitter release under conditions that would otherwise result in synaptic depression. We propose that a shift in the balance from synaptic depression towards synaptic potentiation in sleep-promoting neurons underlies the increased sleep pressure of Adar-deficient animals. Our findings provide a plausible molecular mechanism linking sleep and synaptic plasticity

Mechanisms of synaptic depression at the hair cell ribbon synapse that support auditory nerve function

Inner hair cells (IHCs) in the cochlea are the mammalian phono-receptors, transducing sound energy into graded changes in membrane potentials, the so called “receptor potentials.” Ribbon synapses between IHCs and auditory nerve neurons are responsible for converting receptor potentials into spike rates. The characteristics of auditory nerve responses to sound have been described extensively. For instance, persistent acoustic stimulation produces sensory adaptation, which is revealed as a reduction in neuronal spike rate with time constants in the range of milliseconds to seconds. Since the amplitude of IHC receptor potentials is invariant during this period, the classic hypothesis pointed to vesicle depletion at the IHC as responsible for auditory adaptation. In this study, we observed that fast synaptic depression occurred in responses to stimuli of varying intensities. Nevertheless, release continued after this initial depression, via synaptic vesicles with slower exocytotic kinetics. Heterogeneity in kinetic elements, therefore, favored synaptic responses with an early peak and a sustained phase. The application of cyclothiazide (CTZ) revealed that desensitization of postsynaptic receptors contributed to synaptic depression, which was more pronounced during stronger stimulation. Thus, desensitization had a twofold effect: It abbreviated signaling between IHC and the auditory nerve and also balanced differences in decay kinetics between responses to different stimulation strengths. We therefore propose that both pre- and postsynaptic mechanisms at the IHC ribbon synapse contribute to synaptic depression at the IHC ribbon synapse and spike rate adaptation in the auditory nerve.Fil: Goutman, Juan Diego. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentin

Synaptic Depression and Cortical Gain Control

Defense Advanced Research Projects Agency and Office of Naval Research (N00014-92-J-1309, N00014-95-1-0409, N00014-95-I-0657

Short term synaptic depression improves information transfer in perceptual multistability

Competitive neural networks are often used to model the dynamics of perceptual bistability. Switching between percepts can occur through fluctuations and/or a slow adaptive process. Here, we analyze switching statistics in competitive networks with short term synaptic depression and noise. We start by analyzing a ring model that yields spatially structured solutions and complement this with a study of a space-free network whose populations are coupled with mutual inhibition. Dominance times arising from depression driven switching can be approximated using a separation of timescales in the ring and space-free model. For purely noise-driven switching, we use energy arguments to justify how dominance times are exponentially related to input strength. We also show that a combination of depression and noise generates realistic distributions of dominance times. Unimodal functions of dominance times are more easily differentiated from one another using Bayesian sampling, suggesting synaptic depression induced switching transfers more information about stimuli than noise-driven switching. Finally, we analyze a competitive network model of perceptual tristability, showing depression generates a memory of previous percepts based on the ordering of percepts.Comment: 26 pages, 15 figure

Stationary bumps in a piecewise smooth neural field model with synaptic depression

We analyze the existence and stability of stationary pulses or bumps in a one–dimensional piecewise smooth neural field model with synaptic depression. The continuum dynamics is described in terms of a nonlocal integrodifferential equation, in which the integral kernel represents the spatial distribution of synaptic weights between populations of neurons whose mean firing rate is taken to be a Heaviside function of local activity. Synaptic depression dynamically reduces the strength of synaptic weights in response to increases in activity. We show that in the case of a Mexican hat weight distribution, there exists a stable bump for sufficiently weak synaptic depression. However, as synaptic depression becomes stronger, the bump became unstable with respect to perturbations that shift the boundary of the bump, leading to the formation of a traveling pulse. The local stability of a bump is determined by the spectrum of a piecewise linear operator that keeps track of the sign of perturbations of the bump boundary. This results in a number of differences from previous studies of neural field models with Heaviside firing rate functions, where any discontinuities appear inside convolutions so that the resulting dynamical system is smooth. We also extend our results to the case of radially symmetric bumps in two–dimensional neural field models

Presynaptic adenosine receptor-mediated regulation of diverse thalamocortical short-term plasticity in the mouse whisker pathway

Short-term synaptic plasticity (STP) sets the sensitivity of a synapse to incoming activity and determines the temporal patterns that it best transmits. In “driver” thalamocortical (TC) synaptic populations, STP is dominated by depression during stimulation from rest. However, during ongoing stimulation, lemniscal TC connections onto layer 4 neurons in mouse barrel cortex express variable STP. Each synapse responds to input trains with a distinct pattern of depression or facilitation around its mean steady-state response. As a result, in common with other synaptic populations, lemniscal TC synapses express diverse rather than uniform dynamics, allowing for a rich representation of temporally varying stimuli. Here, we show that this STP diversity is regulated presynaptically. Presynaptic adenosine receptors of the A1R type, but not kainate receptors (KARs), modulate STP behavior. Blocking the receptors does not eliminate diversity, indicating that diversity is related to heterogeneous expression of multiple mechanisms in the pathway from presynaptic calcium influx to neurotransmitter release