Topic: short-term plasticity

One elementary brain function that underlies many of our cognitive behaviors is the ability to maintain parametric information briefly in mind, in the time scale of seconds, to span delays between sensory information and actions. This component of working memory is fragile and quickly degrades with delay length. Under the assumption that behavioral delay-dependencies mark core functions of the working memory system, our goal is to find a neural circuit model that represents their neural mechanisms and apply it to research on working memory deficits in neuropsychiatric disorders. We have constr

Cortical circuits process information by rich recurrent interactions between excitatory neurons and inhibitory interneurons. One of the prime functions of interneurons is to stabilize the circuit by feedback inhibition, but the level of specificity on which inhibitory feedback operates is not fully resolved. We hypothesized that inhibitory circuits could enable separate feedback control loops for different synaptic input streams, by means of specific feedback inhibition to different neuronal compartments. To investigate this hypothesis, we adopted an optimization approach. Leveraging recent ad

CA3-CA1 synapses in the hippocampus are the initial locus of episodic memory. The action of acetylcholine alters cellular excitability, modifies neuronal networks, and triggers secondary signaling that directly affects long-term plasticity (LTP) (the cellular underpinning of memory). It is therefore considered a critical regulator of learning and memory in the brain. Its action via M4 metabotropic receptors in the presynaptic terminal of the CA3 neurons and M1 metabotropic receptors in the postsynaptic spines of CA1 neurons produce rich dynamics across multiple timescales. We developed a model

The exclusive attribution of working memory (WM) retention to persistent frontal activity [1,2] has been questioned by implications of spike-silent WM [3] in early visual cortex (EVC) [4,5,6]. Spike-silent WM might partly be explained by short-term plasticity (STP) [7], where perceptual encoding leaves a neural trace that can be retrieved using perturbation methods [8,9]. However, STP traces cannot easily withstand continual visual stimulation. In contrast, $modulatory$ top-down feedback [10] (i.e., altering spiking propensity without inducing spiking directly [11]) from frontal regions to EVC

Various working memory (WM) models based on a diverse set of biologically plausible synaptic and neural plasticity mechanisms have been proposed. We show that these proposed short-term plasticity mechanisms may not necessarily be competing explanations, but instead yield interesting functional interactions on a wide set of WM tasks and enhance the biological plausibility of spiking neural network models of WM. While reductionist models (WM explained by one particular mechanism) are theoretically appealing and have increased our understanding of specific mechanisms, they are insufficient. WM mo