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Recently, upregulation of metabotropic glutamate receptors (mGluRs) on hippocampal astrocytes in epileptic tissues has become part of the etiology of epilepsy and suggests the involvement of astrocytes in the disease. Through computational modeling, we have shown in previous work that upregulated mGluRs on astrocytes can give rise to positive feedback in closed loop neuron-astrocyte circuits with epilepsy-type spontaneous neuronal spiking. In this paper we further quantify the necessary degree of upregulation of astrocytic mGluRs, relate it to recent clinical and experimental studies, and address through computational modeling the role of synaptic inhibition through interneurons in this form of hyperexcitability. We conclude that inhibitive circuitry cannot tame this form of hyperexcitability.

In the visual cortex some neurons respond more strongly to short stimuli than to long ones. This is referred to as "end-stopping" and has been generally attributed to inhibition. The role of inhibition, however, has been difficult to demonstrate. Moreover, modeling has shown that end-stopping can be created solely from excitation. The roles of excitation and inhibition were investigated using intracellular recordings (Anderson et al., 2001, J. Neurosci. 21: 2104–2112). The results of that study were interpreted in favor of inhibition. The present report re-examines these results and finds that they may be in good, perhaps even better, agreement with an excitation model of end-stopping.

Consciousness is a topic of considerable human curiosity with a long history of philosophical analysis and debate. We consider there is nothing particularly complicated about consciousness when viewed as a necessary process of the vertebrate nervous system. Here, we propose a physiological "explanatory gap" is created during each present moment by the temporal requirements of neuronal activity. The gap extends from the time exteroceptive and proprioceptive stimuli activate the nervous system until they emerge into consciousness. During this "moment", it is impossible for an organism to have any conscious knowledge of the ongoing evolution of its environment. In our schematic model, a mechanism of "afference copy" is employed to bridge the explanatory gap with consciously experienced percepts. These percepts are fabricated from the conjunction of the cumulative memory of previous relevant experience and the given stimuli. They are structured to provide the best possible prediction of the expected content of subjective conscious experience likely to occur during the period of the gap. The model is based on the proposition that the neural circuitry necessary to support consciousness is a product of sub/preconscious reflexive learning and recall processes. Based on a review of various psychological and neurophysiological findings, we develop a framework which contextualizes the model and briefly discuss further implications.

Two experiments are reported in which participants perceived different physical quantities: size and speed. The perceptual tasks were performed in the context of motor performance problems. Participants perceived the size of objects in order to grasp the objects single handed or with both hands. Likewise, participants perceived the speed of a moving treadmill in order to control walking or running at that speed. In both experiments, the perceptual tasks were repeatedly performed by the participants while the to-be-perceived quantity was gradually varied from small to large objects (Experiment 1) and from low to high speeds (Experiment 2). Hysteresis with negative sign was found when participants were not allowed to execute the motor component, that is, when the execution stage was decoupled from the planning stage. No such effect was found in the control condition, when participants were allowed to execute the motor action. Using a Lotka–Volterra–Haken model for two competing neural populations, it is argued that the observations are consistent with the notion that the repetitions induce an adaptation effect of the perceptual system via top-down regulation. Moreover, the amount of synaptic modulation involved in the adaptation is estimated from participant data.

Rationale: Benzylpiperazine (BZP) has been found to increase neural activation in the dorsal striatum when compared to placebo in response to a Stroop paradigm, in addition, subjective effects have been compared to dexamphetamine (DEX). Despite their similarities, the two have not been directly compared in respect to their effects on selective attention and inhibition. Objectives: To use a double-blind placebo-controlled crossover study to compare the acute effects of BZP and DEX on executive function using functional magnetic resonance imaging (fMRI) and an event-related Stroop task. Methods: Eleven healthy participants aged 18–40 years undertook the Stroop task 90min after taking an oral dose of either BZP (200mg), DEX (20mg) or placebo. Results: BZP induced a greater increase in activation than DEX in the inferior frontal gyrus (IFG) during the Stroop task. DEX increased BOLD signal in the thalamus and decreased it in the IFG in comparison to placebo. Conclusion: Despite BZP and DEX reportedly inducing similar subjective effects, there are different patterns of neural activation. We believe this differential activity is due to pharmacological differences in their receptor binding profiles and that subsequent inhibitory effects might be due to their direct effect on dopaminergic activity.