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Vito Di Maio

Publications and source records attributed to Vito Di Maio.

5 recordsLinked to original sources

Multisynaptic activity in a pyramidal neuron model and neural code.

The highly irregular firing of mammalian cortical pyramidal neurons is one of the most striking observation of the brain activity. This result affects greatly the discussion on the neural code, i.e. how the brain codes information transmitted along the different cortical stages. In fact it seems to be in favor of one of the two main hypotheses about this issue, named the rate code. But the supporters of the contrasting hypothesis, the temporal code, consider this evidence inconclusive. We discuss here a leaky integrate-and-fire model of a hippocampal pyramidal neuron intended to be biologically sound to investigate the genesis of the irregular pyramidal firing and to give useful information about the coding problem. To this aim, the complete set of excitatory and inhibitory synapses impinging on such a neuron has been taken into account. The firing activity of the neuron model has been studied by computer simulation both in basic conditions and allowing brief periods of over-stimulation in specific regions of its synaptic constellation. Our results show neuronal firing conditions similar to those observed in experimental investigations on pyramidal cortical neurons. In particular, the variation coefficient (CV) computed from the inter-spike intervals (ISIs) in our simulations for basic conditions is close to the unity as that computed from experimental data. Our simulation shows also different behaviors in firing sequences for different frequencies of stimulation.

Computer Simulation↗

Topographic activation of the medial entorhinal cortex by presubicular commissural projections.

Previous investigations have shown that presubicular commissural fibers traveling in the caudal part of the dorsal hippocampal commissure (PSD) selectively activated the dorsalmost portion of the entorhinal cortex (EC), where they discharged perforant path neurons to the dorsal dentate gyrus. The dentate activation was followed by that of the dorsal hippocampus. The aim of the present study was to ascertain whether presubiculum commissural projections traveling in the PSD can also activate ventral levels of the EC and, if so, whether this activation is followed by that of the dentate gyrus-hippocampal system in the ventral hippocampus. The experiments were carried out in adult, anesthetized guinea pigs by field potential analysis. The results showed that presubicular fibers traveling at different PSD loci selectively activated specific EC portions, with caudal fibers activating only the dorsal EC and more rostral fibers activating ventral EC points. The region activated by PSD projections corresponded to the medial EC. Current source-density (CSD) analysis revealed that at both dorsal and ventral EC levels excitatory synaptic potentials followed by neuron discharge were generated in layer II, site of origin of the perforant path to the dentate gyrus. Activation of either dorsal or ventral levels of the EC was followed by activation of the dentate gyrus-hippocampal system in corresponding hippocampal segments. The results provide physiological evidence that the commissural presubicular projections activate the EC in a topographic manner. The massive activation of perforant path neurons at all EC levels suggests that presubicular signals may strongly influence the functions played by the EC-dentate-hippocampal system.

Action Potentials↗

Synaptic fusion pore structure and AMPA receptor activation according to Brownian simulation of glutamate diffusion.

The rising phase of fast, AMPA-mediated Excitatory Post Synaptic Currents (EPSCs) has a primary role in the computational ability of neurons. The structure and radial expansion velocity of the fusion pore between the vesicle and the presynaptic membrane could be important factors in determining the time course of the EPSC. We have used a Brownian simulation model for glutamate neurotransmitter diffusion to test two hypotheses on the fusion pore structure, namely, the proteinaceous pore and the purely lipidic pore. Three more hypotheses on the radial expansion velocity were also tested. The rising phases of the EPSC, computed under various conditions, were compared with experimental data from the literature. Our present results show that a proteinaceous fusion pore should produce a more marked foot at the beginning of the rising phase of the EPSC. They also confirm the hypothesis that the structure of the fusion pore and its radial expansion velocity play significant roles in shaping the fast EPSC time course.

Animals↗

Stochastic fluctuations of the quantal EPSC amplitude in computer simulated excitatory synapses of hippocampus.

The postsynaptic response in glutamatergic synapses of hippocampus, produced by the release of a single presynaptic vesicle, shows a large variability in amplitude not only among the synapses, but also for a single synapse. A mathematical modelling based on a Brownian motion for the diffusion of glutamate molecules and receptor binding was applied to study the possible sources of the quantal variability. Detailed, geometric and functional, descriptions of the vesicle, of the fusion pore and of the synaptic cleft were used and quantal (or miniature) EPSCs were computed. Our results show non-saturation of AMPA receptors, attributable to the small number of molecules contained in the glutamate vesicles of hippocampus. NMDA receptor saturation was obtained rarely, only in very specific instances. We concluded that the lack of AMPA saturation and intrinsic random variations in basic presynaptic elements, such as the vesicle volume and the vesicle docking position, are the main causes of the observed stochastic variability of the quantal EPSC amplitude. Only minor effects can be ascribed to postsynaptic sources.

Animals↗

Stochastic fluctuations of the synaptic function.

The peak amplitudes of the quantal Excitatory Post Synaptic Currents in single hippocampal synapses show a large variability. Here, we present the results of a mathematical, computational investigation on the main sources of this variability. A detailed description of the synaptic cleft, rigorously based on empirically-derived parameters, was used. By using a Brownian motion model of neurotransmitter molecule diffusion, quantal EPSCs were computed by a simple kinetic schema of AMPA receptor dynamics. Our results show that the lack of saturation of AMPA receptors obtained in these conditions, combined with stochastic variations in basic presynaptic elements, such as the vesicle volume, the vesicle docking position, and the vesicle neurotransmitter concentration can explain almost the entire range of EPSC variability experimentally observed.

Stochastic Processes↗