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Biomedical subjects

L A de Carvalho

Publications and source records attributed to L A de Carvalho.

3 recordsLinked to original sources

A computational model for the neurobiological substrates of visual attention.

Two interesting and complex tasks are performed by the brain in the process of perception: the integration of characteristics leading to an easier recognition of a pattern as a whole (binding), and the extraction of properties that need to be detailed and analyzed (attention). Attention seems to have a reciprocal relation with binding, inasmuch as the latter promotes the composition of features and their dependencies, while the former selects a single characteristic independently of the remainder. Classically, binding is viewed as a process whereby sets of properties are gathered in representative entities, which are themselves linked to form higher level structures, in a sequence that culminates in the total integration of the pattern features in a localized construct. The convergent axonal projections from one cortical area to another would be the neurobiological mechanism through which binding is achieved. Attention comprises the selective excitation of neuronal networks or pathways that stand for specific pattern properties. The thalamus and its reticular nucleus would then be the anatomical substrate of the attentional focus. In this paper we propose a computational model aiming at bringing together the main (and apparently diverging) ideas about binding and attention. Based on experimental data, a neuronal network representing cortical pyramidal cells is assembled, and its structure and function are related to the binding and attention phenomena. Actually, the convergent projections that enlarge the visual receptive field are associated to binding, while a specific change in the pyramidal cell behavior is responsible for attention. Computer simulations are shown which reproduce the electrophysiology of pyramidal cells and mimic some interesting experimental results in visual attention. We conclude by conjecturing that attention is a driven interruption in the regular process of binding.

Algorithms↗

Modeling the thalamocortical loop.

This work proposes a mathematical model for the thalamic gateway to the cortex. In this model, the ionic currents considered and the structural details are in accordance with the biomedical experimental data. To validate the model, three series of simulations were performed in different levels of complexity. First, some experiments show that the model captures the electrophysiological properties of a single thalamic cell, that is, the relay and burst modes of operation. Second, a complete neural network representing the thalamic gateway to the cortex is assembled and the influences of the cortical projections over the thalamus are analysed. Some interesting results about how the cortex opens and closes the thalamic gate, and the relation of this control policy with the phenomenon of attention, are shown. Finally, a third set of simulations establishes some mechanisms of interaction between neighboring thalamic regions, especially a form of somatosensory competition. The paper also hints at possible theoretical explanations for clinical facts like counterirritation, acupuncture analgesia and variations in the sensibility of somatosensory perception. The model seems to be an interesting and new way of understanding the thalamocortical interactions.

Action Potentials↗

Convulsive action of (25S)-isosolafloridine isolated from Solanum pseudo-quina bark.

The crude ethanolic extract prepared from the stem bark of Solanum pseudo-quina produced excitatory effects dominated by convulsions in rats and mice. Solvent extraction followed by alumina column chromatography resulted in the isolation of a pharmacologically active material (AP) which was identified to be (25S)-isosolafloridine. The convulsions produced by AP were predominantly clonic and invariably preceded by generalized fine and coarse tremors. This convulsive behaviour did not entirely resemble the convulsions produced by strychnine, pentylenetetrazol, bicuculline, picrotoxin or 3-mercaptopropionic acid. The tremor and convulsions were only slightly affected by drugs interfering with cholinergic, catecholaminergic, serotoninergic or encephalinergic neurotransmission. Only diazepam and particularly gamma-vinyl-GABA blocked AP-induced effects. After section of the spinal cord at a mid-theoretic level, AP produced convulsions only in the anterior part of the body. After intracerebroventricular administration, AP produced only sedation. A depressive effect was also observed on the blood pressure of conscious rats before and after the convulsions. In subconvulsive doses AP enhanced spontaneous motor activity in mice.

Animals↗