Dendritic structure varies as a function of eccentricity in V1: a quantitative study of NADPH diaphorase neurons in the diurnal South American rodent agouti, Dasyprocta prymnolopha.

The cerebral cortex is often described as a composite of repeated units or columns, integrating the same basic circuit. The 'ice-cube' model of cortical organization, and 'canonical' circuit, born from insights into functional architecture, still require systematic comparative data. Here we probed the anatomy of an individual neuronal type within V1 to determine whether or not its dendritic trees are consistent with the 'ice-cube' model and theories of canonical circuits. In a previous report we studied the morphometric variability of NADPH-diaphorase (NADPH-d) neurons in the rat auditory, visual and somatosensory primary cortical areas. Our results suggested that the nitrergic cortical circuitry of primary sensory areas are differentially specialized, probably reflecting peculiarities of both habit and behavior of the species. In the present report we specifically quantified the dendritic trees of NADPH-d type I neurons as a function of eccentricity within V1. Individual neurons were reconstructed in 3D, and the size, branching and space-filling of their dendritic trees were correlated with their location within the visuotopic map. We found that NADPH-d neurons became progressively smaller and less branched with progression from the central visual representation to the intermediate and peripheral visual representation. This finding suggests that aspects of cortical circuitry may vary across the cortical mantle to a greater extent that envisaged as natural variation among columns in the 'ice-cube' model. The systematic variation in neuronal structure as a function of eccentricity warrants further investigation to probe the general applicability of columnar models of cortical organization and canonical circuits.

Morphometric variability of nicotinamide adenine dinucleotide phosphate diaphorase neurons in the primary sensory areas of the rat.

Even though there is great regional variation in the distribution of inhibitory neurons in the mammalian isocortex, relatively little is known about their morphological differences across areal borders. To obtain a better understanding of particularities of inhibitory circuits in cortical areas that correspond to different sensory modalities, we investigated the morphometric differences of a subset of inhibitory neurons reactive to the enzyme nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) within the primary auditory (A1), somatosensory (S1), and visual (V1) areas of the rat. One hundred and twenty NADPH-d-reactive neurons from cortical layer IV (40 cells in each cortical area) were reconstructed using the Neurolucida system. We collected morphometric data on cell body area, dendritic field area, number of dendrites per branching order, total dendritic length, dendritic complexity (Sholl analysis), and fractal dimension. To characterize different cell groups based on morphology, we performed a cluster analysis based on the previously mentioned parameters and searched for correlations among these variables. Morphometric analysis of NADPH-d neurons allowed us to distinguish three groups of cells, corresponding to the three analyzed areas. S1 neurons have a higher morphological complexity than those found in both A1 and V1. The difference among these groups, based on cluster analysis, was mainly related to the size and complexity of dendritic branching. A principal component analysis (PCA) applied to the data showed that area of dendritic field and fractal dimension are the parameters mostly responsible for dataset variance among the three areas. Our results suggest that the nitrergic cortical circuitry of primary sensory areas of the rat is differentially specialized, probably reflecting peculiarities of both habit and behavior of the species.

Pathophysiology of neurodegeneration following traumatic brain injury.

Acute neuropathological conditions, including brain and spinal cord trauma, are leading causes of death and disabilities worldwide, especially in children and young adults. The causes of brain and spinal cord injuries include automobile accidents, accidents during recreational activities, falls and violent attacks. In the United States of America alone, around 1.7 million people each year seek medical care for some kind of head injury. About fifty-two thousand of these people will die, while the same number will present with permanent functional disability. Considering the high worldwide prevalence of these acute pathological conditions, research on the mechanisms underlying central nervous system damage is of extreme importance. Nowadays, a number of experimental models of acute neural disorders have been developed and the mechanisms of tissue loss have been investigated. These mechanisms include both primary and secondary pathological events contributing to tissue damage and functional impairment. The main secondary pathological mechanisms encompass excitotoxicity, ionic imbalances, inflammatory response, oxidative stress and apoptosis. The proper elucidation of how neural tissue is lost following brain and spinal cord trauma is fundamental to developing effective therapies to human diseases. The present review evaluates the main mechanisms of secondary tissue damage following traumatic brain and spinal cord injuries.

[Mechanisms of secondary degeneration in the central nervous system during acute neural disorders and white matter damage]. / Mecanismos de degeneración secundaria en el sistema nervioso central durante los trastornos neuronales agudos y el daño en la sustancia blanca.

INTRODUCTION: Acute neurodegenerative diseases, including stroke and traumatic brain and spinal cord injury, possess an elevated worldwide incidence. Two distinct lesive patterns can be identified after these destructive events: primary damage, an early consequence of the primary pathological event, and secondary neural degeneration (SND), a group of pathological events inducing late degeneration in cells not or even only partially affected by the primary damage. This pathological mechanism is an important contributing factor for functional deficits and target for therapeutic approaches. Several factors are involved on the SND etiology, including excitotoxicity, inflammation, and oxidative stress. AIM: To review the main mechanisms underlying the SND occurring after acute neural disorders. DEVELOPMENT: The more recent findings about the eliciting processes of SND degeneration are discussed, as well as their significance to degeneration of white matter tracts. CONCLUSIONS: The characterization of the events underlying SND is of fundamental importance for the development of new therapeutic approaches effective enough to decrease the functional deficits, contributing to the improvement of the quality of life of people suffering neurological diseases. These therapeutic approaches must be validated in experimental models of both brain and spinal cord diseases, which effectively simulate human neural disorders protecting both gray and white matters for a better neuroprotective efficacy.

The organizational variability of the rodent somatosensory cortex.

Rodentia is the largest mammalian order, with more than 2,000 species displaying a great diversity of morphological characteristics and living in different ecological niches (terrestrial, semi-aquatic, arboreal and fossorial). Analysis of the organization of the somatosensory areas in six species of rodents allowed us to demonstrate that although these species share a similar neocortical blueprint with other eutherian mammals, important differences exist between homologous areas across different species, probably as a function of both lifestyle and peripheral sensory specializations typical of each species. We based this generalization on a phylogenetic comparison of the intrinsic organization of the primary somatosensory area (SI) across representatives of different rodent suborders. This analysis revealed considerable structural variability, including the differential expansion of cortical representation of specific body parts (cortical amplification) as well as the parcellation of areas into processing modules.

Callosal axon arbors in the limb representations of the somatosensory cortex (SI) in the agouti (Dasyprocta primnolopha).

The present report compares the morphology of callosal axon arbors projecting from and to the hind- or forelimb representations in the primary somatosensory cortex (SI) of the agouti (Dasyprocta primnolopha), a large, lisencephlic Brazilian rodent that uses forelimb coordination for feeding. Callosal axons were labeled after single pressure (n = 6) or iontophoretic injections (n = 2) of the neuronal tracer biotinylated dextran amine (BDA, 10 kD), either into the hind- (n = 4) or forelimb (n = 4) representations of SI, as identified by electrophysiological recording. Sixty-nine labeled axon fragments located across all layers of contralateral SI representations of the hindlimb (n = 35) and forelimb (n = 34) were analyzed. Quantitative morphometric features such as densities of branching points and boutons, segments length, branching angles, and terminal field areas were measured. Cluster analysis of these values revealed the existence of two types of axon terminals: Type I (46.4%), less branched and more widespread, and Type II (53.6%), more branched and compact. Both axon types were asymmetrically distributed; Type I axonal fragments being more frequent in hindlimb (71.9%) vs. forelimb (28.13%) representation, while most of Type II axonal arbors were found in the forelimb representation (67.56%). We concluded that the sets of callosal axon connecting fore- and hindlimb regions in SI are morphometrically distinct from each other. As callosal projections in somatosensory and motor cortices seem to be essential for bimanual interaction, we suggest that the morphological specialization of callosal axons in SI of the agouti may be correlated with this particular function.

Neurotropism and neuropathological effects of selected rhabdoviruses on intranasally-infected newborn mice.

Viral neurotropism is the ability of viruses to infect neuronal cells. This is well studied for herpesviruses, rabies-related viruses, and a few others, but it is poorly investigated among almost all arboviruses. In this study, we describe both the neurotropism and the neuropathological effects of Amazonian rhabdoviruses on the brains of experimentally infected-newborn mice. Suckling mice were intranasally infected with 10(-4) to 10(-8) LD50 of viruses. Animals were anaesthetized and perfused after they had become sick. Immunohistochemistry using specific anti-virus and anti-active caspase three antibodies was performed. All infected animals developed fatal encephalitis. Survival time ranged from 18 h to 15 days. Viruses presented distinct species-dependent neurotropism for CNS regions. Histopathological analysis revealed variable degrees of necrosis and apoptosis in different brain regions. These results showed that viruses belonging to the Rhabdoviridae family possess distinct tropism for CNS structures and induce different pattern of cell death depending on the CNS region.