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Neuroanatomia dell'uomo. 2a Edizione
Questa seconda edizione si presenta aggiornata e arricchita di alcune significative recenti acquisizioni nel campo delle neuroscienze sperimentali e clinich
Density and distribution of dendritic spines in neocortical pyramidal neurons of rats exposed to alcohol during the first postnatal week
Reduced density of dendritic spines in pyramidal neurons of rats exposed to alcohol during early postnatal life
Dendritic spines are the main postsynaptic sites of excitatory connections of neocortical pyramidal neurons. Alterations of spine shape, number, and density can be observed in different mental diseases, including those caused by developmental alcohol exposure. Pyramidal neurons of layer 2/3 are the most abundant cells of the neocortex and represent the main source of associative cortico-cortical connections. These neurons are essential for higher functions mediated by the cortex such as feature selection and perceptual grouping. Furthermore, their connections have been shown to be altered in experimental models of fetal alcohol spectrum disorders. Here, we used a Golgi-like tracing method to study the spine density of layer 2/3 associative pyramidal neurons in the somatosensory cortex of adult rats exposed to alcohol during the first postnatal week. The main result of the present study is represented by the decreased spine density in the apical dendrite of alcohol-treated rats, as compared to controls. As to the basal dendritic tree, there were no significant differences between the experimental and the control group. A decreased density of dendritic spines in the apical dendrite may impair the excitatory input onto pyramidal neurons, thus resulting in a widespread alteration of the cortical information flow
Experimental models of early exposure to alcohol: a way to unravel the neurobiology of mental retardation
As of November 2014, a PubMed search for “fetal alcohol” retrieved more than 14,500 articles. Alcohol consumption during pregnancy and its detrimental consequences on the developing brain raise major public health, social, and economic issues. However, the research on fetal alcohol spectrum disorders (FASD) in the real world is challenging, given that it is largely based on retrospective analysis. Therefore, establishing the relationship between brain damage and drinking habits proves particularly hard. One of the advantages of FASD studies carried out in the laboratory environment derives from the tight control of time, dose, and modality of alcohol exposure
Neuronal circuitry dissected by immunocytochemistry combined with retrograde tracing and electrophysiology
Several substances, once injected in a given central structure, are taken up by axon terminals and transported
retrogradely over long distances, to the cell bodies of neurons projecting to the injection area. They are
then visualized by means of histochemical (or immunohistochemical) reactions, making it possible to trace
neural pathways .
Here we describe a method to label retrogradely neocortical pyramidal neurons in a Golgi-like fashion.
This method allows reconstructing the entire dendritic tree of retrogradely labeled cells and can be easily combined with immunohistochemical techniques. Methods suitable to establish relationships
between morphological and functional features of projecting neurons are also discussed
Modelling the Effects of Early Exposure to Alcohol on the Excitability of Cortical Neurons
In recent years, a novel approach based on multi-objective optimization has been developed to automatically tune biophysically realistic, multi-compartmental neuron models starting from electrophysiological recordings. Here, we apply this methodology to the optimization of model neurons capable of reproducing the reduced excitability observed in experiments carried out in cortical pyramidal cells in a rodent model of fetal alcohol spectrum disorder. We find that both control and ethanol-exposed model cells present an excellent match with the experiments in terms of membrane voltage dynamics, with the latter group displaying a small but significant rightward shift of their current-frequency relationship. We identify a possible interplay between model parameters and cellular morphology and suggest future improvements to better capture the features of dendritic voltage dynamics
Alterations of neocortical pyramidal neurons: turning points in the genesis of mental retardation
Pyramidal neurons represent the majority of neocortical cells and their involvement in cognitive functions is decisive. Therefore, they are the most obvious target of developmental disorders characterized by mental retardation. Genetic and non-genetic forms of intellectual disability share a few basic pathogenetic signatures that result in the anomalous function of pyramidal neurons. Here we review the key mechanisms impairing these neurons and their participation in the cortical network, with special focus on experimental models of fetal exposure to alcohol. Due to the heterogeneity of pyramidal neurons, some alterations affect selectively a given cell population, which may also differ depending on the considered pathology. These specific features open new possibilities for the interpretation of cognitive defects observed in mental retardation syndromes, as well as for novel therapeutic interventions
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