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Ramasco, J. J.

Publications and source records attributed to Ramasco, J. J..

2 recordsLinked to original sources

Competition between bottom-up visual input and internal inhibition generates error neurons in a model of the mouse primary visual cortex

The predictive coding theory, although attractive, is far from being proven. Supporters of this theory agree that bottom-up sensory inputs and top-down predictions of these inputs must be compared in certain types of neurons called error neurons. Excitatory neurons in layer 2/3 (E2/3) of the primary visual cortex (V1) are ideal candidates to act as error neurons, although how these error neurons are generated is poorly understood. In this study, we aimed to gain insight into how the genetically encoded structure of canonical microcircuits in the neocortex implements the emergence of error neurons. To this end, we used a biologically realistic computational model of V1, developed by the Allen Institute, to study the effect that sudden changes in bottom-up input had on the dynamics of E2/3 neurons. We found that the responses of these neurons can be divided into two main classes: one that depolarized (reporting positive errors; dVf neurons) and one that hyperpolarized (reporting negative errors; hVf neurons). Detailed analysis of both network and effective connectivity allowed us to uncover the mechanism that led to the dynamic segregation of these neurons. This mechanism was found to be the competition between the external visual input, originating in the thalamus, and the recurrent inhibition, originating mainly in layers 2/3 and 4. In contrast, we found no evidence of similar division and responses in excitatory infragranular neurons of layers 5 and 6. Our results are in agreement with recent experimental findings and shed light on the mechanisms responsible for the emergence of error neurons.

neuroscience↗

Global predictions for the risk of establishment of Pierce's disease of grapevines

The vector-borne bacterium Xylella fastidiosa is responsible for Pierces disease (PD), a lethal grapevine illness that originated in the Americas. The international plant trade is expanding the geographic range of this pathogen, posing a new threat to viticulture worldwide. To assess the potential incidence of PD, we have built a dynamic epidemiological model based on the response of 36-grapevine varieties to the pathogen in inoculation assays and on the vectors distribution when this information is available. Key temperature-driven epidemiological processes, such as PD symptom development and recovery, are mechanistically modelled. Integrating into the model highresolution spatiotemporal climatic data from 1981 onward and different infectivity (R0) scenarios, we show how the main wine-producing areas thrive mostly in non-risk, transient, or epidemic-risk zones with potentially low growth rates in PD incidence. Epidemic-risk zones with moderate to high growth rates are currently marginal outside the United States. However, a global expansion of epidemic-risk zones coupled with small increments in the disease growth rate is projected for 2050. Our study globally downscales the risk of PD establishment while highlighting the importance of considering climate variability, vector distribution and an invasive criterion in obtaining accurate risk maps to guide policy decision-making in plant health.

plant biology↗