Search bioRxiv⌕ Search

Biology subjects

Gornet, J. A.

Publications and source records attributed to Gornet, J. A..

2 recordsLinked to original sources

Automated construction of cognitive maps with predictive coding

Humans construct internal cognitive maps of their environment directly from sensory inputs without access to a system of explicit coordinates or distance measurements. While machine learning algorithms like SLAM utilize specialized inference procedures to identify visual features and construct spatial maps from visual and odometry data, the general nature of cognitive maps in the brain suggests a unified mapping algorithmic strategy that can generalize to auditory, tactile, and linguistic inputs. Here, we demonstrate that predictive coding provides a natural and versatile neural network algorithm for constructing spatial maps using sensory data. We introduce a framework in which an agent navigates a virtual environment while engaging in visual predictive coding using a self-attention-equipped convolutional neural network. While learning a next image prediction task, the agent automatically constructs an internal representation of the environment that quantitatively reflects spatial distances. The internal map enables the agent to pinpoint its location relative to landmarks using only visual information.The predictive coding network generates a vectorized encoding of the environment that supports vector navigation where individual latent space units delineate localized, overlapping neighborhoods in the environment. Broadly, our work introduces predictive coding as a unified algorithmic framework for constructing cognitive maps that can naturally extend to the mapping of auditory, sensorimotor, and linguistic inputs.

neuroscience↗

A brain network basis of Fragile X syndrome behavioral penetrance determined by X chromosome inactivation in female mice

Non-random (skewed) X chromosome inactivation (XCI) in the female brain can ameliorate X-linked phenotypes, though clinical studies typically consider 80-90% skewing favoring the healthy allele as necessary for this effect1-10. Here we quantify for the first time whole-brain XCI at single-cell resolution and discover a preferential inactivation of paternal to maternal X at [~]60:40 ratio, which surprisingly impacts disease penetrance. In Fragile-X-syndrome mouse model, Fmr1-KO allele transmitted maternally in [~]60% brain cells causes phenotypes, but paternal transmission in [~]40% cells is unexpectedly tolerated. In the affected maternal Fmr1-KO(m)/+ mice, local XCI variability within distinct brain networks further determines sensory versus social manifestations, revealing a stochastic source of X-linked phenotypic diversity. Taken together, our data show that a modest [~]60% bias favoring the healthy allele is sufficient to ameliorate X-linked phenotypic penetrance, suggesting that conclusions of many clinical XCI studies using the 80-90% threshold should be re-evaluated. Furthermore, the paternal origin of the XCI bias points to a novel evolutionary mechanism acting to counter the higher rate of de novo mutations in male germiline11-16. Finally, the brain capacity to tolerate a major genetic lesion in [~]40% cells is also relevant for interpreting other neurodevelopmental genetic conditions, such as brain somatic mosaicism.

neuroscience↗