Neurocomputing aspects in modelling cursive handwriting.

P Morasso; V Sanguineti

doi:10.1016/0001-6918(93)90013-h

Home/Archive/PubMed

PubMed · 8475767

Neurocomputing aspects in modelling cursive handwriting.

P Morasso·V Sanguineti

View original source ↗Export metadata ↓

Abstract

This paper describes a distributed modelling framework of the motor control processes that underly the planning of cursive handwriting. The model, that focuses on the hypothetical functions of the posterior parietal cortex combines a paradigm of self-organization (for building robust and coherent maps of the different motor spaces) with relaxation dynamics (for run-time incorporation of task constraints) and non-linear integration (for a smooth integration between via-points).

Explore related subjects

Cerebral Cortex Handwriting Humans Models, Neurological Muscles Neural Networks, Computer Psychomotor Performance Psychophysiology Journal Article Research Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

P Morasso, V Sanguineti. 1993. Neurocomputing aspects in modelling cursive handwriting.. https://doi.org/10.1016/0001-6918(93)90013-h

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Histone H3K9 methyltransferases regulate cortical growth by coordinating heterochromatin formation and neural progenitor dynamics.

DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.

Cerebral Cortex↗

PubMed2000

P300, a state and a trait marker in schizophrenia.

Explore the source record for details and available documents.

Cerebral Cortex↗

PubMed2000

Complementary neural mechanisms for tracking items in human working memory.

Recognition of a specific visual target among equally familiar distracters requires neural mechanisms for tracking items in working memory. Event-related functional magnetic resonance imaging revealed evidence for two such mechanisms: (i) Enhanced neural responses, primarily in the frontal cortex, were associated with the target and were maintained across repetitions of the target. (ii) Reduced responses, primarily in the extrastriate visual cortex, were associated with stimulus repetition, regardless of whether the stimulus was a target or a distracter. These complementary neural mechanisms track the status of familiar items in working memory, allowing for the efficient recognition of a currently relevant object and rejection of irrelevant distracters.

Cerebral Cortex↗