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Loss of protein tyrosine phosphatase receptor delta PTPRD increases the number of cortical neurons, impairs synaptic function and induces autistic-like behaviors in adult mice
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Loss of protein tyrosine phosphatase receptor delta PTPRD increases the number of cortical neurons, impairs synaptic function and induces autistic-like behaviors in adult mice
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Loss of protein tyrosine phosphatase receptor delta PTPRD increases the number of cortical neurons, impairs synaptic function and induces autistic-like behaviors in adult mice
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Journal Article
Loss of protein tyrosine phosphatase receptor delta PTPRD increases the number of cortical neurons, impairs synaptic function and induces autistic-like behaviors in adult mice
2024
Overview
Background
The brain cortex is responsible for many higher-level cognitive functions. Disruptions during cortical development have long-lasting consequences on brain function and are associated with the etiology of brain disorders. We previously found that the protein tyrosine phosphatase receptor delta Ptprd, which is genetically associated with several human neurodevelopmental disorders, is essential to cortical brain development. Loss of
Ptprd
expression induced an aberrant increase of excitatory neurons in embryonic and neonatal mice by hyper-activating the pro-neurogenic receptors TrkB and PDGFRβ in neural precursor cells. However, whether these alterations have long-lasting consequences in adulthood remains unknown.
Results
Here, we found that in
Ptprd+/-
or
Ptprd-/-
mice, the developmental increase of excitatory neurons persists through adulthood, affecting excitatory synaptic function in the medial prefrontal cortex. Likewise, heterozygosity or homozygosity for
Ptprd
also induced an increase of inhibitory cortical GABAergic neurons and impaired inhibitory synaptic transmission. Lastly,
Ptprd+/-
or
Ptprd-/-
mice displayed autistic-like behaviors and no learning and memory impairments or anxiety.
Conclusions
These results indicate that loss of
Ptprd
has long-lasting effects on cortical neuron number and synaptic function that may aberrantly impact ASD-like behaviors.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,Sociedad de Biología de Chile,BMC
Subject
/ Anxiety
/ Autism
/ Autistic Disorder - genetics
/ Autistic Disorder - physiopathology
/ Behavior
/ BIOLOGY
/ Biomedical and Life Sciences
/ Brain
/ Cerebral Cortex - metabolism
/ Female
/ GABA
/ Glucose
/ Kinases
/ Learning
/ Male
/ Memory
/ Mice
/ Neonates
/ Neurodevelopmental disorders
/ Neurons
/ Phenols
/ Protein tyrosine phosphatase receptor delta
/ Protein-tyrosine-phosphatase
/ Proteins
/ Receptor-Like Protein Tyrosine Phosphatases, Class 2 - genetics
/ Receptor-Like Protein Tyrosine Phosphatases, Class 2 - metabolism
/ Synaptic Transmission - physiology
/ Tyrosine
