Absence of parvalbumin increases mitochondria volume and branching of dendrites in inhibitory Pvalb neurons in vivo: a point of convergence of autism spectrum disorder (ASD) risk gene phenotypes.
Lucia Janickova, Karin Farah Rechberger, Lucas Wey and 1 others
PMID 32517751WHAT IT FOUND
Removing the parvalbumin protein in mice caused their inhibitory neurons to grow larger mitochondria and branch more extensively.
This structural change suggests a mechanism for autism-related brain hyperconnectivity, but it is a basic science finding in animals.
Key findings
01In mice lacking the parvalbumin protein, the volume of mitochondria in inhibitory neurons increased significantly, with the largest increase in neurons that normally express the highest levels of this protein.
02The absence of parvalbumin also led to increased branching and length of dendrites in specific populations of inhibitory neurons, suggesting a link to local hyperconnectivity.
STILL TO COME
How it was doneWhat they found
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What it does not show
This is an animal study using mice. The authors explicitly state that the changes in brain structure observed here are restricted to the mouse brain and have not been demonstrated in human autism brains. The study measures physical structure (morphology) but does not provide direct evidence of how these changes affect the actual firing or connectivity of the neural circuits (function). The density of these specific inhibitory neurons is lower in humans than in mice, so the impact of these structural changes on human brain networks may be different.
Declared interests
The work was funded by the Swiss National Science Foundation. The authors declared no conflicts of interest.
The easy way to misread this
Do not interpret these cellular changes as a confirmed mechanism for human autism or a target for therapy. This is a basic science observation in mice that has not been replicated in human patients, and the clinical relevance to human neurodevelopmental disorders remains hypothetical.