Stimulant restores cell signaling, eases behavior issues in animals missing autism gene

Stimulant restores cell signaling, eases behavior issues in animals missing autism gene

Publication date: May 29, 2021

Disrupted signals: Zebrafish missing both copies of the gene CHD7 (right) have fewer brain cells that produce the inhibitory neurotransmitter GABA than fish with two intact copies (left). Zebrafish lacking both copies of the gene are hyperactive at night, unlike controls and fish missing just one copy, the new study shows. Patten and his colleagues found that the fish show dysregulation along the MAPK/ERK signaling pathway, which is involved in cell growth and implicated in other autism-related neurodevelopmental conditions. Worms and zebrafish missing both copies of the gene CHD7 have a disrupted cellular signaling pathway, a dearth of inhibitory neurons and behavioral challenges. People with a mutated copy of CHD7 often have CHARGE syndrome, a condition that can cause heart and eye defects, stunted growth, attention deficit hyperactivity disorder and autism. People with CHARGE syndrome generally have only one altered copy of the gene, whereas the fish have two. They found that one, the stimulant ephedrine, significantly restored GABA neuron function and suppressed hyperactivity in the fish.

Concepts Keywords
Amphetamine Inhibitory postsynaptic potential
Autism Interneuron
Fish MTOR
Mutant Zebrafish
Neurodegenerative CHD7
Worms Gamma-Aminobutyric acid
Zebrafish Danio
Regenerative biomedicine
Neurotransmitters
Neurons
Branches of biology
Study CHARGE syndrome

Semantics

Type Source Name
drug DRUGBANK Amphetamine
disease MESH defects
disease MESH stunted growth
disease MESH attention deficit hyperactivity disorder
disease MESH neurodegenerative disease
drug DRUGBANK gamma-Aminobutyric acid
drug DRUGBANK Ephedrine
disease MESH CHARGE syndrome
disease MESH autism

Original Article

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