Tweaks to autism-linked pathway tilt circuits’ signaling balance
Altered expression of TSC2 and the mTOR pathway reshape the formation of certain synapses between inhibitory and excitatory neurons in mice.
Altered expression of TSC2 and the mTOR pathway reshape the formation of certain synapses between inhibitory and excitatory neurons in mice.
The in-depth approach shows mutations in the autism-linked gene disrupt neuronal growth and communication, as well as mitochondrial gene expression.
The method yields complex organoids that more closely mimic embryonic brain development than do those cultured in other ways.
People’s brains have a larger network of inhibitory interneurons than mouse brains do, according to a new study. Changes to that network could contribute to autism or other conditions, says lead investigator Moritz Helmstaedter.
The approach, tested in mice, selectively boosts the expression of the autism-linked gene SCN1A in a subgroup of inhibitory cells.
Interneurons that fail to propagate electrical signals in mice that model Dravet syndrome may cause the animals, like people with the autism-linked condition, to die suddenly.
Together, the neurons are part of the corticostriatal circuit, which has been implicated in autism.
Worms and zebrafish missing both copies of the gene CHD7 have disrupted cellular signaling, a dearth of inhibitory neurons and behavior changes — all of which are reversed by the stimulant drug ephedrine.
Female mice missing a copy of the autism-linked gene MECP2 in a specific set of inhibitory neurons have a hard time heeding pups’ calls and herding litters.
Sensory problems in people with fragile X syndrome may stem from hyperactive neurons, a mouse model study suggests.