Most working scientists aren’t optimistic about their career prospects, according to a Nature survey; expecting passion may be detrimental in academia; and there are new funding opportunities on the horizon, with upcoming deadlines.
Mice missing a copy of the gene SENP1 have atypical social behavior likely due to a signaling imbalance in the retrosplenial cortex.
Model mice of the subtype also show hyperactivity in a signaling pathway called mTOR, bolstering the idea that distinct forms of autism have different biological roots and may require different treatment approaches.
The work fills in gaps about how synapses change before and after birth — essential knowledge for understanding whether synapse development differs in autism.
An online community is helping many new principal investigators through a tricky time, plus other resources for early-career autism researchers.
These short reports from Spectrum journalists highlight some of the autism-related findings that caught our attention at the meeting this past week.
Activating certain receptors in the amygdala — a treatment that runs counter to a leading theory of what causes the condition — can reverse some traits in rats.
Animal models of autism rooted in exposure to maternal antibodies hint at different mechanisms.
Social memory, which may be altered in autism, depends on serotonin-sensitive neurons that send signals from the medial septum to the hippocampus.
Even partial loss of the gene impairs the mouse brain’s ability to respond to sensory experiences, which may explain why people with SYNGAP1 mutations tend to have learning difficulties and a high pain tolerance.
