The Role of Nicotinic Receptors in the Attenuation of Autism-Related Behaviors in a Murine BTBR T + tf/J Autistic Model.
Nicotine improved social play and cut repetitive moves in autism-model mice by switching on nicotinic receptors.
01Research in Context
What this study did
Scientists gave nicotine to BTBR mice. These mice show autism-like behaviors.
The team watched how the mice played and repeated movements. They also gave a drug that blocks nicotine receptors to check if effects reversed.
What they found
Nicotine made the mice spend more time with new friends. It also cut repetitive jumping and grooming.
When the blocker was added, the gains vanished. This shows the benefit came through nicotinic receptors.
How this fits with other research
Weissman-Fogel et al. (2015) extends this work. They placed a nicotine patch on one hospitalized teen. Aggressive episodes and restraints dropped.
Luo et al. (2020) used the same BTBR mouse strain. They changed a genetic RNA instead of nicotine. Both teams saw better social behavior, pointing to shared brain pathways.
Moerkerke et al. (2024) tested oxytocin spray in children. They found no clear change in face-processing activity. Their null result contrasts with the positive mouse nicotine data, but the drugs and measures differ, so the papers do not truly clash.
Why it matters
Nicotine turned on receptors that calmed core autism signs in mice. A single teen case shows similar promise for irritability. You cannot prescribe nicotine, but you can watch future drugs that hit these same receptors. Track social time and stereotypy in your sessions. If safer nicotinic medicines arrive, you will have baseline data ready.
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02At a glance
03Original abstract
Nicotinic receptors are distributed throughout the central and peripheral nervous system. Postmortem studies have reported that some nicotinic receptor subtypes are altered in the brains of autistic people. Recent studies have demonstrated the importance of nicotinic acetylcholine receptors (nAChRs) in the autistic behavior of BTBR T + tf/J mouse model of autism. This study was undertaken to examine the behavioral effects of targeted nAChRs using pharmacological ligands, including nicotine and mecamylamine in BTBR T + tf/J and C57BL/6J mice in a panel of behavioral tests relating to autism. These behavioral tests included the three-chamber social interaction, self-grooming, marble burying, locomotor activity, and rotarod test. We examined the effect of various oral doses of nicotine (50, 100, and 400 mcg/mL; po) over a period of 2 weeks in BTBR T + tf/J mouse model. The results indicated that the chronic administration of nicotine modulated sociability and repetitive behavior in BTBR T + tf/J mice while no effects observed in C57BL/6J mice. Furthermore, the nonselective nAChR antagonist, mecamylamine, reversed nicotine effects on sociability and increased repetitive behaviors in BTBR T + tf/J mice. Overall, the findings indicate that the pharmacological modulation of nicotinic receptors is involved in modulating core behavioral phenotypes in the BTBR T + tf/J mouse model. LAY SUMMARY: The involvement of brain nicotinic neurotransmission system plays a crucial role in regulating autism-related behavioral features. In addition, the brain of the autistic-like mouse model has a low acetylcholine level. Here, we report that nicotine, at certain doses, improved sociability and reduced repetitive behaviors in a mouse model of autism, implicating the potential therapeutic values of a pharmacological intervention targeting nicotinic receptors for autism therapy. Autism Res 2020, 13: 1311-1334. © 2020 International Society for Autism Research, Wiley Periodicals, Inc.
Autism research : official journal of the International Society for Autism Research, 2020 · doi:10.1002/aur.2342