| Aggressive behavior,a major feature of autism,is evident in more than 25%of autistic patients and has been demonstrated in many model mice.Great breakthroughs have been made in the research of neural circuits related to social disorders and stereotyped behaviors,but little is known about the aggressive behavior field of autism up to now.Neuroligins(NLs)are critical for synaptic formation and function,and NL3 R451C is an autism-related mutation.NL3 R451C knockin(KI)mice showed autistic behavioral abnormalities,including social novelty deficits.In this model,we found that KI mice were accompanied by severe aggressive behavior,and this aggressive behavior was different for different manifestations of intruders.At the same time,we examined the expression of c-fos in different brain regions of KI mice related to the attack,and found that the c-fos cells in the medial prefrontal cortex(mPFC)of KI mice were more activated than the wild-type mice in the same number of attacks.In KI mice,c-fos cells in the ventromedial hypothalamus(VMH)and the dorsal medial nucleus(DM)of the hypothalamus were less activated than wild-type mice.In addition,we also recorded the calcium signal release in mPFC brain region of mice during the attack by in vivo fiber recording.We found that the excitability(CamkII-positive)neurons of KI mice increased rapidly at the beginning of the attack.In the control group,wild-type(WT)mice did not significantly change the calcium signal release during challenge;while the inhibitory(PV)neurons of KI mice remained in an irregular state after the start of the attack,the control group WT mice started after the attack.Inhibitory(PV)neurons are in a state of sustained high release,which continues until the end of the attack.These findings suggest that there may be abnormalities in the neural circuits of autistic mice’s aggressive behavior,and this study will provide insights into the treatment of autistic behavioral symptoms in autistic patients. |
PDF Full Text Request