Related Experiment Video
Updated: Jan 15, 2026
The Unpredictable Chronic Mild Stress Protocol for Inducing Anhedonia in Mice
Published on: October 24, 2018
Cuminaldehyde, a Hopeful Agent, Mitigates Autistic-Like Behaviors, Combating Hippocampal Neuroinflammation in
Alireza Gholipour Shahraki1, Fariba Houshmand2, Elham Saghaei2
1Student Research Committee, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Background And Aim:
Autism spectrum disorder (ASD) is a neurodevelopmental disorder that appears in the earliest ages of the lifespan. The causes of ASD remain anonymous, although immunological, genetic, biological, and psychosocial theories have been proposed. Stresses during early life, such as maternal separation (MS), are one of the psychosocial causes of ASD. The neuroimmune response is complicated in the pathophysiology of ASD. Cuminaldehyde (CA) has different pharmacological effects, such as anti-inflammatory properties. This study aimed to explore effects of CA on autistic-like behaviors in maternally separated mice with respect to its probable anti-neuroinflammatory effects.
Methods:
Forty male mice were randomly allocated to five groups, including control mice administered with normal saline, and MS groups received normal saline and CA with doses of 5, 25, 50 mg/kg intraperitoneally for 14 continuous days. The three-chamber sociability, the resident-intruder, and shuttle box tests were performed. Subsequently, mice were euthanized, and the expression of the NLRP3, TLR4, HMGB1, and IL-1β genes in the hippocampus was investigated using real-time PCR.
Results:
MS mice showed diminished sociability preference, damaged passive avoidance memory, as well as aggressive behaviors. Behaviors related to autism in MS mice are associated with a rise in the expression of inflammatory markers in the hippocampus. CA reversed the deleterious effects of MS on behaviors, in addition to a decrease in the expression of inflammatory genes in the hippocampus.
Conclusion:
CA, via attenuation of neuroimmune reaction in the hippocampus, partially mitigated autistic-like behaviors in the MS mouse model.
