A new model as an early life manipulation: Fake mother

2017 ◽  
Vol 41 (S1) ◽  
pp. S346-S346
Author(s):  
M. Kucukkarapinar ◽  
A. Dönmez ◽  
S. Candansayar ◽  
A. Bozkurt ◽  
E. Akçay

IntroductionEarly life stressful events cause long-term neural changes that are associated with psychiatric disorders.ObjectiveEarly life manipulations focus on commonly the impact of remaining separate from the mother in a specific period of time. The maternal odor is required for pups to approach the mother for nursing. What happens when there is a mother that smell like a real mother but does not take care her own pups?AimTo investigate the fake mother effects on adult rat's behavioral changes, NMDR2B protein level changes in prefrontal cortex and hippocampus.MethodsWistar rats were used. Fake mother (n:13), early handling (n:12), maternal separation (n:14) and control (n:12) were the study groups. A fake mother is an object that smells like a real dam. When the real mother is separated from own pups fake mother stays with the pups for an hour. Manipulations were made during the postnatal first 14 days. Behavioral tests (social interaction test, elevated plus maze, novel object recognition test) were made between postnatal 62 and 78 days. NMDAR2B protein levels in prefrontal cortex and hippocampus were evaluated by using ELISA at postnatal 78 days.ResultsIn social interaction test, fake mother group exhibited less social behavior and more aggressive behavior than the other groups. Their long-term memory functions were the lowest. NMDAR2B protein levels in the hippocampus increased in rats that exposed to early stressful life events.ConclusionThese results support that being raised by fake mother increases aggressive behavior and decrease social behavior in adulthood.Disclosure of interestThe authors have not supplied their declaration of competing interest.

2013 ◽  
Vol 63 (4) ◽  
pp. 309-315 ◽  
Author(s):  
Fukie Niijima-Yaoita ◽  
Masahiro Tsuchiya ◽  
Hiroko Saito ◽  
Yuka Nagasawa ◽  
Shigeo Murai ◽  
...  

2019 ◽  
Vol 28 (2) ◽  
pp. 247-260 ◽  
Author(s):  
Do Gyeong Kim ◽  
Edson Luck Gonzales ◽  
Seonmin Kim ◽  
Yujeong Kim ◽  
Keremkleroo Jym Adil ◽  
...  

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A11-A12
Author(s):  
Carolyn Jones ◽  
Randall Olson ◽  
Alex Chau ◽  
Peyton Wickham ◽  
Ryan Leriche ◽  
...  

Abstract Introduction Glutamate concentrations in the cortex fluctuate with the sleep wake cycle in both rodents and humans. Altered glutamatergic signaling, as well as the early life onset of sleep disturbances have been implicated in neurodevelopmental disorders such as autism spectrum disorder. In order to study how sleep modulates glutamate activity in brain regions relevant to social behavior and development, we disrupted sleep in the socially monogamous prairie vole (Microtus ochrogaster) rodent species and quantified markers of glutamate neurotransmission within the prefrontal cortex, an area of the brain responsible for advanced cognition and complex social behaviors. Methods Male and female prairie voles were sleep disrupted using an orbital shaker to deliver automated gentle cage agitation at continuous intervals. Sleep was measured using EEG/EMG signals and paired with real time glutamate concentrations in the prefrontal cortex using an amperometric glutamate biosensor. This same method of sleep disruption was applied early in development (postnatal days 14–21) and the long term effects on brain development were quantified by examining glutamatergic synapses in adulthood. Results Consistent with previous research in rats, glutamate concentration in the prefrontal cortex increased during periods of wake in the prairie vole. Sleep disruption using the orbital shaker method resulted in brief cortical arousals and reduced time in REM sleep. When applied during development, early life sleep disruption resulted in long-term changes in both pre- and post-synaptic components of glutamatergic synapses in the prairie vole prefrontal cortex including increased density of immature spines. Conclusion In the prairie vole rodent model, sleep disruption on an orbital shaker produces a sleep, behavioral, and neurological phenotype that mirrors aspects of autism spectrum disorder including altered features of excitatory neurotransmission within the prefrontal cortex. Studies using this method of sleep disruption combined with real time biosensors for excitatory neurotransmitters will enhance our understanding of modifiable risk factors, such as sleep, that contribute to the altered development of glutamatergic synapses in the brain and their relationship to social behavior. Support (if any) NSF #1926818, VA CDA #IK2 BX002712, Portland VA Research Foundation, NIH NHLBI 5T32HL083808-10, VA Merit Review #I01BX001643


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