Summary: Babies removed from their mothers for 24 hours when they were 9 days old exhibited significant behavioral and brain structural abnormalities in adulthood, a new study reports. Researchers noted memory impairment and less communication between specific brain regions in those removed from maternal care.
When a baby is taken from its mother for even a brief period early in life, this traumatic event significantly alters the future, adult function of the brain, according to a new animal model study from the School of Science at IUPUI. These changes in the brain are similar to disturbances in brain structure and function that are found in people at risk for neuropsychiatric disorders, such as schizophrenia.
The study was conducted in the laboratory of associate professor of psychology Christopher Lapish. In the study, young rats were removed from their mothers for 24 hours when they were nine days old, which is a critical period of brain development. The resulting scans revealed that, unlike animals that were not separated from their mother during this crucial period, the separated rats exhibited significant behavioral, as well as biological and physiological, brain abnormalities in adulthood.
“Rat and human brains have similar structure and connectivity,” Lapish said. “Understanding what happens in the brain of a young rat that’s removed from its mother gives us important insight into how this type of early trauma — perhaps comparable to the incarceration of a human mother — affects the young human brain.”
“The more we understand how the brain responds, the closer we come to being able to address and hopefully develop novel treatment strategies to reverse these neurological changes.” Lapish said.
“In this study, we found memory impairment, as well as less communication between brain regions, in the animals that had been removed from their mothers, among other neurological changes,” said study corresponding author Sarine Janetsian-Fritz, formerly a graduate student in the Lapish lab and now a postdoctoral fellow in neuropsychology at the Indiana University School of Medicine. “These are all clues to how a traumatic event early in life could increase a person’s risk of receiving a schizophrenia diagnosis in the future.”
The causes of schizophrenia and the delay in the appearance of symptoms of this lifelong disease remain a mystery.
“Children exposed to early-life stress or deprivation are at higher risk for mental illness and addictions later in life, including schizophrenia,” said study co-author Brian F. O’Donnell, professor of psychological and brain sciences at IU Bloomington. “We have identified enduring changes in the brain and behavior that result from one type of stress in a rodent. These types of brain changes might mediate the effects of adverse events on children. Thus, policies or interventions that mitigate stress to children could reduce vulnerability to emotional disorders in adulthood.”
Funding: The study was funded by an Indiana University Collaborative Research Grant awarded jointly to Lapish, who studies the neurophysiological basis of cognition; O’Donnell, who studies schizophrenia in humans; and Baucum, who conducts brain chemical analyses.
Source: Cindy Fox Aisen – IUPUI
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “Maternal deprivation induces alterations in cognitive and cortical function in adulthood” by Sarine S. Janetsian-Fritz, Nicholas M. Timme, Aqilah M. McCane, Anthony J. Baucum II, Brian F. O’Donnell & Christopher C. Lapish in Translational Psychiatry. Published March 28 2018.
Maternal deprivation induces alterations in cognitive and cortical function in adulthood
Early life trauma is a risk factor for a number of neuropsychiatric disorders, including schizophrenia (SZ). The current study assessed how an early life traumatic event, maternal deprivation (MD), alters cognition and brain function in rodents. Rats were maternally deprived in the early postnatal period and then recognition memory (RM) was tested in adulthood using the novel object recognition task. The expression of catechol-o-methyl transferase (COMT) and glutamic acid decarboxylase (GAD67) were quantified in the medial prefrontal cortex (mPFC), ventral striatum, and temporal cortex (TC). In addition, depth EEG recordings were obtained from the mPFC, vertex, and TC during a paired-click paradigm to assess the effects of MD on sensory gating. MD animals exhibited impaired RM, lower expression of COMT in the mPFC and TC, and lower expression of GAD67 in the TC. Increased bioelectric noise was observed at each recording site of MD animals. MD animals also exhibited altered information theoretic measures of stimulus encoding. These data indicate that a neurodevelopmental perturbation yields persistent alterations in cognition and brain function, and are consistent with human studies that identified relationships between allelic differences in COMT and GAD67 and bioelectric noise. These changes evoked by MD also lead to alterations in shared information between cognitive and primary sensory processing areas, which provides insight into how early life trauma confers a risk for neurodevelopmental disorders, such as SZ, later in life.