Abstract
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.
Highlights
The prenatal or early neonatal period is critical for brain development and can be powerfully influenced by environmental factors[1]
The current study examined a number of behavioral, biochemical, and neurophysiological markers to determine how maternal deprivation (MD) alters brain structure and function in adulthood
MD impairs recognition memory (RM) Variances between groups were similar based on F tests
Summary
The prenatal or early neonatal period is critical for brain development and can be powerfully influenced by environmental factors[1]. Early-life adverse events such as malnutrition, maternal separation, or viral infection[2,3,4,5] may disrupt brain development[6], possibly leading to psychopathology later in life, including schizophrenia (SZ)[7,8]. Determining how early life trauma alters neural circuit composition/function is important to understand the link with an increased risk for psychopathology. Altered hippocampal NMDA receptor subunit expression has been observed following MD11, which is associated with impairments in learning and memory later in life[12]. Administering a NMDA receptor antagonist (Memantine), prevents impaired social cognition typically observed in adulthood following MD13, further supporting that early life trauma can alter the glutamatergic system. Janetsian-Fritz et al Translational Psychiatry (2018)8:71 decreases in brain derived neurotrophic factor (BDNF)
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