Abstract
Early life exposure to stressful situations impairs cognitive performance of adults and contributes to the etiology of several psychiatric disorders. Most of affected cognitive abilities rely on coupling by synchrony within complex neuronal networks, including prefrontal cortex (PFC), hippocampus (HP), and perirhinal cortex (PRH). Yet it remains poorly understood how early life stress (ELS) induces dysfunction within these networks during the course of development. Here we used intermittent maternal separation during the first 2 postnatal weeks to mimic ELS and monitored the recognition memory and functional coupling within prefrontal-hippocampal-perirhinal circuits in juvenile rats. While maternally-separated female rats showed largely normal behavior, male rats experiencing this form of ELS had poorer location and recency recognition memory. Simultaneous multi-site extracellular recordings of network oscillations and neuronal spiking from PFC, HP, and PRH in vivo revealed corresponding decrease of oscillatory activity in theta and beta frequency bands in the PFC of male but not female rats experiencing maternal separation. This deficit was accompanied by weaker cross-frequency coupling within juvenile prefrontal-hippocampal networks. These results indicate that already at juvenile age ELS mimicked by maternal separation induces sex-specific deficits in recognition memory that might have as underlying mechanism a disturbed communication between PFC and HP.
Highlights
We used different recognition memory paradigms to decide whether already at early stages of juvenile development, the cognitive behavior of rats maternally deprived during the first postnatal weeks is affected
We combined behavioral testing with electrophysiology in vivo from urethane-anesthetized rats to decide how adversity during early life perturbs the functional development of neuronal networks and related behavioral performance
We showed that the ontogeny of cognitive performance at juvenile age was severely affected in males and to a lesser extent, in female rats with a history of ELS
Summary
Disruption of cortical excitability, dendritic atrophy and spine loss have been proposed as synaptic and cellular substrate of ELS-induced cognitive dysfunction at adulthood[10,20,21,22,23,24]. It is still fully unknown whether and at which developmental time point the wiring and function of neuronal networks is affected by ELS. We show that decreased oscillatory activity in the PFC and abnormal prefrontal-hippocampal coupling are present already at juvenile age in male rats This dysfunction correlates with poorer object location and recency recognition. These findings provide mechanistic insights into the developmental dynamics of ELS-induced circuit dysfunction
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