Abstract
Adverse experiences during childhood are among the most prominent risk factors for developing mood and anxiety disorders later in life. Early-life stress interventions have been established as suitable models to study the neurobiological basis of childhood adversity in rodents. Different models such as maternal separation, impaired maternal care and juvenile stress during the postweaning/prepubertal life phase are utilized. Especially within the limbic system, they induce lasting alterations in neuronal circuits, neurotransmitter systems, neuronal architecture and plasticity that are further associated with emotional and cognitive information processing. Recent studies found that astrocytes, a special group of glial cells, have altered functions following early-life stress as well. As part of the tripartite synapse, astrocytes interact with neurons in multiple ways by affecting neurotransmitter uptake and metabolism, by providing gliotransmitters and by providing energy to neurons within local circuits. Thus, astrocytes comprise powerful modulators of neuronal plasticity and are well suited to mediate the long-term effects of early-life stress on neuronal circuits. In this review, we will summarize current findings on altered astrocyte function and hippocampal plasticity following early-life stress. Highlighting studies for astrocyte-related plasticity modulation as well as open questions, we will elucidate the potential of astrocytes as new targets for interventions against stress-induced neuropsychiatric disorders.
Highlights
Adverse events causing feelings of emotional strain are part of our daily life
With a similar stress exposure protocol, we investigated dorsal and ventral Schaffer collateral (SC)-Cornu Ammonis area 1 (CA1)-LTP, and found that the previously reported increase of LTP in the ventral CA1 of rats with a history of juvenile stress (JS) can be mimicked with a pharmacological blockage of the enzyme glutamine synthetase, which breaks down glutamate to glutamine within astrocytes
Studies in humans and rodents have demonstrated that early-life stress shapes how individuals respond to stress later in life [1,137,138]
Summary
Adverse events causing feelings of emotional strain are part of our daily life. Usually, our system adapts well to such stressors. The maturation of brain areas and circuits associated with emotion control and emotional memory such as the amygdala, hippocampus and medial prefrontal cortex (PFC) undergo restructuring processes during childhood and periadolescence Such developmental trajectories are observed in humans, and in the rodent brain during the prepubertal life phase [7], allowing for the use of animal models to study the impact of early life adversity on cognition and emotional behavior later in life. In response to new events, neural circuits constantly change in order to adapt their function to new environmental requirements, a process called plasticity, which occurs on different temporal scales These changes can be expressed as an altered short-term (millisecond-to-minutes) adaptation to a multisensory input, the formation of short-forms of memories or sustenance of working memory (see [13] for an excellent review). We can identify current gaps in knowledge and themes for further research regarding the putative mechanisms of a lasting astrocytic modulation of plasticity after early-life stress
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