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Adolescent-like Processing of Behaviorally Salient Cues in Sensory and Prefrontal Cortices of Adult Preterm-Born Mice
Insights
Preterm birth impairs cognitive function by altering neural activity in visual and prefrontal cortex circuits. Early interventions like environmental enrichment may not fully restore performance in preterm mice.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Cognitive Neuroscience
Background:
- Preterm birth is a significant risk factor for cognitive and sensory processing deficits.
- The specific neural circuit mechanisms underlying these atypicalities remain poorly understood.
Purpose of the Study:
- To investigate the impact of preterm birth on visual processing and prefrontal cortex function.
- To identify potential circuit-level alterations contributing to cognitive deficits in preterm individuals.
Main Methods:
- Adult mice born a day early (preterm) were trained on a visual discrimination task.
- In vivo electrophysiology was used to record neural activity in the primary visual cortex (V1) and anterior cingulate cortex (ACC).
- The effects of environmental enrichment were assessed.
Main Results:
- Preterm mice exhibited poorer performance on the visual task, committing more errors.
- V1 and ACC neurons showed hyper-responsiveness to reward cues and reduced activation to non-rewarded cues during errors.
- Fast-spiking (FS) interneurons in the prefrontal cortex displayed elevated error-related activity.
- Environmental enrichment did not improve performance in preterm mice.
Conclusions:
- Preterm birth disrupts neural circuits involved in reward processing and error monitoring.
- Prefrontal cortex circuits, particularly FS interneurons, appear vulnerable to altered extrauterine experiences.
- Early environmental interventions may have limited efficacy in mitigating cognitive deficits associated with preterm birth.
Abstract:
Preterm birth is a leading risk factor for atypicalities in cognitive and sensory processing, but it is unclear how prematurity impacts circuits that support these functions. To address this, we trained adult mice born a day early (preterm mice) on a visual discrimination task and found that they commit more errors and fail to achieve high levels of performance. Using in vivo electrophysiology , we found that the neurons in the primary visual cortex (V1) and the V1-projecting prefrontal anterior cingulate cortex (ACC) are hyper-responsive to the reward, reminiscent of cue processing in adolescence. Moreover, the non-rewarded cue fails to robustly activate the V1 and V1-projecting ACC neurons during error trials, in contrast to prefrontal fast-spiking (FS) interneurons which show elevated error-related activity, suggesting that preterm birth impairs the function of prefrontal circuits for error monitoring. Finally, environmental enrichment, a well-established paradigm that promotes sensory maturation, failed to improve the performance of preterm mice, suggesting limited capacity of early interventions for reducing the risk of cognitive deficits after preterm birth. Altogether, our study for the first time identifies potential circuit mechanisms of cognitive atypicalities in the preterm population and highlights the vulnerability of prefrontal circuits to advanced onset of extrauterine experience.
