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Published on: December 4, 2013
Maternal deprivation induces deficits in temporal memory and cognitive flexibility and exaggerates synaptic
Aurélie Baudin1, Kévin Blot, Catherine Verney
1INSERM, UMRs, Physiopathologie des Maladies du Système Nerveux Central, Paris, France.
Insights
Early life maternal deprivation (MD) impairs executive functions in adult rats by altering prefrontal cortex (PFC) synaptic plasticity, not neuron numbers. This suggests exaggerated plasticity contributes to cognitive deficits.
Area of Science:
- Neuroscience
- Developmental Psychology
- Behavioral Neuroscience
Background:
- Early life adverse events, such as maternal deprivation (MD), can negatively impact brain development.
- The prefrontal cortex (PFC) is particularly vulnerable to early life stress and is crucial for executive functions.
Purpose of the Study:
- To investigate the long-term effects of MD on PFC-dependent executive functions, neuronal and astrocyte populations, and synaptic plasticity in adult male rats.
- To determine if observed cognitive deficits correlate with structural or functional changes in the medial PFC (mPFC).
Main Methods:
- Male Long-Evans rats underwent daily maternal deprivation from postnatal day 1-14.
- Cognitive functions were assessed in adulthood using the temporal order memory task (TMT), attentional set-shifting task (ASST), and Morris water maze task (WMT).
- Neuronal and astrocyte counts in the prelimbic area of the mPFC were quantified using stereology, and in vivo field potentials were recorded to assess long-term potentiation (LTP) in the PrL area.
Main Results:
- MD induced cognitive deficits in PFC-dependent TMT and ASST, but not in the non-PFC-dependent WMT.
- Maternal deprivation resulted in an upregulation of LTP in the prelimbic area of the mPFC.
- No significant changes were observed in the number of neurons or astrocytes in the mPFC following MD.
Conclusions:
- Maternal deprivation in early life leads to lasting impairments in PFC-dependent executive functions in adult male rats.
- Exaggerated synaptic plasticity (LTP) in the mPFC, without changes in cell numbers, may underlie these cognitive deficits.
- These findings highlight the critical role of early life experiences in shaping PFC function and cognitive abilities throughout life.
Abstract:
Early life adverse events can lead to structural and functional impairments in the prefrontal cortex (PFC). Here, we investigated whether maternal deprivation (MD) alters PFC-dependent executive functions, neurons and astrocytes number and synaptic plasticity in adult male Long-Evans rats. The deprivation protocol consisted of a daily separation of newborn Long-Evans pups from their mothers and littermates 3h/day postnatal day 1-14. Cognitive performances were assessed in adulthood using the temporal order memory task (TMT) and the attentional set-shifting task (ASST) that principally implicates the PFC and the Morris water maze task (WMT) that does not essentially rely on the PFC. The neurons and astrocytes of the prelimbic (PrL) area of the medial PFC (mPFC) were immunolabelled respectively with anti-NeuN and anti-GFAP antibodies and quantified by stereology. The field potentials evoked by electrical stimulation of ventral hippocampus (ventral HPC) were recorded in vivo in the PrL area. In adulthood, MD produced cognitive deficits in two PFC-dependent tasks, the TMT and ASST, but not in the WMT. In parallel, MD induced in the prelimbic area of the medial PFC an upregulation of long-term potentiation (LTP), without any change in the number of neurons and astrocytes. We provide evidence that MD leads in adults to an alteration of the cognitive abilities dependent on the PFC, and to an exaggerated synaptic plasticity in this region. We suggest that this latter phenomenon may contribute to the impairments in the cognitive tasks.
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