ArticleCerebral cortex (New York, N.Y. : 1991)2021
Knock-Down of Hippocampal DISC1 in Immune-Challenged Mice Impairs the Prefrontal-Hippocampal Coupling and the Cognitive Performance Throughout Development.
Article in Cerebral cortex (New York, N.Y. : 1991), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Prefrontal Cortex Dysfunction as a Precipitating Factor for Schizophrenia and Depression.Journal of neurochemistry · 2026Review
- Developmental Olfactory Dysfunction and Abnormal Odor Memory in Immune-ChallengedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A developmental increase of inhibition promotes the emergence of hippocampal ripples.Nature communications · 2024Article
- Sparser and Less Efficient Hippocampal-Prefrontal Projections account for Developmental Network Dysfunction in a Model of Psychiatric Risk Mediated by Gene-Environment Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Developmental decrease of entorhinal-hippocampal communication in immune-challenged DISC1 knockdown mice.Nature communications · 2021Article
- The Logic of Developing Neocortical Circuits in Health and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
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Authors and funding
3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Disrupted-in-schizophrenia 1 (DISC1) gene represents an intracellular hub of developmental processes. When combined with early environmental stressors, such as maternal immune activation, but not in the absence of thereof, whole-brain DISC1 knock-down leads to memory and executive deficits as result of impaired prefrontal-hippocampal communication throughout development. While synaptic dysfunction in neonatal prefrontal cortex (PFC) has been recently identified as one source of abnormal long-range coupling, the contribution of hippocampus (HP) is still unknown. Here, we aim to fill this knowledge gap by combining in vivo electrophysiology and optogenetics with morphological and behavioral assessment of immune-challenged mice with DISC1 knock-down either in the whole brain (GE) or restricted to pyramidal neurons in hippocampal CA1 area (GHPE). We found abnormal network activity, sharp-waves, and neuronal firing in CA1 that complement the deficits in upper layer of PFC. Moreover, optogenetic activating CA1 pyramidal neurons fails to activate the prefrontal local circuits. These deficits that persist till prejuvenile age relate to dendrite sparsification and loss of spines of CA1 pyramidal neurons. As a long-term consequence, DISC1 knock-down in HP leads to poorer recognition memory at prejuvenile age. Thus, DISC1-controlled developmental processes in HP in immune-challenged mice are critical for circuit function and cognitive behavior.
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