ArticleBiological psychiatry2018
Mature Hippocampal Neurons Require LIS1 for Synaptic Integrity: Implications for Cognition.
Article in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Article
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- BALB/c mice challenged with SARS-CoV-2 B.1.351 β variant cause pathophysiological and neurological changes within the lungs and brains.The Journal of general virology · 2024Article
- Brain region-specific action of ketamine as a rapid antidepressant.Science (New York, N.Y.) · 2024Article
- LIS1 RNA-binding orchestrates the mechanosensitive properties of embryonic stem cells in AGO2-dependent and independent ways.Nature communications · 2023Article
- Recent advances in understanding neuronal diversity and neural circuit complexity across different brain regions using single-cell sequencing.Frontiers in neural circuits · 2023Review
- Activation of RhoC by regulatory ubiquitination is mediated by LNX1 and suppressed by LIS1.Scientific reports · 2022Article
- Abnormalities in Cortical GABAergic Interneurons of the Primary Motor Cortex Caused byFrontiers in cell and developmental biology · 2022Article
- Long-Term Effects of Ionizing Radiation on the Hippocampus: Linking Effects of the Sonic Hedgehog Pathway Activation with Radiation Response.International journal of molecular sciences · 2021Article
- Interplay of LIS1 and MeCP2: Interactions and Implications With the Neurodevelopmental Disorders Lissencephaly and Rett Syndrome.Frontiers in cellular neuroscience · 2019Article
- Causal relationship between genetically predicted Enzyme and Tinnitus risk: a two-sample bi-directional mendelian randomization study.Brazilian journal of otorhinolaryngologyArticle
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundPlatelet-activating factor acetylhydrolase 1B1 (LIS1), a critical mediator of neuronal migration in developing brain, is expressed throughout life. However, relatively little is known about LIS1 function in the mature brain. We previously demonstrated that LIS1 involvement in the formation and turnover of synaptic protrusions and synapses of young brain after neuronal migration is complete. Here we examine the requirement for LIS1 to maintain hippocampal circuit function in adulthood.
methodsEffects of conditional Lis1 inactivation in excitatory pyramidal neurons, starting in juvenile mouse brain, were probed using high-resolution approaches combining mouse genetics, designer receptor exclusively activated by designer drug technology to specifically manipulate CA1 pyramidal neuron excitatory activity, electrophysiology, hippocampus-selective behavioral testing, and magnetic resonance imaging tractography to examine the connectivity of LIS1-deficient neurons.
resultsWe found progressive excitatory and inhibitory postsynaptic dysfunction as soon as 10 days after conditional inactivation of Lis1 targeting CA1 pyramidal neurons. Surprisingly, by postnatal day 60 it also caused CA1 histological disorganization, with a selective decline in parvalbumin-expressing interneurons and further reduction in inhibitory neurotransmission. Accompanying these changes were behavioral and cognitive deficits that could be rescued by either designer receptor exclusively activated by designer drug-directed specific increases in CA1 excitatory transmission or pharmacological enhancement of gamma-aminobutyric acid transmission. Lagging behind electrophysiological changes was a progressive, selective decline in neural connectivity, affecting hippocampal efferent pathways documented by magnetic resonance imaging tractography.
conclusionsLIS1 supports synaptic function and plasticity of mature CA1 neurons. Postjuvenile loss of LIS1 disrupts the structure and cellular composition of the hippocampus, its connectivity with other brain regions, and cognition dependent on hippocampal circuits.
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