Impaired hippocampal–prefrontal synchrony in a genetic mouse model of schizophrenia
Open accessAbstract
Abnormalities in functional connectivity between brain areas have been postulated as an important pathophysiological mechanism underlying schizophrenia. In particular, macroscopic measurements of brain activity in patients suggest that functional connectivity between the frontal and temporal lobes may be altered. However, it remains unclear whether such dysconnectivity relates to the aetiology of the illness, and how it is manifested in the activity of neural circuits. Because schizophrenia has a strong genetic component, animal models of genetic risk factors are likely to aid our understanding of the pathogenesis and pathophysiology of the disease. Here we study Df(16)A(+/-) mice, which model a microdeletion on human chromosome 22 (22q11.2) that constitutes one of the largest known genetic risk factors for schizophrenia. To examine functional connectivity in these mice, we measured the synchronization of neural activity between the hippocampus and the prefrontal cortex during the performance of a task requiring working memory, which is one of the cognitive functions disrupted in the disease. In wild-type mice, hippocampal-prefrontal synchrony increased during working memory performance, consistent with previous reports in rats. Df(16)A(+/-) mice, which are impaired in the acquisition of the task, showed drastically reduced synchrony, measured both by phase-locking of prefrontal cells to hippocampal theta oscillations and by coherence of prefrontal and hippocampal local field potentials. Furthermore, the magnitude of hippocampal-prefrontal coherence at the onset of training could be used to predict the time it took the Df(16)A(+/-) mice to learn the task and increased more slowly during task acquisition. These data suggest how the deficits in functional connectivity observed in patients with schizophrenia may be realized at the single-neuron level. Our findings further suggest that impaired long-range synchrony of neural activity is one consequence of the 22q11.2 deletion and may be a fundamental component of the pathophysiology underlying schizophrenia.
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Df(16)A +/- mice have prominent working memory deficits that are likely caused by impaired functional connectivity between the hippocampus and the prefrontal cortex.
“Df(16)A +/-mice have prominent working memory deficits that are likely caused by impaired functional connectivity between the hippocampus and the prefrontal cortex 77”
From Developmental timing and critical windows for the treatment of psychiatric disorders (2016) · cites this paper as [77]
Recent evidence suggests that relations exist between aberrant synchronization across prefrontal and hippocampal ensembles in rodents and observations in schizophrenia patients.
“Recent evidence suggests that this is feasible and that relations exist between aberrant synchronization across prefrontal and hippocampal ensembles in rodents and observations in schizophrenia patients (Meyer-Lindenberg et al., 2005”
From Neuronal Dynamics and Neuropsychiatric Disorders: Toward a Translational Paradigm for Dysfunctional Large-Scale Networks (2012) · cites this paper as Sigurdsson et al., 2010
Rodent models of 22q11DS have provided important insights, including descriptions of circuit dysfunction.
“Rodent models of 22q11DS have provided important insights3,9,10, including describing circuit dysfunction11–13.”
From Neuronal defects in a human cellular model of 22q11.2 deletion syndrome (2020) · cites this paper as [12]
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- Authors
- Sigurdsson, T., Stark, K. L., Karayiorgou, M., Gogos, J. A., & Gordon, J. A.
- Affiliations
- Columbia University (US)
- New York State Psychiatric Institute (US)
- Corresponding author
- Gogos, Joseph A.
- Gordon, Joshua A.
- Venue
- Nature
- Published
- 2010-04
- Volume
- 464
- Issue
- 7289
- Pages
- 763-767
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2864584
- OpenAlex
- W2065738753
- Cited by
- 702
- References
- 4
- Citations by year
- 2026: 22 · 2025: 34 · 2024: 26 · 2023: 51 · 2022: 38 · 2021: 53 · 2020: 41 · 2019: 56 · 2018: 43 · 2017: 46 · 2016: 35 · 2015: 63 · 2014: 35 · 2013: 49 · 2012: 44
- FWCI
- 34.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Foundation for the National Institutes of Health
- Simons Foundation
- National Institutes of Health
- National Institute of Mental Health (R01MH067068, MH 67068, MH081968, R01MH081968)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- schizophrenia, 22q11.2 microdeletion, working memory, functional connectivity, theta oscillations, phase locking, local field potentials, prefrontal cortex, hippocampus, neuronal synchronization, genetic risk factors, mouse model of schizophrenia, cognitive impairment, synaptic plasticity
- MeSH terms
- Action Potentials, Alleles, Animals, Behavior, Animal, Chromosomes, Human, Pair 22, Disease Models, Animal, Female, Hippocampus, Humans, Male, Memory, Mice, Inbred C57BL, Models, Genetic, Models, Neurological, Schizophrenia, Prefrontal Cortex, Genetic Predisposition to Disease, Chromosomes, Mammalian, Mice
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