Impairment of cognitive performance after reelin knockdown in the medial prefrontal cortex of pubertal or adult rats
Open accessAbstract
The glycoprotein reelin is important for embryonic neuronal migration. During adulthood reelin possibly acts as a modulator of synaptic plasticity. Several studies link reduced levels of reelin messenger RNA and protein to the pathophysiology of certain neuropsychiatric disorders. However, little is known about reelin's role for behavioral and cognitive functions in vivo. Therefore, the effect of a reelin knockdown in the medial prefrontal cortex (mPFC) of Wistar rats was examined in behavioral tasks related to neuropsychiatric disorders, such as schizophrenia. Rats treated with reelin antisense phosphothioate oligonucleotides in the mPFC during puberty or adulthood were tested for prepulse inhibition (PPI) of the acoustic startle reflex, spatial working memory, object recognition, and locomotor activity. Reelin quantification in the mPFC was assessed by Western blotting. Local reelin knockdown during puberty or adulthood induced (1) a PPI deficit as well as (2) an impairment of spatial working memory and object recognition following pubertal injections. Western blot analyses showed a distinct and highly selective reelin knockdown in the rats' mPFC. These results indicate that mPFC reelin signaling plays an important role in behavioral tasks with relevance to e.g. schizophrenia. Understanding reelin's function as a neurotrophic modulator of the extracellular matrix may help to achieve new insights into the etiology of certain neuropsychiatric diseases and foster prospective treatment strategies.
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The time and place at which Reelin signaling is reduced may prove to be the deciding factor for the extent of cognitive impact that defective Reelin signaling may have.
“The time and place at which Reelin signaling is reduced may prove to be the deciding factor for the extent of cognitive impact that defective Reelin signaling may have (97).”
From Reelin: Neurodevelopmental Architect and Homeostatic Regulator of Excitatory Synapses (2017) · cites this paper as [97]
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Reelin: Neurodevelopmental Architect and Homeostatic Regulator of Excitatory Synapses
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“The time and place at which Reelin signaling is reduced may prove to be the deciding factor for the extent of cognitive impact that defective Reelin signaling may have (97).”
BackgroundCanonical and non-canonical Reelin signaling
Bock, H. H., & May, P. (2016) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2016.00166 · Cited by 107 · see citing works
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Hypervulnerability of the adolescent prefrontal cortex to nutritional stress via reelin deficiency
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Maternal Pravastatin Prevents Altered Fetal Brain Development in a Preeclamptic CD-1 Mouse Model
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Reelin in Alzheimer’s Disease, Increased Levels but Impaired Signaling: When More is Less
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Decisive role of Reelin signaling during early stages of Alzheimer’s disease
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Identification of RELN variation p.Thr3192Ser in a Chinese family with schizophrenia
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F-spondin gene transfer improves memory performance and reduces amyloid-β levels in mice
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The Candidate Schizophrenia Risk Gene DGCR2 Regulates Early Steps of Corticogenesis
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Modulation of Hippocampal Gamma Oscillations by Dopamine in Heterozygous Reeler Mice in vitro
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Self-citationOlfaction, among the First Senses to Develop and Decline
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OCRL1 Deficiency Affects the Intracellular Traffic of ApoER2 and Impairs Reelin-Induced Responses
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Self-citationExamining reelin expression and neural plasticity in animal models of depression
Lussier, A. L. (2012) · University Library - University of Saskatchewan (University of Saskatchewan)
Bouamrane, L. (2015) · theses.fr (ABES) · doi:10.70675/00597159za953z4221z95b8z57a6c1d48c8e
Reelin in vulnerability and sex-dependent maturational trajectories of the prefrontal cortex
Silva-Hurtado, T. J. (2021) · theses.fr (ABES) · doi:10.70675/ecf0031ez1ac8z4688za735za4cd9acfc52c
- Authors
- Brosda, J., Dietz, F., & Koch, M.
- Affiliations
- University of Bremen (DE)
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2011-11
- Volume
- 44
- Issue
- 2
- Pages
- 239-247
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2041055359
- Cited by
- 37
- References
- 95
- Citations by year
- 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 8 · 2015: 1 · 2014: 3 · 2013: 3 · 2012: 6
- FWCI
- 2.62
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- reelin, medial prefrontal cortex, antisense oligonucleotides, prepulse inhibition, acoustic startle response, spatial working memory, object recognition, puberty, schizophrenia, neuropsychiatric disorders, synaptic plasticity, neurotrophic factors, extracellular matrix
- MeSH terms
- Reelin Protein, Age Factors, Animals, Cognition Disorders, Disease Models, Animal, Male, Nerve Tissue Proteins, Serine Endopeptidases, Sexual Maturation, Cell Adhesion Molecules, Neuronal, Extracellular Matrix Proteins, Rats, Wistar, Prefrontal Cortex, Mood Disorders, Oligoribonucleotides, Antisense, Rats, Gene Knockdown Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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