Deficits in LTP and recognition memory in the genetically hypertensive rat are associated with decreased expression of neurotrophic factors and their receptors in the dentate gyrus
Abstract
We have previously reported that a genetically hypertensive strain of Wistar rat (GH), is deficient in nerve growth factor (NGF) and Trk receptors in dentate gyrus and that these deficits are accompanied by impaired expression of long-term potentiation (LTP) in perforant path-granule cell synapses. Here we confirm this deficit in LTP and report that this strain of rat also displays impairments in long-term recognition memory when compared with normotensive controls. Further analysis of neurotrophin expression in dentate gyrus confirmed the previously-reported deficit in NGF and revealed a decrease in expression of brain-derived neurotrophic factor (BDNF), but not neurotrophin 3 (NT3) or neurotrophin 4 (NT4), in GH rats. These alterations in ligand expression were accompanied by changes in Trk receptor expression; specifically, a decrease in expression of TrkA and TrkB, but not TrkC, in the dentate gyrus of GH, compared with normotensive, rats. We conclude that the impairments in LTP and learning and memory observed in the GH strain are associated with aberrant expression of specific neurotrophic factors and their receptors in the dentate gyrus, adding weight to the evidence indicating a role for these proteins in several forms of synaptic plasticity.
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In spontaneously hypertensive rats, expression of neurotrophic factors and receptors in dentate gyrus is subtly abnormal, with reduced BDNF, neurotrophins 3 and 4, TrkA, and TrkB.
“In spontaneously hypertensive rats, subtle abnormalities in the expression of neuro trophic factors and their receptors, namely reduced levels of BDNF, neutrophins 3 and 4, TrkA, and TrkB, have been described in the dentate gyrus.82”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [82]
The preserved response to NogoA antibodies suggests that growth factor abnormalities in hypertensive rats might not be clinically relevant.
“This preserved response to NogoA antibodies suggests that the growth factor abnormalities might not be clinically relevant.”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [82]
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- Authors
- Hennigan, A., Callaghan, C. K., Kealy, J., Rouine, J., & Kelly, Á. M.
- Affiliations
- Trinity College Dublin (IE)
- Venue
- Behavioural Brain Research
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 197
- Issue
- 2
- Pages
- 371-377
- ISSN
- 0166-4328 (ISSN-L)
- OpenAlex
- W1987340931
- Cited by
- 51
- References
- 45
- Citations by year
- 2024: 3 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 4 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 3 · 2014: 6 · 2013: 6 · 2012: 3
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Behavioural Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Higher Education Authority
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- genetically hypertensive rats, long-term potentiation, recognition memory, neurotrophic factors, nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, neurotrophin-4, TrkA, TrkB, TrkC, dentate gyrus, synaptic plasticity, learning and memory impairment, hypertension
- MeSH terms
- Analysis of Variance, Animals, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Hypertension, Male, Memory, Nerve Growth Factors, Blotting, Western, Rats, Wistar, Long-Term Potentiation, Dentate Gyrus, Brain-Derived Neurotrophic Factor, Receptor, trkC, Receptor, trkB, Receptor, trkA, Neurotrophin 3, Rats
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