The omega-3 fatty acid-derived neuroprotectin D1 limits hippocampal hyperexcitability and seizure susceptibility in kindling epileptogenesis: NPD1 Limits Kindling Epileptogenesis
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PURPOSE: Temporal lobe epilepsy, one of the most common epilepsy syndromes, is characterized by hippocampal hyperexcitability and progressive seizure susceptibility. Omega-3 fatty acids are involved in neuronal excitability and have anticonvulsant properties. We studied the effect of docosahexaenoic acid (DHA) or its derived lipid mediator, neuroprotectin D1 (NPD1, 10R,17S-dihydroxy-docosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid), in evoked seizures using a rapid kindling model of temporal lobe epilepsy. METHODS: DHA or NPD1 was administered in rodents with or without kindling acquisition. Locomotor seizures and evoked epileptiform hippocampal activity immediately after hippocampal stimulations were analyzed. KEY FINDINGS: DHA or NPD1 limits hippocampal electrically induced hyperexcitability. Seizures induced by kindling triggered NPD1 synthesis in the hippocampus. Supplying its precursor, DHA, or direct injection of NPD1 into the third ventricle resulted in attenuation of kindling progression and hippocampal hyperexcitability. SIGNIFICANCE: The significance of NPD1 in temporal lobe epilepsy could open new pathways for understanding the initiation and propagation of seizures and the role this lipid mediator plays in the neuronal network.
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NPD1 is decreased in the CA1 area of hippocampus from Alzheimer's disease, increases after seizures, and attenuates seizure severity progression and hippocampal hyper-excitability in a kindling model of temporal lobe epilepsy.
“NPD1 is decreased in CA1 area of hippocampus from Alzheimer’s disease (Bazan et al., 2011a), increases after seizures (Musto et al., 2011) and attenuates seizure severity progression and hippocampal hyper-excitability in a kindling model of temporal lobe epilepsy (Musto et al., 2011).”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Musto et al., 2011
NPD1 reduced the amplitudes of microseizures in hippocampal layers and limits the development of hippocampal hyper-excitability in a rapid kindling model of temporal lobe epilepsy.
“Also, NPD1 reduced the amplitudes of microseizures in hippocampal layers and limits the development of hippocampal hyper-excitability in a rapid kindling model of temporal lobe epilepsy (Musto et al., 2011) that displays a subtle alteration in hippocampal neuronal plasticity and damage (Morimoto et al., 2004).”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Musto et al., 2011
Seizure progression severity and hippocampal hyperexcitability are attenuated upon intraventricular administration of NPD1.
“Moreover, seizure progression severity and hippocampal hyperexcitability are attenuated upon intraventricular administration of NPD1 [15].”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [15]
Omega-3 essential fatty acid improves neurological outcomes in models of epilepsy and is neuroprotective.
“Recent evidence suggests that omega-3 essential fatty acid improves neurological outcomes in models of epilepsy [14, 15] and is neuroprotective [12, 16, 17].”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [15]
Hippocampal NPD1 pool size increases after seizures.
“Hippocampal NPD1 pool size increases after seizures [15].”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [15]
NPD1 modulates the neuronal network in the CA1 during ictogenesis.
“suggesting that NPD1 modulates the neuronal network in the CA1 during ictogenesis, which is critical in kindling epileptogenesis [15] and in human and experimental TLE [48].”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [15]
Intra-cerebral NPD1 administration reduces seizure susceptibility in a kindling mouse model.
“Intra-cerebral NPD1 administration reduces seizure susceptibility in a kindling mouse model [15]”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [15]
Previously, hippocampal hyperexcitability followed by electrical stimulation in the CA1 region was observed to be attenuated by NPD1.
“Previously, we observed that hippocampal hyperexcitability, followed by electrical stimulation in the CA1 region, is attenuated by NPD1 [15].”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [15]
After intra-ventricular administration of NPD1 during kindling epileptogenesis, NPD1 limits progression of seizure severity and hippocampal hyper-excitability, including abnormal patterns of the electrical seizures.
“After intra-ventricular administration of NPD1 during kindling epileptogenesis, we observed that NPD1 limits progression of seizure severity and hippocampal hyper-excitability, including abnormal patterns of the electrical seizures [15]”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [15]
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- Authors
- Musto, A. E., Gjorstrup, P., & Bazan, N. G.
- Affiliations
- Louisiana State University (US)
- Corresponding author
- Bazan, Nicolas G.
- Venue
- Epilepsia
- Publisher
- Wiley
- Published
- 2011-05-13
- Volume
- 52
- Issue
- 9
- Pages
- 1601-1608
- ISSN
- 0013-9580 (ISSN-L)
- OpenAlex
- W1577144537
- Cited by
- 71
- References
- 55
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 5 · 2023: 1 · 2022: 6 · 2021: 5 · 2020: 5 · 2019: 5 · 2018: 8 · 2017: 2 · 2016: 8 · 2015: 4 · 2014: 6 · 2013: 6 · 2012: 5
- FWCI
- 3.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Epilepsia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (RR016816)
- U.S. Public Health Service
- National Institute of Neurological Disorders and Stroke (R01NS023002)
- National Center for Research Resources (P20RR016816)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Physiology › Diet and metabolism studies
- Keywords
- neuroprotectin D1, omega-3 fatty acids, docosahexaenoic acid, temporal lobe epilepsy, kindling, epileptogenesis, hippocampal hyperexcitability, seizure susceptibility, lipid mediators, anticonvulsant activity
- MeSH terms
- Animals, Biophysics, Disease Models, Animal, Docosahexaenoic Acids, Drug Administration Routes, Electric Stimulation, Electroencephalography, Epilepsy, Temporal Lobe, Hippocampus, Kindling, Neurologic, Male, Mice, Inbred C57BL, Rats, Wistar, Neuroprotective Agents, Mice, Rats
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