Synaptic Zn2+ and febrile seizure susceptibility
- Author(s)
- Reid, CA; Hildebrand, MS; Mullen, SA; Hildebrand, JM; Berkovic, SF; Petrou, S;
- Details
- Publication Year 2017,Volume 174,Issue #2,Page 119-125
- Journal Title
- British Journal of Pharmacology
- Publication Type
- Journal Article
- Abstract
- Zn2+ , the second most prevalent trace element in the body, is essential for supporting a wide range of biological functions. While the majority of Zn2+ in the brain is protein-bound, a significant proportion of free Zn2+ is found co-localized with glutamate in synaptic vesicles and is released in an activity-dependent manner. Clinical studies have shown Zn2+ levels are significantly lower in blood and cerebrospinal fluid of children that suffer febrile seizures. Likewise, investigations in multiple animal models demonstrate that low levels of brain Zn2+ increase seizure susceptibility. Recent work provides human genetic evidence that disruption of brain Zn2+ homeostasis at the level of the synapse is associated with increased seizure susceptibility. In this review we will explore the clinical, functional and genetic data supporting the view that low synaptic Zn2+ increases cellular excitability and febrile seizure susceptibility. Finally, the review will focus on the potential of therapeutic Zn2+ supplementation for at risk patients.
- Publisher
- Wiley
- Research Division(s)
- Cell Signalling And Cell Death
- PubMed ID
- 27771943
- Link To PubMed Central Version
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5192799/
- Publisher's Version
- https://doi.org/10.1111/bph.13658
- NHMRC Grants
- NHMRC/1105023,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2016-10-26 01:19:30
Last Modified: 2018-07-05 08:37:35