Abstract
During neuroinflammation T-cells invade the CNS, and may lead to the development and progression of several pathologies, of which multiple sclerosis is the most common. In these pathologies neuroinflammation is often associated with cognitive dysfunction. Using mouse hippocampal slices, we show here that CD4(+)CD25(-) T-cells inhibit long-term potentiation (LTP) induced by high-frequency stimulation. The T-cell-mediated inhibition of LTP can be prevented by blockade of gamma-aminobutyric acid (GABA)(A) receptors. These findings provide additional insight into the multiple functions of T-cells in CNS pathologies.
Publication types
- Research Support, N.I.H., Extramural
- Research Support, Non-U.S. Gov't
MeSH terms
- Animals
- CD4-Positive T-Lymphocytes / physiology*
- Cytokines / metabolism
- Electric Stimulation
- Electrophysiology
- GABA Antagonists / pharmacology
- GABA-A Receptor Antagonists
- Hippocampus / physiology*
- Immunohistochemistry
- In Vitro Techniques
- Inflammation / pathology
- Interleukin-2 Receptor alpha Subunit / physiology*
- Long-Term Potentiation / physiology*
- Male
- Mice
- Mice, Inbred C57BL
- Picrotoxin / pharmacology
- Synapses / drug effects
- Synapses / physiology
- gamma-Aminobutyric Acid / physiology
Substances
- Cytokines
- GABA Antagonists
- GABA-A Receptor Antagonists
- Interleukin-2 Receptor alpha Subunit
- Picrotoxin
- gamma-Aminobutyric Acid