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Inflammation inhibits GABA transmission in multiple sclerosis
Silvia Rossi1, Valeria Studer, Caterina Motta
1Clinica Neurologica, Dipartimento di Neuroscienze, Università Tor Vergata, Rome, Italy.
Multiple Sclerosis (Houndmills, Basingstoke, England)
|March 16, 2012
Summary
Cerebrospinal fluid from multiple sclerosis (MS) patients with active brain lesions inhibits GABA transmission. This effect is mediated by Interleukin-1 beta (IL-1β), indicating inflammation alters neuronal function in MS.
Area of Science:
- Neuroscience
- Immunology
Background:
- Multiple sclerosis (MS) involves abnormal glutamate-dependent neuronal excitation and damage.
- The role of the gamma-aminobutyric acid (GABA) system in MS pathogenesis is poorly understood.
Purpose of the Study:
- To investigate the involvement of the GABA system in MS.
- To determine the impact of cerebrospinal fluid (CSF) from MS patients on GABAergic transmission.
Main Methods:
- Analysis of CSF from MS patients with active brain lesions.
- Electrophysiological recordings of GABA transmission in mouse brain slices.
- Assessment of Interleukin-1 beta (IL-1β) involvement using receptor antagonists and exogenous IL-1β.
Main Results:
- CSF from MS patients with active lesions inhibited GABA transmission in mouse brain slices.
- This inhibition was attributed to enhanced Interleukin-1 beta (IL-1β) activity.
- IL-1β receptor antagonist blocked the inhibitory effect, and exogenous IL-1β mimicked it.
Conclusions:
- Focal inflammation in MS alters the cytokine profile in CSF.
- This altered cytokine milieu, specifically IL-1β, leads to widespread GABAergic dysfunction in neurons.
- These findings highlight a novel mechanism of neuronal dysfunction in MS.
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