Research: Inflammation can influence nerve signalling

Rossi S, Studer V, Motta C, De Chiara V, Barbieri F, Bernardi G, Centonze D. Inflammation inhibits GABA transmission in multiple sclerosis.Mult Scler. 2012 Mar 14. [Epub ahead of print]

Abnormal glutamate-dependent synaptic excitation contributes to neuronal damage in multiple sclerosis (MS). Little is known about the involvement of the GABA system in this disorder. Here we found that cerebrospinal fluid (CSF) from MS patients with enhanced brain lesions on magnetic resonance imaging inhibited GABA transmission in mouse brain slices. Enhanced IL-1β neuronal action was responsible for this effect, because IL-1β receptor antagonist blocked, and exogenous IL-1β mimicked the synaptic effect of inflamed CSF. Our results provide evidence that focal inflammation in MS perturbs the cytokine milieu within the circulating CSF, resulting in diffuse GABAergic alteration in neurons.

Nerve transmitter there signals using chemicals that can excite or inhibit the excitiment of nerves. The major excitory chemical is glutamate, which is vital for nerve function. But it there is too much excitation it can cause damage to the nerve. GABA producing nerves abut onto nerves that produce glutamate and inhibit glutamate-producing nerves from signalling their nerve impulses. They have found that there is something in the cerebrospinal fluid of MSers/pwMS (whats the term you want let us to use…….have a quick pole Prof G!) that have evidence of active inflammation that blocks GABA signalling, which means there will be more gluatamate signalling, which can be damaging. They believe that a chemical called interleukin 1 triggers this problem.

Interleukin 1 does a great many things and has been called: fibroblast-activating factor (FAF), lymphocyte-activating factor (LAF), B-cell-activating factor (BAF), leucocyte (white blood cell) endogenous mediator (LEM), epidermal cell-derived thymocyte-activating factor (ETAF), serum amyloid A inducer of hepatocyte (liver cell)-stimulating factor (HSP), catabolin, haemopoetin-1 (H-1), endogenous pyrogen (EP. Causing fever), osteoclast-(bone cell) activating factor (OAF), and proteolysis-inducing factor (PIF) and therefore the prospect for specifically targeting this molecule is probably unlikely, because there could be lots of side-effects because it does so many thing.

However, by taking human tissue fluids and then adding them onto animal tissues which can be assayed we can definantively show that things in the brains of MSers/PwMS are not good.

About the author



By MouseDoctor



Recent Posts

Recent Comments