Researchers in China have discovered a new way in which epilepsy can develop, and this revolves largely around the structure of neurons and their ability to adapt to their environment. At this point, therefore, it would be useful to have a recap on neuronal structure.

Neurons vary greatly in structure depending on their location and function, but typically they have three parts - a cell body or 'soma', an axon and many dendrites - made largely of a protein called actin. See the diagram below:

The cell body is the co-ordinating centre for the neuron's growth and activity, and is where information from the external environment, for example other neurons, is processed. Dendrites carry this information to the cell body in the form of electrical impulses, and the axon transmits information away from the cell body in the same way.

Dendrites and axons are the means by which neurons communicate with each other, and they do this via gateways called synapses. Synapses can either be excitatory or inhibitory, and neurons have an ability to alter the number and types of synapse they form, depending on their environment. This is thanks to the actin in their make-up, which is highly versatile. If too many excitatory synapses are present at one time, neurons risk becoming hyperexcitable and seizures can result.

Each axon / dendrite is able to form several synapses at once, and they do this by developing tiny spine-like extensions from their terminals. These spine-like extensions are formed from layers of actin and their growth is partly controlled by a protein called actin-related protein 2/3 (ARP2/3). In turn, ARP2/3 is regulated by another protein known as neuronal Wiskott-Aldrich syndrome protein (N-WASP). If the level of N-WASP in the brain is decreased, this will have a direct effect upon the amount of ARP2/3, which will also decrease.

A study published earlier this year in the Journal of Biological Chemistry, showed that if the function of either N-WASP or ARP2/3 is blocked in the neurons of the hippocampus, fewer spine-like extensions develop and the number of excitatory synapses decreases. This suggests that the synapses built by ARP2/3 are largely excitatory in nature.
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More recently, the aforementioned researchers in China studied the brains of forty surgical patients with intractable epilepsy (IE) - i.e. epilepsy that has not responded to medication - and compared them with 20 control (or 'normal') brains. Interestingly they found that in the temporal lobes of all of the IE brains, there were greater amounts of N-WASP and therefore ARP2/3 present than in the controls.
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Given the results of the previous study, it is feasible that increased N-WASP and therefore ARP2/3 caused an abnormally high number of excitatory synapses to develop, leading to epilepsy in the IE brains studied.

This is an exciting discovery, because it identifies excess N-WASP, and therefore ARP2/3, as a potential cause of epilepsy. New treatments that target and decrease N-WASP and ARP2/3 to normal levels could possibly be developed in the future.