Before continuing, a glossary of terms that will be used in this article might be helpful:

Synapse
A gateway of communication between a neuron and another cell type, across which signals are carried in a chemical form, by neurotransmitters. Signals travel down neurons as electrical impulses, but are unable to cross synapses in this form.

Neurotransmitter
A chemical that carries signals between a neuron and another cell, across a synapse.

A neurotransmitter is stored in a small package at the end of a neuron, near the edge of a synapse. On the surface of the next cell are special receptors for the neurotransmitter. When the neurotransmitter combines to its receptor, a chain of events is triggered that causes the signal to be transferred over.

A neurotransmitter can be excitatory, meaning that it triggers the next cell to become active; or inhibitory, meaning that it suppresses activity in the next cell.

Gap junction
A specialized connection between certain types of cell, which allows ions such as calcium (Ca2+), sodium (Na+) and potassium (K+) to pass freely between cells.

Hemichannel
A gap junction is made of two hemichannels, which connect to each other across the space between the two cells.

Ion channels
Pores that help to control electrical activity in cells, by allowing the flow of ions such as calcium (Ca2+), sodium (Na+) and potassium (K+) into or out of the cell.

What is the link between stroke and epilepsy?
Glutamate is the main excitatory neurotransmitter in the brain, and it combines to a receptor known as NMDA. The combining of glutamate to its receptor triggers the opening of ion channels. This allows particular ions to enter and leave the cell, generating an electrical signal.

Under normal circumstances, once glutamate has activated a cell in this way, it is cleared from the synapse into surrounding cells, by special transporters. However when oxygen to the brain is cut off, as in a stroke, this no longer happens and glutamate remains active. One consequence of this is that a stream of calcium ions passes through the glutamate receptor into the cell. This causes cell death.

In addition, both the stroke itself and the increased glutamate can also cause the uncontrolled opening of hemichannels in the brain. This causes the uncontrolled flow of ions (particularly calcium) between cells, and ultimately cell death.

It was whilst exploring the effect upon hemichannels that researchers from the University of British Columbia and the Vancouver Coastal Health Institute made an exciting discovery about stroke and epilepsy.

They examined the effect of glutamate at slightly lower levels than those reached during stroke, upon hemichannels in neurons. Interestingly, they found that more moderate activation of glutamate receptors opened the hemichannels, but caused seizure activity, not cell death. They also noticed that the seizures themselves caused hemichannels to open.

When the scientists repeated the experiment, but blocked the function of the hemichannels, they noticed that the seizure activity in the neurons was markedly reduced.

These results are very exciting, as not only do they increase our understanding of epilepsy, but also show hemichannels to be a new target for drug treatment. The researchers are confident that hemichannel blockers will soon be in development.

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