The brain's capacity to learn and make memories is an ongoing focus of research, but the precise mechanisms involved are not clearly understood.

In a recent breakthrough, scientists at the Duke Medical Centre, Durham, USA, have identified a protein that could play a vital part, not only in the formation of memories, but also in the development of epilepsy. The protein, called myosin Vb, was already known to play an important role in the brain's synapses, but its precise function had not been established.

Synapses are essentially narrow gaps between two neurons, or between a neuron and a different type of cell, across which information is transported. They can be either excitatory or inhibitory, meaning that the 'recipient' neuron / cell will be stimulated or suppressed respectively.

Electrical signals that travel down neurons cannot cross synapses. To overcome this, when a signal reaches the end of a particular neuron (neuron 1), a substance called a neurotransmitter is released into the synapse. The neurotransmitter takes the information across the synapse in a chemical form. The Recipient cell / neuron (we'll call this 'neuron 2') has special receptors for the neurotransmitter on its surface.

When the neurotransmitter combines with these receptors, the signal is converted back to an electrical form, and this either continues its journey down neuron 2, or exerts specific effects upon a recipient cell. The more neurotransmitter receptors that are present for the neurotransmitter to combine with, the more amplified the electrical signal in neuron 2, or the greater the effect seen in a recipient cell, will be. The synapse is then said to have been strengthened.

This is believed to form the basis of memory. For example if two neurons fire at the same time in response to different stimuli, e.g. a person's face and their name, the synapses between them grow stronger. In this way this a person's face becomes linked to a particular name. Similarly, in order to learn new associations, such as where the person is standing, these neurons form stronger synapses with the cells that compute these associations. In this way, bundles of information become tied together.

The aforementioned scientists at Duke Medical Centre discovered that myosin Vb is, in fact, responsible for transporting new neurotransmitter receptors into position on neuron 2 / recipient cells and strengthening synapses.

In a series of experiments using neurons in the hippocampus (an important memory centre in the brain), they found that mysosin Vb became activated when an electrical signal crossed a particular synapse.

They observed that one end of the myosin Vb molecule was attached to a structural protein in neuron 2, known as actin, whilst the other end carried a 'packet' called an endosome, containing neurotransmitter receptors. The two proteins (actin and myosin) interacted with each other and the new receptors were moved into position on the membrane of neuron 2.

When the researchers measured the electrical current in neuron 2, they found that it was markedly greater than in neuron 1. Moreover, when the activity of myosin Vb was blocked, new receptors were prevented from moving to the surface of neuron 2 and the electrical signal in both neurons remained the same. This indicates that myosin is necessary for strengthening nerve connections.

The significance of these findings is enormous. Not only could myosin Vb be a new drug target for conditions such as Alzheimer's disease, where memory is severely affected, but the scientists suspect that myosin Vb plays a role in many other conditions, including epilepsy.

How might myosin Vb cause epilepsy? Seizures are caused by overexcitability of neurons in the brain. In theory, if myosin Vb function is defective for some reason, and too many neurotransmitter receptors are moved into position on neuron 2, synapses will be strengthened too much, causing neuron 2 to fire excessively. Alternatively, it could be that too few receptors are moved into position in inhibitory synapses, meaning that the signal fails to counteract the excitation of certain neurons.

What about uncontrolled seizures and their detrimental effect upon memory? Could myosin Vb be also be the vital link in this process?

If further research confirms the role of myosin Vb in epilepsy, it could become an exciting target for the development of new treatments for this condition.

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