Wednesday, August 25, 2010

Stuttering and Neurotransmitters

The brain consists of neurons which are basically nerve cells organized to perform specialized functions such as speech. In addition, there are chemicals called neurotransmitters that help to transfer messages in the form of electrical impulses from neuron to neuron.

To understand what happens in the brain when a person stutters as well as how various medications work to reduce stuttering, it is first important to learn about the function of neurons and neurotransmitters.

As shown in the top diagram in the picture at the left, the neuron consists of a cell body, an axon, and numerous branching dendrites at both ends. Messages pass through the brain by traveling through these neuronal structures, beginning as an electrical impulse that is picked up by one of the dendrites of the neuron. Next, the impulse moves through the cell body then travels down the axon. By the time it reaches the end of the axon the electrical impulse is changed to a chemical impulse in the form of a neurotransmitter. These neurotransmitters, released by the axon carry messages from one neuron to another. When the message is picked up by the dendrite of a neighboring neuron, it is changed back to an electrical impulse and the process begins again. Since neurons do not touch each other, the neurotransmitter passes from one neuron to the next through a narrow gap, called a synapse.

Neurotransmitters are specifically shaped so that when they pass from a presynaptic neuron into a synapse, they can chemically bind onto certain sites, called receptors, on a neighboring postsynaptic neuron. Neurotransmitters can fit a number of different receptors, but receptor sites can only receive specific types of neurotransmitters. Upon binding to a receptor site of a neuron, the chemical message of the neurotransmitter may lead to an electrical impulse that continues on its way toward the next neuron, or it may stop where it is. In either case the neurotransmitter releases from the receptor site and floats back into the synapse. It is then removed from the synapse in one of two ways. The neurotransmitter may be broken down by a chemical called monoamine oxidase, or it may be taken back in by the presynaptic neuron that originally released it. This last process is called neurotransmitter reuptake.

The current hypothesis regarding stuttering is that it is caused by excessive dopaminergic activity in the motor neuron section of the brain. The bottom diagram of the picture above shows the detail of a neuronal synapse. The neurotransmitter, dopamine, is released from the dendrite of a presynaptic neuron at the left of the diagram and binds to a dendrite of a postsynaptic neuron (shown as a "tail") in the middle of the diagram.  Dopamine is an excitatory neurotransmitter.  On the right is another dendrite which releases GABA that happens to be an inhibiting neurotransmitter. What this means is that when GABA binds to the postsynaptic neuron, it inhibits or blocks the action of dopamine and hence modulates its excitatory action. So if stuttering is caused by excessive dopaminergic activity, we have several courses of action. The first is to directly block dopaminergic activity in various ways and the second is to increase GABAergic activity by various means.

Dopamine is an agonist, which is a chemical that binds to a receptor of a neuron and triggers a response by that neuron. In addition to dopamine, there are other neurotransmitters in the brain that act as agonists.  Also, drugs introduced exogenously into the brain may act as agonists.  On the other hand, GABA is an antagonist in that it blocks the action of the agonist. And similarly to an agonist, there are other neurotransmitters that are antagonists and drugs may act as antagonists.
In the next post we will discuss drugs that may affect dopaminergic activity in different ways.

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