Last week, we were discussing the intersection of the brain with the mind. One way of describing the structure is the brain is the computer and the mind is software. The brain can't do anything without a program to run it and the program can't be executed without a computer to operate on.
This analogy has been used a number of times. It paints a reasonable, but flawed, picture of how the whole thing works.
The flaws arise from brain plasticity - the ability of different parts of the brain to be rewired and take on entirely new tasks if necessary.
It also doesn't address the peripheral nervous system and the role it plays.
That said, the mechanics of brain function are reasonably well understood. Signals are passed from neuron to neuron through synapses. Electrical impulses enter dendrites attached to the cell body, propagate across the neuronal membrane and down the axon and are transmitted to a receiving neuron across a synaptic cleft.
Synapses come in two forms - electrical and chemical. The direct transmission of an electrical signal is rare and requires a very small synaptic cleft. Most synapses involve the chemical compounds called neurotransmitters.
Neurotransmitters are synthesized within the sending neuron and stored in vesicles prior to being released into the synapse.
One way of envisioning the pre-synaptic neuron is a bag filled with thousands of water balloons or a mass of soap bubbles. Each vesicle is filled and waiting to merge with the external membrane whereupon it dumps its contents into the synapse. It's a bit like a soap bubble popping and releasing the air within.
Within the synapse, a neurotransmitter is free to move and can face any number of possible fates. Ideally, for the purpose of signal transmission, it crosses the small gap between the neurons to engage with a receptor on the surface of the post-synaptic neuron. In doing so, it can instigate a series of reactions which results in a nerve impulse being generated.
The signal carries on.
However, each neurotransmitter is like a key and can only act upon an appropriate receptor or lock.
The neurotransmitter and receptor site recognize one another. If the receptor site is damaged or already occupied, the neurotransmitter does nothing and floats away.
The neurotransmitter might also be swept from the synapse before engaging with the receptor or might react with other molecules present. Both result in a loss of signal strength.
For proper function of the brain, a multitude of receptor sites need to be turned on at the same time to generate a strong signal or a burst of activity. As soon as the neurotransmitter has done its job of stimulating the receiving neuron, it is discarded from the receptor site thereby clearing the field for the next wave of neurotransmitter molecules.
Further, since the electrical signal carried by each neuron is always the same voltage, the strength of a signal is not determined by the size of the electrical pulse but the frequency. Strong signals involve the rapid firing of a neuron. It is also possible for a neurotransmitter to inhibit a cell resulting in no or very few electrical pulses.
The ability to speed up or slow down the rate at which each neuron fires electrical impulses along its length lies at the heart of how the neurotransmitters and the brain work. Collectively, the total of all of the electrical pulses occurring at varying rates results in what we call our thoughts.
Drugs can influence the actions of our neurons in a number of different ways. Some interfere with the storage vesicles causing them to leak their contents before they engage with the neuron's membrane. They are like a water balloon with a small hole - by the time you want to throw it there is nothing left inside.
Others drugs replace the contents of the vesicle thereby allowing the neuron to release the contents but with no action. Some drugs even create empty vesicles with no content to be released at all. And some drugs prevent the vesicles from binding to the neuronal membrane making it impossible for them to release their contents. (Imagine a water balloon which refuses to pop.)
But many of our therapeutic agents act within the synaptic cleft by inhibiting the enzymes which degrade the neurotransmitters once they have activated a receptor site. Having triggered a response on the receiving neuron and been swept away, neurotransmitters are typically broken down by enzymes. Many antidepressants - such as Mono-Amine Oxidase Inhibitors or MAOIs - act by preventing enzymes from destroying these molecules.
This allows a large concentration of a neurotransmitter to accumulate in the synapse resulting in the rapid and repeated firing of the receiving neuron.
Understanding the way drugs interact with the brain is one of the more interesting and challenging problems in science today.
