The Believing Brain - Michael Shermer [62]
Of course, we are not aware of the workings of our own electrochemical systems. What we actually experience is what philosophers call qualia, or subjective states of thoughts and feelings that arise from a concatenation of neural events. But even qualia is itself a type of neural binding effect, integrating inputs from countless other neural networks downstream. It really does all come down to the electrochemical process of neuronal action potentials, or neurons firing and communicating with one another, passing information along the way. How do they do this? More chemistry.
Communication between neurons happens in that impossibly tiny synaptic cleft between neurons. When the action potential of a neuron rushes down the axon and reaches the terminals it triggers the release of tiny packets of chemical transmitter substances (CTS) into the synapse. When taken up by the connecting neuron, the CTS act as an EPSP to change the voltage and permeability of the postsynaptic neuron, thereby causing it to fire and propagate its action potential down its axon to its terminals to release its CTS into the next synaptic gap, and so on down the line in a neural network. When you stub your toe the pain signal travels along a circuitry from the pain receptors in the tissues in your toe all the way up to the brain, which registers the pain and processes the signal to other areas of the brain that send additional signals to contract muscles to pull your foot away from the offending object, all at a speed that feels almost instantaneous.
There are many types of CTS. The most common are known as the catecholamines and include dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline). The CTS act like keys for the locks on the postsynaptic neuron. If the key fits and turns, the neuron fires; if it doesn’t the door remains closed and the postsynaptic neuron quiet. After the firing process occurs, most unused CTS go back to the presynaptic neuron where it is either reused or destroyed by monoamine oxidase (MAO) in a process called Uptake I. If there are too much CTS floating around in the synaptic gap, then the rest gets sucked up into the postsynaptic neuron in a process called Uptake II.
Drugs act on synapses and the release of CTS and subsequent uptake processes. Amphetamines, for example, speed up the release of CTS into the synapse, thereby accelerating the neural communication process—that’s why they’re called speed. Reserpine, once commonly prescribed for psychosis, breaks up CTS vesicles in the presynaptic neuron so that the MAO destroys them before they are used, thereby slowing neural networks and controlling mania, hypertension, and other symptoms of an overactive nervous system. Cocaine blocks Uptake I so that the CTS just stay in the synapse and keep the neurons firing away at an accelerated rate, cranking up neural networks into a frenzied state—think Robin Williams with a microphone and an audience; in point of fact, Williams attributes much of his manic comedy in the 1980s to his cocaine addiction. As one of the most common CTS, dopamine is critical to the smooth communication between neurons and muscles, and when there isn’t enough of it patients lose motor control and shake uncontrollably. This is called Parkinson’s disease, one treatment for which is L-dopa, a dopamine agonist that stimulates the production of more dopamine.
How do we build a system from the bottom up, starting with a chemical transmitter substance such as dopamine, and bind the inputs into an integrated belief system? Through behavior. Remember, the primary function of the brain is to run the body and help it survive. One way it does that is through association