Nerve cells, called neurons, are one of the building blocks of behaviour. It is estimated that there are between 10 and 100 billion neurons in the nervous system and that neurons make 13 trillion connections with each other. The neurons send electrochemical messages to the brain so that people can respond to stimuli—either from the environment or from internal changes in the body.

The following video explains how neurotransmitters were discovered.

The process by which these messages are sent is called neurotransmission.  The electrical impulse that travels along the body of the neuron is called an action potential. When an action potential travels down the body, or axon, of the neuron, it releases neurotransmitters that are stored in the neuron’s terminal buttons. The neurotransmitters are then released into the gap between the neurons – called the synapse. The synaptic gap is an incredible one-millionth of a centimeter! Neurotransmitters are the body’s natural chemical messengers that transmit information from one neuron to another. After crossing the synapse, the neurotransmitters fit into receptor sites on the post-synaptic membrane, like a key in a lock. Once the message is passed on, the neurotransmitters are either broken down by an enzyme or reabsorbed by the terminal buttons, in a process called reuptake.

Neurotransmitters have been shown to have a range of different effects on human behaviour. In fact, neurotransmission underlies behaviour as varied as mood, sleep, learning and memory, sexual arousal, and mental illness. The table below, which highlights just a few neurotransmitters, gives an idea of the variety of behaviours that are influenced by these neurochemicals.

Neurotransmitters

Because neurotransmitters fit tightly into receptor sites, like a key in a lock, drugs have been developed to either simulate the neurotransmitter if there is not enough of a specific neurotransmitter or to block the site if it is excessive. The application of such research has improved the lives of many people.

There has been criticism of reducing the explanation of behaviour to the workings of neurotransmitters alone. It is said to be reductionist. Can a complex human behaviour like falling in love with someone be attributed to a simple “love cocktail” of dopamine and norepinephrine? Can your mood during the summer holidays be attributed simply to serotonin levels? Once again, most psychologists consider that neurotransmitters play a role, but do not rely solely on neurotransmission to explain behaviour.

There are many strengths to carrying out an experiment like the one by Rogers and Kesner.  First, the procedure is very simple.  In this way, the study can be easily replicated and the reliability of the results can be tested. In addition, the experiment was highly controlled.  The only difference in the conditions is the level of acetylcholine.  To make sure that receiving the injection was not the factor that influenced the rats’ ability to run the maze, the saline solution was injected. In this way, the researchers could rule out the placebo effect as a reason for their results.

However, there are also limitations to the study.  It is not clear to what extent we can generalize the findings from rats to human beings.  However, researchers have found that there are lower levels of acetylcholine in Alzheimer’s patients. 

In a study by Antonova et al (2011), researchers demonstrated that blocking acetylcholine receptors in the brain can affect spatial memory tasks in humans. In their study, they used a sample of twenty healthy male adults, with a mean age of 28 years old. The study used a double-blind procedure and participants were randomly allocated to one of two conditions. They were injected with either Scopolamine or a placebo.

The participants were then put into an fMRI where they were scanned while playing the "Arena task."  This is a rather complex virtual reality game in which the researchers are observing how well the participants are able to create spatial memories.   The goal is for the participants to navigate around an "arena" with the goal of reaching a pole. After they have learned where the pole is located, the screen would go blank for 30 seconds.  During this time, the participants were told to actively rehearse how to get to the pole in the arena. When the arena reappeared, the participant was now at a new starting point in the arena. The participants would have to use their spatial memory to determine how to get to the location of the pole.

The procedure was repeated three to four weeks later, each participant received the other treatment.

The researchers found that when participants were injected with scopolamine, they demonstrated a significant reduction in the activation of the hippocampus compared to when they received a placebo. It appears that acetylcholine could play a key role in the encoding of spatial memories in humans, as well as in rats.

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