The soma of a neuron is electrically charged reacting to electrical disturbances from either sensory or neighbouring neurons via its dendrites. These brief changes of electrical voltage (action potentials) are conducted away from the soma and along the neurons axon. Action potentials travel quickly to the tip of the axon (synapse) where it stimulates the secretion of a particular neurotransmitter. The neurotransmitter acts as a chemical message able to bridge the fluid filled synaptic gap between neighbouring neurons so that communication between cells can occur.
The amount of neurotransmitter released into the synaptic gap depends on the frequency of the incoming action potential. On reaching compatible receptors on the postsynaptic neuron the neurotransmitter has an effect on the neighbouring cells action potential, either creating anew or increasing the frequency of an already present action potential (excitation) or suppressing action potential activity (inhibition). Crucially the neurotransmitter only has a short time to stimulate the receptors as it is quickly taken back by the presynaptic neuron in the process of re-uptake.
In this way the brain can receive incoming messages from the external world, process the information and transmit instructions of response to the body which reacts appropriately. Understanding the biological behaviour of neurons and applying this knowledge to symptoms of neurological disease has led to some important discoveries and theories regarding the nature of the brain and its relationship to human behaviour.
For example neuronal activity can explain why the breaking or blocking of a blood vessel (a stroke) and resulting lesion in a region of the motor cortex can cause loss of speech and use of corresponding limbs, neurons are no longer able to communicate to the appropriate motor neurons (Toates, 2007). The inherent adaptability or plasticity of the brains neurons which enables other brain regions to take over a damaged region (Mareschal, Johnson and Grayson, 2004) also offers an explanation for the recovery of bodily function seen in stroke patients.
However the vast differences in levels and speed of recovery in stroke patients indicates that the creation of new connections is most likely affected by many variables placing limits on theories of cause and effect. In recent years non-invasive methods such as positron emission tomography (PET) and magnetic resonance imaging (MRI) have revolutionised biological psychology research. Researchers are now able to provide visual evidence of participants neuronal activity as cognitive and motor tasks are performed.
This has armed psychology with credible biologically based data with which to generate hypothesis regarding the relationship between neurons and human behaviour. However Toates (2007) warns that the interpretation of material data in itself may limit the reliability of its use as evidence. A further area of psychological interest enriched by our understanding of neuronal systems is that of mood disorders.
For example depression is argued to be caused by abnormalities in the neurotransmission of key neural systems including the serotonergic synapse which results in inadequate levels of serotonin being present in the nervous system (Toates, 2007). The theory for a neurochemical cause of depression is supported through the use of antidepressants which inhibit the re-uptake of serotonin and increase serotonin levels (Martin, Carlson and Buskit, 2010).
This example illustrates how viewing a psychological state at the level of biology can be useful in both increasing understanding and developing interventions A strictly biological explanation for mood disorders therefore appears logical and valid but there are limits to this approach. For example if depression is simply a case of not enough of the right neurotransmitter then we could expect antidepressants to be prescribed and depression to disappear but for an estimated 35-50% of people antidepressants are ineffective (Royal College of Psychiatrists, 2012).
There is also the opposite phenomenon of placebos successfully treating depression which suggests that the idea of taking pharmaceuticals or perhaps the very act of getting medical support itself has a psychological impact which must somehow cause biochemical changes in the brain. The idea that conscious awareness can influence physiological processes in the brain is also supported by cases of psychoactive drug use . i. e. heroin where an appropriate social context is needed to experience their effects (Toates, 2007).
Psychologists are mostly in agreement that biological processes do not solely determine psychological processes but that the two are in fact reciprocal in nature, interacting and influencing each other over time and in different contexts. In other words a person may have a genetic predisposition for low levels of serotonin leading to depression but the biochemical state of depression may also be a consequence of an environmental experience.
This is supported by Anisman and Zacharko (1982) who found that depression is often proceeded with a high frequency of stressful life events, although this does not equate to a cause and effect relationship. To conclude this essay has highlighted the importance of recent technological advancements in providing scientifically reliable evidence to develop and support our understanding of neurological processes.
However it has also revealed the flaws of the outdated extreme reductionist view that all psychological phenomenon begin at the level of biology and are determined by physiological causes. Human behaviour is clearly too complex for this and in order to gain a more reliable and useful picture, must always be considered in a social and cultural context. At this point we may be closer to knowing how neurons communicate but the elusive cause and effect relationship between brain and behaviour is far from ready to be fully understood.