As a result of ever-changing conditions and environments, humans have evolved to adapt. Evolution has changed how we respond to fear. Fear can be defined as an intense negative emotion when an organism encounters a threat or dangerous situation (Gullone, 2020). In humans, fear can be displayed in multiple ways. For example, physiological symptoms of fear can include but are not limited to chest pain, shortness of breath and an increased heart rate (Fritscher, 2020). The individual may also feel overwhelmed or distressed. This fear can often manifest itself into phobias, an anxiety disorder involving the feeling of fear and distress whilst also incorporating avoidance behaviour to reduce the intensity of negative emotions (Eaton, Bienvenu & Miloyan, 2018). Consequently, phobias can result in freeze, flight, fight or fright reactions (Bracha, 2004). Phobias can be classified into three categories: specific phobias, agoraphobia and social phobias (American Psychiatric Association, 2013). Specific phobias can be sub-categorized into the four categories of the natural environment, animal, situational and blood-injection-injury types (LeBeau et al., 2010). Phobias can significantly damage a person’s quality of life if triggered by a common stimulus, for example, hydrophobia (the fear of water). As a result, it is essential to understand the causes of fear and consequently phobias. Theoretically, human evolution should have created a way for us to minimise or remove fear as humans are intelligent and versatile enough to survive in a vast range of environments. This essay will therefore discuss the neurological explanations of fear and phobia behaviours and their limitations and applications by looking at the role of the amygdala.
In general, the most common area associated with fear and phobias is the amygdala, located at the base of the brain, specifically the medial temporal lobe. Research suggests that the amygdala plays a large role in the detection of fear with it often being an essential component in identifying facial expressions (Öhman, 2005), thus explaining why individuals with social phobias are triggered by the presence of faces (for example large crowds). In addition, the amygdala plays a significant role in fear conditioning, which works in a similar way to classical conditioning – the amygdala causes an association with a negative stimulus which induces a fear response in the individual; this is what leads to a phobia being formed. Through the use of fMRI studies, Goossens et al. (2007) found increased levels of baseline amygdala activity in participants before being exposed to a phobic stimulus. This research suggests that the amygdala may influence fear conditioning as well as suggesting that subcortical structures can be changed as a result of exposure therapy. In addition, the use of fMRI imaging increases the reliability of the results as it is a standardised and objective technique. The amygdala has also been shown to be involved in memory consolidation – more specifically the basolateral amygdala (McIntyre, 2003). This can be done by neurone excitability via the collective efforts of dopamine, cholinergic and beta-2 adrenergic receptors, which cause the activation of phospholipase C resulting in the inhibition of potassium-voltage gated channels that conduct M current; the M current regulates neurone excitability (Schroeder et al., 2000). When a neurone becomes excitable, the chances of a memory being consolidated is improved (Young & Thomas, 2014). These results, therefore, highlight the role of the amygdala in the production and storage of phobias. The following results could be applied as to why phobias are difficult to extinguish after the association between the phobic cue and the feeling of fear has been made.
In addition to the role of the amygdala itself, it can also cause the secretion of hormones and neurotransmitters that influence behaviour. There is research to suggest that these neurotransmitters and hormones are part of the mechanism of fear and reinforcement. For example, dopamine (a hormone and neurotransmitter required for reward processing) is released should avoidance behaviour occur. Research from Gentry, Lee & Roesch (2016) found that when looking at dopamine levels in rats, there was a higher release of dopamine during avoidance and reward behaviour. Similar results have also been found in mice (Menegas et al., 2018). When engaging in avoidance behaviour, the secretion of dopamine causes the individual to feel pleasure from not engaging with the phobic stimulus. As a result, the avoidant behaviour is reinforced as the individual can avoid the distress and negative emotions related to the phobic stimulus. As mice and rats can be genetically similar to humans, some generalisations can be made regarding the role of dopamine as a reinforcing agent. However, it should not be taken as concrete evidence as factors such as previous experiences and complex emotions cannot be considered.
Another set of neurotransmitters that are involved in a response to phobias are those that cause the ‘fight-or-flight’ response- this occurs when an individual encounter’s a phobic stimulus (Bracha, 2004). The fight-or-flight response can be defined as a physiological response to a stimulus perceived as harmful in order to aid survival. The fight-or-flight response is controlled by the autonomous nervous system resulting in responses such as increased heart rate and respiratory rate and decreased digestion. Upon seeing a phobic stimulus, the sympathetic nervous system activates physiological changes in the autonomous nervous system. The amygdala activates a neural response in the hypothalamus which is soon followed by the secretion of adrenocorticotropic hormone from the adrenal glands which encourages the production of epinephrine (adrenaline) and thus, cortisol in order to create more energy (McCarty, 2016). There is research to suggest that individuals that suffer from social phobias, may exhibit signs of increased levels of adrenaline and noradrenaline (Van Zijderveld et al., 1991) for example, shaking. In addition, more recent research has shown norepinephrine (noradrenaline) to play a vital role in the identification of fearful stimuli. Onur et al. (2009) used 18 healthy participants in a double-blind trial and administered reboxetine (a type of norepinephrine reuptake inhibitor) or a sugar placebo – the use of reboxetine encourages the uptake of norepinephrine in the synapse rather than presynaptically. Through fMRI imaging, it was shown that the use of reboxetine produced a response via the basolateral amygdala in response to fearful stimuli. It could therefore be suggested that the disinhibition of internal norepinephrine could be a reason for an exaggerated reaction from the basolateral amygdala should fear stimuli be encountered. Although this research initiative focuses on the role of norepinephrine in stress-related disorders such as post-traumatic stress disorder, the research could explain why people with phobias may experience certain symptoms such as shaking and sweating.
There is also evidence to suggest that Hebbian synaptic plasticity is also a factor in fear detection. Originally suggested by Donald Hebb in 1949, Hebbian theory claims that ‘neurones that fire together, wire together (Chechik & Horn, 2000). The main concept of Hebbian theory is that the persistent and repeated stimulation of a postsynaptic cell from a presynaptic cell causes an increase in synaptic effectiveness (Hebb, 2005). Some research has shown that the Hebbian theory can be used to explain fear acquisition and memory consolidation. Langwieser et al., (2010) investigated the role of postsynaptic voltage-gated calcium channels involved in the thalamus-amygdala pathway in mice; more specifically the Cav1.2 channels (these channels could possibly be involved in the process of Hebbian plasticity). Through the use of auditory fear conditioning, the study found that when these pathways are blocked pharmaceutically (by a class of calcium blockers called isradipine), the fear acquisition was minimised due to the blocking of Cav1.2 channels. Consequently, this research could provide evidence for the use of voltage-gated calcium channels in Hebbian plasticity in the amygdala pathway, and therefore fear acquisition. It could provide possible biological treatments for people with phobias through the use of calcium channel blockers. However, this area would have to be thoroughly researched as present research use mice and therefore may lack external validity when generalising to human neurological processes. There is also cause to believe that N-methyl-d-aspartate receptors (NMDARs) are associated with Hebbian plasticity as they allow for an influx of calcium, inducing long-term potentiation. However, there is a type of long-term potentiation that requires NMDARs which occur in the lateral nucleus of the amygdala (Fourcaudot et al., 2009). This could suggest that fear acquisition is not due to Hebbian plasticity as the depolarisation of the postsynaptic neurone is not required. It could be possible for this research to influence extensive research in the role of Hebbian plasticity and phobia acquisition.
There is no question that the acquisition of phobias can be largely influenced by the role of neurological factors as stated above. In addition to research, there is also evidence to support these claims by looking at deficits when these areas are damaged. For instance, damage to the cortical areas of the brain, more specifically areas in the limbic system can result in severe emotional variations (Bear, Conors & Paradisco, 2007). There is also evidence to suggest that damage to the amygdala can inhibit a person’s ability to identify facial expressions and therefore fear. Patient SM endured a rare form of bilateral amygdala damage as a result of Urbach-Wiethe disease (a rare genetic disorder affecting the medial temporal lobes and causing calcification of the surrounding areas of the amygdala (Hurlemann et al., 2007)). Patient SM, therefore, didn’t respond to fearful stimuli in a way that would be expected; they often responded with expressions of excitement and curiosity (Feinstein et al., 2011). One advantage of the case study of Patient SM is that it has allowed for a rich collection of data regarding the effects of damage to the amygdala and its relationship with fear. However, the case of Patient SM should be used as evidence with caution. As the case of Patient SM is a case study, it is difficult to generalise to the public as the results are not replicated with more than one participant- this replication would also not be ethical as it would involve the surgical damage of the amygdala.
To conclude, there are multiple neurological aspects that must be considered when looking at what may cause fear and consequently the behaviour that can be observed when individuals are exposed to a phobic stimulus. It can be argued that the amygdala plays a significant role in the acquisition of fear and how a person may respond to a phobic stimulus. Whilst there is research to suggest other components of the brain are involved, the vast majority of these involve the amygdala one way or another. For example, the release of epinephrine and norepinephrine when the fight-or-flight response occurs. It should be noted that the majority of studies investigating the role of neurological components on the fear acquisition and consequently the following behaviour use animals – usually mice or rats. There are a few advantages when using mice and rats in research. For example, they are similar to humans in terms of genetics as they have a 99% match to the human genome (Vandamme, 2014), in addition to being a relatively cost-effective option should a large-scale study be conducted. However, it must be noted that the research must ethically comply with the appropriate governing body (such as BPS or APA) in addition to the use of animals being a last resort as a research participant. It could be argued that the use of rodents is ethical in this scenario as it could be considered unethical to subject a participant to phobic stimuli, knowing it will cause distress. It could also be argued that the use of animals decreases the external validity of results when applying the data to humans – for example, it cannot be assumed that the amygdala and Cav1.2 channels would work in the same way in humans as they do in mice. However, when looking at human participants, objective methods such as fMRI are used in order to investigate the roles of brain structures such as the amygdala (Goossens et al., 2007). Consequently, the internal validity of studies that use such methods increases, making results more reliable and generalisable. In addition, fMRI is a non-invasive method of measurement thus making the drop-out rate for these studies relatively low. One advantage of research into neurological explanations of phobic behaviour is that it may be possible to produce relevant treatments for individuals should their phobia become difficult to handle, for example, it could be possible to produce a treatment involving voltage-gated calcium channels should further research suggest this as a viable option. However, it is important to note that whilst the majority of research suggests the amygdala plays a large role in the production of phobia responses, it is important to recognise that there may be other explanations as to why people respond this way. For example, a popular theory to explain phobia behaviour is rooted in evolutionary psychology. Evolutionary psychology states that individuals respond to phobic stimuli as a result of a natural instinct to survive and that relevant evolutionary fears such as heights or predators could present themselves without a relevant cue or experience (Coelho & Purkins, 2009). In conclusion, it can be shown that the amygdala plays a significant role in phobia acquisition and behaviour, but other factors must be considered in order to appreciate the complexity of fear.