Fear conditioning refers to a behavioral model whereby organisms learn to anticipate aversive events. Blanchard & Blanchard (1972) consider fear conditioning as a form of learning whereby a particular aversive stimulus, such as an electric shock, is often linked to a given neutral context or stimulus such as a tone or a room, which lead to the expression of fear responses to initial neutral context or stimulus. This is often achieved through the pairing of the neutral stimulus with an aversive stimulus. In due course, exposure to the neutral stimulus alone is enough to bring out a state of fear. In the domain of classical conditioning, the neutral stimulus or context is equivalent to the conditional stimulus (CS), the aversive stimulus is equivalent to the unconditional stimulus and the fear is equivalent to the conditional response (CR) (Cahill, Vardarjanova & Setlow, 2000).

Among humans, conditioned fear is usually evaluated using the galvanic skin response and verbal report whereas in animals, conditioned fear is usually determined using freezing (a duration characterized by watchful immobility) and fear potentiated startle, wherein the fearful stimulus augments the startle reflex. Several scholars have hypothesized that the amygdala plays an instrumental role in fear condition (Campeau & Davis, 1995). Deactivation or ablation of the amygdala plays an instrumental role in inhibiting both the expression and learning of fear. In some types of fear conditioning such as trace and contextual fear conditioning, the hippocampus is involved, which is believed to obtain affective impulses originating from the amygdala after which it integrates these impulses with earlier information in order to make the information useful (Campeau, Miserendino & Davis, 1992; Kluver, 1937).

There are a number of theoretical accounts of traumatic experiences that propose that amygdala-based fear tends to bypass the hippocampus during cases of strong stress and can be archived somatically or in the form of images that often reveal themselves as flashbacks that lack cognitive meaning (Coco et al., 1992). The goal of this literature is to describe the role of the amygdala in the acquisition and expression of conditioned fear. In order to highlight the role of amygdala in fear conditioning, this paper provides an overview of the neurobiology of fear and the neurobiology of fear-potentiated startle, the acquisition of fear, cellular biology of the amygdala during the process of fear condition and the emotional brain with regard to fear; all these reviews will attempt to pinpoint the role the amygdala plays in the expression and acquisition of conditioned fear.

Neurobiology of Conditioned Fear

In order for a brain region to have the capability of mediating learning, Davis (1986) sets forth two fundamental preconditions that a brain region must satisfy. First, the brain area should receive input from the sensory systems involved in the processing of dangerous stimuli such as the tactile system for shock or the visual system used for processing light. The second precondition is that the brain area should be extended to other brain areas that play a role in controlling fear responses such as the pareventricular nucleus and lateral hypothalamus. Basing on these criteria, Davis (1986) argues that the amygdala positions itself as a vital brain area for mediating fear conditioning.

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Campeau, Miserendino & and Davis (1992) characterize the amygdala as a tiny almond shaped nuclei cluster located in the temporal lobe. According to Campeau, Miserendino & Davis (1992), the amygdala is perfectly situated as a locus of fear learning. This is because the lateral nucleus of the amygdala relays input from the thalamus and cortical areas, which are a fundamental relay station of the brain. In addition, the central nucleus of the amygdala plays an instrumental role in sending output to numerous brain sections such as the hypothalamus, which is recognized to arbitrate fear responses. Basing on this basis, substantial progress has been made with regard to understanding the amygdaloid fear system (Coco et al., 1992).

The first clues regarding the neural substrates associated with fear conditioning were derived from studies undertaken by Kluver & Bucy (1937), who revealed that the temporal lobe resections found in monkeys generated an electric deficit (Kluver-Bucy Syndrome) typified by loss of fear, lessened neophobia, hyper sexuality and by visual Agnosia. Further work pointed out that lessened fear in monkeys was because of the damage in the amygdala. After the consistency of these results, reports emerged pointing the crucial role that the amygdala plays in aversive learning as well as the acquisition of conditioned fear responses in cats and conditional emotional responses reported in experiments involving cats. Combined together, these reports provided a basis for the involvement of the amygdala in aversively motivated learning and fear responses (Campeau, Miserendino & Davis, 1992).

This foundation provided ground for further research with regard to the neurobiology of the amygdaloid fear system as shown in figure 1 below. It is now evident that the amygdaloid fear system comprises of two subsystems having distinctive roles in the process of fear conditioning (Campeau & Davis, 1995). The basolateral complex (BLA) of the amygdala, which is made up of the lateral nucleus (LA), basolateral nucleus (BL) and basomedial nuclei (BM), is the neuro-substrate that facilitates the sensory convergence between sub cortical and cortical areas of the brain. Campeau, Miserendino & Davis (1992) consider the basolateral complex as the putative locus for US-CS association during the process of fear conditioning. On the other hand, the central nucleus (CE) of the amygdala projects into other brain regions, such as the pariaqueductal gray (PAG) and the lateral hypothalamus (LH), which take part in the mediation of fear responses. Therefore, Cahill, Vardarjanova & Setlow (2000) consider the central nucleus of the amygdala as the final common output pathway that plays an instrumental role in the generation of conditional responses. Davis (1986) affirms that damage to neurons found in the central nucleus or the basolateral complex impairs the expression and acquisition of conditional fear irrespective of the same stimuli that is used to train fear or the response measure that assesses it. Therefore, the amygdala is perfectly located to facilitate the integration and association of sensory information and the execution of motor functions during instances of fear conditioning.

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Recent research has provided further support with regard to the vital role that the amygdala plays in the process of fear conditioning. In an experiment by Coco et al. (1992), it was reported that a rat having a damaged amygdala will still exhibit a fear response when shock is exerted to the foot although it will fail to establish the association existing between the foot shock and the light. Even after conducting several training sessions, the animals did not show any signs of fear of the light. The case is similar in humans, wherein humans with damaged amygdala exhibit a similar problem. Davis (1986) examined fear conditioning among individuals having a localized damage in the amygdala and reported that the subjects were able to verbalize the association between shock and light; however, they did not exhibit the normal conditioned fear responses such as high heartbeat rates, when the light stimuli was presented alone without shock. Fascinatingly, Blanchard & Blanchard (1972) also found out that fear condition in rats results in lasting alterations with regard to the patterns of communication between the neurons found in the amygdala. According to Clugnet & LeDoux (1990), the cellular response to the sound of the conditioned stimuli tone tends to increase after coupling with the shock; however, there is no increase in the neurological response to other tones that are not linked with foot shock, and the improvement in conditional stimuli tone does not happen in the absence of training. It is apparent that these point out the significant role that the amygdala plays in fear conditioning.

The acquisition of Conditioned Fear

As aforementioned, the amygdala is a crucial component of the neural circuit that influences fear conditioning (Coco et al., 1992). Before the acquisition of fear, the synapses found between the auditory inputs that are tasked with carrying information regarding the conditional stimuli and the cells in the lateral nucleus of the amygdala are weak. As a result, the conditional stimulus is not able to drive neurons in the lateral nucleus in order to fore action potentials; hence, the conditional stimuli fail to bring about fear. On the other hand, an unconditional stimulus, which is extremely aversive, is capable of driving the neurons found in the lateral nucleus, which function as coincidence detectors (Cahill, Vardarjanova & Setlow, 2000). When a neutral conditional stimulus is presented together with an unconditional stimulus, the auditory inputs carrying the conditional stimuli tend to strengthen, a phenomenon known as Hebbian plasticity (Campeau, Miserendino & Davis, 1992).

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The molecular model for explaining the Hebbian plasticity entails the influx of calcium into the post synaptic cell through the NMDA receptors and the L-type voltage gated calcium cells. The calcium plays a role in triggering downstream flows of kinases, which leafs to swift changes in the cystoskeletal; this helps the elasticity to be permanent (Campeau & Davis, 1995). The outcome of these molecular alternations is that the conditional stimuli is now capable of driving cells in the lateral nucleus to fire action potentials, sometimes referred to as spikes. The action potential in the lateral nucleus influences behavior through the efferents emanating from the lateral nucleus to the basal and central nuclei. Freezing behavior is initiated by the outputs of the central nucleus projecting to the pariaqueductal gray. In addition, these outputs also project to the lateral hypothalamus in order for the lateral hypothalamus to initiate the autonomic nervous system (Campeau & Davis, 1995). On the contrary, the basal nucleus is not necessarily needed for Pavlovian fear responses to auditory conditional stimuli; however, it is essential for fear conditioning when the conditional stimuli are extremely complex. For instance, the basal nucleus plays an important role during cases of contextual fear conditioning and for active responses to conditional stimuli such as escape or avoidance (Campeau, Miserendino & Davis, 1992).

As a consequence, a dichotomy exists between the behaviors which brought forth by the basal and central amygdala. For instance, if a rat is freezing, it is not escaping. In addition, intense fear impairs the ability of an animal to escape. However, after an animal learns how to use the conditional stimuli to keep away from danger, then conditional stimuli can no longer bring about automatic defense behaviors as well as the automatic responses linked to fear. Campeau, Miserendino & Davis (1992) assert that this is a significant clinical concept. Possibly, people suffering from PTSD and paralyzed by fear can opt to learn active coping methods that help them to reduce the prevalence of the lateral nucleus to the central nucleus in the amygdala and help them enhance the lateral amygdala to the basal amygdala pathway.

Neurobiology of Fear-Potentiated Startle

Campeau, Miserendino & Davis (1992) assert that another way to perceive the role of the amygdala in the acquisition and expression of conditioned fear is through a review of the neuro anatomy of fear-potentiated startle, which refers to a reflexive physiological response to a stimulus. Fear-potentiated startle (FPS) indicates a fear reaction from an organism. According to Clugnet & LeDoux (1990), the fear-potentiated response can be brought forth when an organism is exposed to any threatening disorders such as situations that are likely to make the organism experience fear. FPS can also be brought forth a neutral stimulus resulting from fear conditioning. The stimulus in question can be either visual or auditory and the measures for startle response include the heart rate and eye blink rates.

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With regard to the neuro anatomy of the FPS, it has been established that the central brain structure linked to FPS is the amygdala. When the central amygdala is stimulated through the activation of the flight-or-fight response, the organism tends to react passively or it exhibits an aggressive physiological reaction (Campeau & Davis, 1995). Passive response is typified by behaviors such as freezing or hyper vigilance whereas aggressive response is typified by rapid breathing and increased pulse rate. The communication between the amygdala and other brain areas, such as the hypothalamus and the brain stem, plays an instrumental role imposing fear-induced reactions. For example, when the amygdala communicates with the lateral hypothalamus, blood pressure increases and pupils dilate. Similarly, when the amygdala communicates with the central grey, freezing takes place whereas the amygdala communicates with paraventricular nucleus results in the release of hormones associated with stress (Campeau & Davis, 1995).

Existing literature has associated fear-potentiated response to the interaction between the central amygdala, to the the nucleus reticular pontis caudalis and the central grey. Damage to these parts of the brain is likely to hinder FPS response. Furthermore, a distinction has been established with regard to the neural activity associated with a reflexive fear potentiated startle, and the response that occurs when a person is exposed to fear-provoking stimulus for long durations of time. Campeau, Miserendino & Davis (1992) suggest that under such situations, fear-potentiated startle stems from the activation of the stria terminals and the bed nucleus of the amygdala. Therefore, damage to these brain areas is likely to inhibit FPS response.

Issues Regarding the Role of Amygdala in Fear Conditioning

A number of concerns have been raised with respect to the role of amygdala in mediating fear. The first issue involves the interpretation of the effects of the lateral and basal lesions in expressing conditioned fear. Research has established that lateral and basal lesions tend to impair the expression of conditioned fear. Davis (1986) interprets these impairments to assert that the L/BL lesions hinder conditioned fear. The second issue relates to the effects that intra-amygdala infusions of NMDA antagonists have on the Pavlovian fear conditioning. A number of studies have pointed out that FPS is propagated by NMDA antagonists that are infused into the amygdala before fear conditioning. In addition, evidence gathered from human subjects points out that non-conscious and conditioned responses can be formed in the absolute absence of the amygdala. Other studies also propose that the amygdala is only active during the acquisition of conditioned fear and does not play any significant role after the acquisition of fear (Davis, 1986).


The paper has discussed the role that the amygdala plays in fear conditioning. It is apparent from the neuro-anatomy of conditioned fear and FPS the significant role that the amygdala plays in fear condition. This is affirmed by the observation that damage to the amygdala hinders conditioned fear response and FPS. This paper has highlighted the amygdala as a vital brain structure in the mediation of fear as evident through its anatomical structure backed by vast evidence from research. Whereas much is known regarding the role of amygdala in fear conditioning, less is known regarding the other comprehensive emotions besides fear; this presents a significant area for further research.


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