Neurological Mechanism Involved in Fear Conditioning - Case Study Example

Running head: fear conditioning What is fear conditioning and what are the neural mechanisms underlying it? Introduction The current discourse is a short explanation on fear conditioning from neurological viewpoint. From classical conditioning perspective, fear conditioning is regarded as the most impactful form of emotional learning and memory processes in animals and humans. Human beings and animals are made to respond to aversive conditions that elicit reactions of fear and anxiety by artificial external stimulation of different types. Motive behind fear conditioning is to understand behavioural aspects and neurological mechanisms involved in specific behavioural responses to fear. Further, it helps in psychotherapeutic intervention and psychological dealing to tackle behavioural as well as other physiological problems in humans. Neural mechanisms involved in fear conditioning have been studied extensively ever since fear conditioning was developed. An understanding of the complex mechanisms of neural circuit has helped scientists and psychotherapists to develop different and more accurate methods of dealing with fear and anxiety related problems in humans. However, psychotherapeutic interventions require deeper understanding of neurological, molecular as well as genetic mechanisms involved in fear conditioning. The present discussion focuses on neurological mechanism involved in fear conditioning, from animal and human perspectives. Fear is an emotion resulting in increased anxiety and disturbance due to expectation of an assumed hazard and can occur at any time and to anybody depending upon the situation that can cause some kind of harm to the individual/animal. This emotion is experienced by every living organism based on previous experiences. These one-time experiences tend to create specific perception that is retained for longer periods; similar emotions recur when the individual/animal encounters similar situation even without experiencing any harm or injury in subsequent encounters. In the sense, the individual/animal has got conditioned to the situation in such a manner that the perception elicits same emotions again and again. Such conditioning to situation that elicits fear is termed as fear conditioning. Fear conditioning was developed from concept of classical conditioning, a behaviour response shown by animals and human beings, which was first recognized by Ivan Pavlov in the behaviour science (Taylor, 2006; 60). Achieving behavioural changes through classical conditioning requires active and willing participation by the individual, and hence may not be applicable in all conditions requiring behavioural change. However, fear conditioning has been found to be very effective in bringing desired change in behaviour and psychology. Evidence indicates that fear conditioning was first tried in animal models and then extended to humans (Delgado, Olsson & Phelps, 2005). The aspect of fear has received much attention in behavioural science because of its two-fold impact on human beings. On one side, fear is a natural adaptive alert mechanism to escape from potential harmful consequences and on the other hand it can result in serious health implications like anxiety, phobia, panic, posttraumatic stress disorders and also abnormal behaviour leading to psychological disorders (LeDoux, 2002). In some cases, inducing fear to specific objects and/or situations also becomes important in order to make people avoid risky activities or behaviours. Both can be achieved through fear conditioning. The bases for human emotions have been studied from psychological as well as neurological perspectives by many people. A link between both has been established after extensive study by LeDoux (2002) by studying neurological mechanisms that take place within the brain during episodes of fear. Fear is one emotion experienced by nonhuman mammals as well as human beings from the beginning. Hence, fear conditioning has been extensively researched on animal models and humans with great success. Fear conditioning is conducted by exposing the experimental model to specific external conditioned stimulus (CS), like a tone or light followed by brief unconditioned stimulus (US) such as electric shock. Before conditioning to particular state, the conditioned stimulus does not produce any defensive reaction. However, after paring the conditioned and intermittent unconditioned stimuli, a range of conditioned responses are produced by the experimental subject. The conditioned responses (CR) are produced both to conditioned stimuli as well as the conditioned atmosphere. In rodents, these responses were found to be in the form of freezing or immobility; in other animals the response were specific to their species-type defensive mechanisms like changes in heart rate and blood pressure, defecation, and increased levels of circulating stress hormones (Schaffe & LeDoux, 2004). Immense work has been carried out to study and understand the neural circuit involved in fear conditioning, both in humans and nonhuman mammals. While most of the studies indicated the involvement and importance of Amygdala nuclei in the entire process, debate about which nuclei ARE actually involved still exists. Some studies have emphasized on the central nucleus of amygdala, which has connections with brain stem and spinal cord controlling the motor expression of emotional LeDoux et al.’s (1985) experiments have identified that fear memory is associated with lateral nucleus of amygdala (LA) that contain cells that recognize and respond to the senses received from the medial division of the thalamic medial geniculate body (MGm), the posterior intralaminar nucleus (PIN) and from cortices (LeDoux, 2004). Based on their experiment on contribution of amygdala and hippocampus regions to fear conditioning, Phillips and LeDoux (1992) had identified that amygdala is involved in formation of connection between a sudden unconditioned external stimulus and a variety of conditioned stimuli that traverse through the sensory processing areas of the thalamus, neo cortex, higher order cortical areas and the hippocampus. If the stimuli are multiple or complex, then the hippocampus transmits more number of signals to the amygdale through thalamus and neo-cortex; from here, all signals unite with the lateral amygdaloid nucleus. In auditory responses, the auditory sections of these parts are involved, which contain the neurotransmitter glutamate. Auditory and shock sensations traverse through the MGm, PIN and cortex to the lateral amygdale where specific cells recognize and react to the external stimuli. This indicates that the LA as well as hippocampus are critical to fear conditioning (LeDoux, 2002; Schaffe & LeDoux, 2004). The lateral amygdala is the site of plasticity where most of the synapses occur. Here, long-term potentiation (LTP) occurs mediated by NMDA receptors that aid in acquisition and storage of memory related to fear conditioning. The synaptic plasticity that occurs at LA and hippocampal regions is much more complex and involves many other neurotransmitters (Schaffe & LeDoux, 2004). In fact, researchers have studied that the long-term potentiation that occurs within the amygdala provides sufficient explanation of the mechanism involved in fear conditioning. The conditioned and unconditioned stimuli elicit neurological responses which converge in the cells present in amygdala where long-term potentiation occurs. Here, the conditioned stimulus is weak and unconditioned stimulus is stronger; the unconditioned stimulus activates postsynaptic cells resulting in repetitive action of fear or creation of memory related to feared object/situation. In the two-way reaction, the conditioned stimulus does not activate postsynaptic cells and hence are not responsible for eliciting fear reaction. However, the conditioned stimulus in conjunction with the unconditioned stimulus tends to create long-term potentiation (LTP) and eventually activates the postsynaptic cells also resulting in fear conditioning. Few studies have reported that pairing of conditioned and unconditioned stimuli (CS-US) has resulted in plasticity of the CS and thereby weakening postsynaptic reactions. However, this is contrary to long-term potentiation. Researchers believe that role of other modalities of basolateral neurons and biochemical basis in fear condition cannot be ignored (Schafe & LeDoux, 2004). Buchel and Dolan (2000) explain that neuroimaging and brain lesion techniques have led investigators to affirm that the neurological mechanism involved in fear conditioning in human adults parallels that found in rodents and nonhuman mammals (McClure & Pine, 2006; 488). Fear conditioning mechanism in humans involves using startle reflexes to explore the emotional state. Like in animal models, human beings also show greater responses to unconditioned stimuli or startle probe than conditioned stimuli. The probe stimuli result in potentiated responses when humans are threatened about unconditioned stimuli, like shock, although no real shock is given. Another method is fear acquisition and extinction followed by exposure to few more unconditioned stimuli without the conditioned stimulus. In humans, contextual and cue fear conditioning have been tried. In all types, the major neural sections involved include the hippocampus, amygdale and the neo-cortex. In conclusion, fear conditioning is used to make nonhuman animals and human beings learn to fear new stimuli or to eliminate previous fears through learning process that involves a conditioned stimulus that is usually neutral one and an unconditioned stimulus meant to elicit aversive response. Immense advances in studying the neural mechanisms involved in fear conditioning have assisted behaviour specialists in addressing many anxiety-related disorders by developing different learning methods. From psychotherapeutic perspective, the synaptic events, neurotransmitters responsible for eliciting associated emotions, and the overall circuit provide sufficient opportunity for therapeutic drug development. References Delgado, M.R, Olsson, A and Phelps, E.A. (2006). Extending animal models of fear conditioning to humans. Biological Psychology. 73: 39-48.p LeDoux, J. E. (2002). Emotion: Clues from the Brain. In Cacioppo, J.T et al (Eds.) Foundations in social neuroscience. USA: MIT Press. McClure, F.B and Pine, D.S. Social anxiety and emotion regulations: A model for developmental psychopathology perspectives on anxiety disorders. Cichetti, D and Cohen, D.J (Eds.) Developmental psychopathology. 2nd Ed. USA: John Wiley and Sons. Phillips, R.G and LeDoux, J.E. (1992). Differential contribution of Amygdala and Hippocampus to Cued and Contextual Fear Conditioning. Behavioral Neuroscience. Vol 106, No.2, pp: 274-285. Schaffe, G.E and LeDoux, J.E. (2004). The Neural Basis of Fear. Gazzaniga, M.S. (Ed.) The cognitive neurosciences. USA: MIT Press. Taylor, S.E. (2006). Health psychology. 6th Ed. Tata McGraw-Hil: New York. Indovina, I, Robbins, T.W, and Nunez-Elizalde, A.O. (2010) Fear-Conditioning Mechanisms Associated with Trait Vulnerability to Anxiety in Humans. Neuron. Vol.69, No.3. pp: 563-571. Read More