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classical conditioning by Pavlov and its current use in treating anxiety
The paper focuses on the development of classical conditioning being used, as suggested by Pavlov, in treating anxiety through using fear-induced techniques. The paper talks about the past experiments that were done on animals and human, those who were suffering from anxiety and those who weren't, and highlights how anxiety is treated through fear induced conditioning.
Combination of neutral stimulus with aversive U.S. (unconditioned stimulus) is what we see involved in fear conditioning. In the first stance, there is no emotional response seen from a neutral stimulus, but after the recurring coupling with unconditioned stimulus, the neutral stimulus turn out to be a CS (conditioned stimulus). CS gives indication about the forth coming unconditioned stimulus and brings to mind the nervousness and expectancy with regard to U.S.. Fear conditioning is commonly an adaptive type of learning. When an uneasy response to the conditioned stimulus takes place in the nonexistence of a CS/U.S. possibility then there are chances that fear conditioning may lead to pathology (Lissek et al., 2005).
For the minimum of eighty years, the formal theories have mixed up fear conditioning in the pathogeneses of disorders relating to nervousness (Pavlov, 1927; Watson & Rayner, 1920). Improved quality of work (e.g., Gorman, Kent, Sullivan, & Coplan, 2000; Grillon & Morgan, 1999; Pine, 1999) is trailed from the prologue of extra composite conditioning models where both the aspects of fear and anxiety are noticeable (e.g., Mineka & Zinbarg, 1996). Introduction is followed with research done on animals which define particular lobe circuits which are occupied by terror (reviewed by Blair, Schafe, Bauer, Rodrigues, & LeDoux, 2001). This is followed by facts which support the assistance of related brain parts to fear learning in human beings (e.g., Bechara et al., 1995; LaBar, Gatenby, Gore, LeDoux, & Phelps, 1998). The fear conditioning disparity identified within the anxiety patients is liable to promote the future endeavors which are subject to the explication of neurobiological loci of clinical anxiety.
The declaration of classical conditioning model of anxiety disorders is that the pathological anxiety (neurosis) is developed by simple classical conditioning (Pavlov, 1927; Watson & Rayner, 1920). After the submission of this theory other writers gave an extension to it by stating that classically conditioned model also acts as an instrument which stimulates prevention (Eysenck, 1976, 1979; Eysenck & Rachman, 1965; Miller, 1948; Mowrer, 1947, 1960). The other versions of this theory stress on the birth and the intensification of terror (Eysenck, 1979), the aversive associations prepared on evolutionary basis (e.g., o hman, 1986; Seligman, 1971), failure to slow down the response to safety signs (Davis, Falls & Gewirtz, 2000), related learning shortfall (Grillon, 2002), stimulus generalization (Mineka & Zinbarg, 1996; Watson & Rayner, 1920), and improved condition ability in the arrangement and perseverance of anxiety disorder (Orr et al., 2000; Peri, Ben Shakhar, Orr, & Shalev, 2000),.
Classical Fear Conditioning
Ivan Pavlov (1927) has the honor of demonstrating the original classical conditioning model most eminently. The model starts with the description of certain stimuli which are considered to be unconditional ones, and tend to bring a consistently yielded UR (unconditional response). The model goes beyond to explain that trough training a neutral stimulus could also give the same response when coupled with U.S.. So, under such a situation the neutral stimulus is regarded as the conditioned one and the response generated is the CR (conditioned response). Pavlov performed an experiment on a dog where the food worked as a U.S. And the salivated mouth of the dog was a UR (Pavlov, 1927).
The next time Pavlov offered the food he also rang the bell (neutral stimulus); he repeated this action many times. Finally, he just rang the bell (CS) without presenting the food; just the mere sound of bell produces saliva in the dog's mouth (conditioned response) (Pavlov, 1927).
When the pairing of neutral stimulus is done with aversive one, it is known as Pavlovian fear conditioning. This can be explained with help of an example related to a little eleven-month-old boy, Albert. Once Albert was provided with a rat to play (CS), the boy showed no response of terror. Second time Albert was given the same rat to play but concurrently with a loud sound (U.S.), Albert started to cry (CR). The second step was repeated a number of times and then finally, in the end Albert started crying (CR) just on the mere glance at the rat, with no presence of any sound (CS). Very small stimuli like rat could bring in such a fearing response on part of a boy. Where on one side reaction to fear can serve as a precious task in protection from possible hazard, but on the other hand it may also act to be maladaptive. Under a maladaptive condition, a contextual stimulus can become linked with recurrent terror and nervousness (i.e. generalization). Under typical models on fear conditioning, a meek electric shock brings out a freezing reaction or a rise in the blood pressure or causes the heart beat to rise (CR) (Pavlov, 1927).
Neuroanatomy of Anxiety
Amygdala is that part of the brain which is liable for getting hold of the fear conditioning (Pare et al., 2004). Amygdala is present in the medial temporal lobe of the brain. Three of the nuclei out of a total of 13 present in amygdala are; basal amygdala (BA), lateral amygdala (LA) and central nuclei. These three nuclei are implicated in the way of fear response (Rosen, 2004). LA receives stimulus from the sensory thalamus which is then transferred to the central nuclei (CA) (short loop pathway). A linkage between LA and central nucleus is made by BA. LA receives signals from the sensory cortex, insula and prefrontal cortex; this is what undergoes in the long loop path (LeDoux, 2000; Sotres-Bayon et al., 2006). From LA information is transferred to the effectors side of the brain and the hypothalamus. Hypothalamus creates involuntary signs of fear responses (Cahill et al., 1998). LA is found to be the part of brain which is accountable for remembrance consolidation and flexibility within fear conditioning (Shumyatsky et al., 2002). A severe memory loss could occur if LA or CA is damaged due to some injury (Wallace et al., 2001; Blair et al., 2005; Goosens and Maren, 2001). Evidences have proved that the damage of BA can adversely affect reactions to fear (Anglada-Figueroa and Quirk, 2005). The molecular mechanism through which fear acquisition takes place within LA is termed as enduring potentiation (LTP) (Chapman et al., 1990). When calcium takes entry into the cell through N- methyl-D-aspartate (NMDA) receptors and voltage-gated calcium channels (VGCCs) (Bauer et al., 2002) then the consolidation of memory takes place. The blockage or damage of VGCCs will have no affect on the long-term memory but will greatly disturb the short-term memory. This clearly signifies that the presence of NMDA receptors is essential for the pathway to be affective (Rodrigues et al., 2001; Walker and Davis, 2000; Cain et al., 2002). The research work which was carried out on animals revealed that when the antagonist blocked the NMDA receptor, L-2-amino-5-phosphonovaleric acid (APV, AP5), acquisition of fear stopped but no harm was caused to expressions (Roesler et al., 2000; Fendt, 2001; Miserendino et al., 1990). But if the latest studies are considered then we get to know that both the processes are stopped (Jasnow et al., 2004; Maren et al., 1996; Lee et al., 2001). The studies of genetic materials have exposed that there is high appearance of NMDA receptors within the hippocampus too. This, thus signifies the worth of this brain structure under Pavlovian conditioning (Mei et al., 2005). Whereas, if inside amygdala, blockage with these receptors takes place, then the result would be the disturbed responses of fear conditioning (Zhao et al., 2005; Melik et al., 2006).
The use of preclinical findings is currently restricted on human beings. But the usage of NMDA receptors and calcium channel blockers is taking place in order to solve damaged memory issues and also for the cure of anxiety indicators. Nowadays, the usage of non-competitive NMDA receptors is becoming very common. These receptors are widely used as agents who carry out the memory enhancement task within the patients who are suffering from Alzheimers disease, which is ranging from a reasonable to a severe level. The receptors accomplish this task by bringing improvement in the neuronal flexibility and also by decreasing excitotoxity within the hippocampus (Parsons et al., 1999). Within few of the animal studies the existence of anxiolytic properties is seen (Bertoglio et al., 2003; 2004), however not in all (Karcz-Kubicha et al., 1997; Harvey et al., 2005). This has not been considered as a primary anxiolytic mediator in humans. Zarate as well as colleagues (Zarate et al., 2006) who initiated a double-blind, placebo-controlled test were not proved to be successful in the treatment of major depressive orders. This thus gave unusual paths for the tone of the mood. For the treatment…[continue]
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