Thursday, April 23, 2015

Fear Conditioning

One form of learning that plays a prominent role in consumer’s behaviour is fear conditioning.

In Watson and Rayner’s seminal experiment with “Little Albert” (1920), they showed how fear can become a conditioned emotional reaction. Marketers may also be incorporating some of Watson and Rayner’s behavioural theories to influence their consumer’s behaviour.

People often learn by information and instruction which situations to fear (Rachman, 1977). Mowrer (1939) argued that fear “may effectively motivate human beings” and that the curtailment of fear “may serve powerfully to reinforce behaviour that brings about such a state of relief or security”.

Accordingly, companies that market their products often use forms of fear conditioning in an attempt to increase their revenue.

Clearasil, a skin care product for the treatment of acne, ran television advertisements portraying spotty teenagers looking glum and downbeat; but joyful and surrounded by attractive women once the product had been discovered. Similar advertising themes exist with Lynx body spray. The product is advertised as a potent solution for men to acquire more attention from women, a “spray more - get more” mantra of fear conditioning.  

Both advertisements suggest an attempt at fear conditioning to promote their product to possibly insecure adolescent males. The fear can be conditioned by frequent repetition of the association between the new conditioned stimulus and the fear. Therefore, individuals (consumers) are driven to purchase these products in an attempt to avoid negative outcomes and successfully reduce their fear (Rachman, 1977). It can be further argued that avoidance conditioning is employed in these advertisements; as the consumer learns a response (buy product) and thus avoid an aversive stimulus (e.g. not being attractive).
"...because then you're watching television, you're watching the news, you're being pumped full of fear, there's floods, there's AIDS, there's murder, cut to commercial, buy the Acura, buy the Colgate, if you have bad breath they're not going to talk to you, if you have pimples, the girl's not going to fuck you, and it's just this campaign of fear, and consumption, and that's what I think it's all based on, the whole idea of keep everyone afraid, and they'll consume." ~ Marilyn Manson (Bowling for Columbine, 2002).

Wednesday, April 01, 2015

Schizophrenia: The Dopamine Hypothesis

Dopamine, a major excitatory neurotransmitter, may play a key role in schizophrenia. According to the dopamine hypothesis, the symptoms of schizophrenia - particularly positive symptoms (e.g. delusions and hallucinations), are produced by over-activity of the dopamine in areas of the brain that regulate emotional expression, motivated behaviour and cognitive functioning.
Having "too much" of this neurotransmitter is probably too simplistic; the better term is a functional excess (Lieberman, 1990). This may be caused by a failure of any of the many processes involved in breaking down and re-creating the neurotransmitter, or disruption to the receptor system (such as the receptor functioning "too well"), or there may be problems with re-uptake into the presynaptic membrane.
Dopamine Pathways
People diagnosed with schizophrenia have more dopamine receptors on neuron membranes than do non-schizophrenics, and these receptors seem to be over-active to dopamine stimulation (Wong, 1986). Additional support comes from the finding that the effectiveness of antipsychotic drugs used to treat schizophrenia is positively related to their ability to reduce dopamine-produced synaptic activity (Green, 1997).
The hypothesis that dopamine and dopaminergic mechanisms are central to schizophrenia has been one of the most enduring ideas about the illness. It was not until the 1970's, however, that the dopamine hypothesis was finally crystallized with the finding that the clinical effectiveness of antipsychotic drugs was directly related to their affinity for dopamine receptors. To date, their have been more than 6800 articles on the topic of dopamine and schizophrenia since 1991.
In summary, molecular imaging studies show that presynaptic striatal dopaminergic function is elevated in patients with schizophrenia; however blockade of this heightened transmission, either by decreasing dopamine levels or blocking dopamine transmission, leads to a resolution of symptoms for most patients (Howes, 2009).