Sample 1

McGaugh and Cahill (1995) and Newcomer et al (1999) examined the roles of adrenaline and cortisol on human memory. Hormones are chemicals that affect human behaviour. They are secreted by glands in the endocrine system and are released into the bloodstream, meaning they take longer to produce changes in human behaviour than neurotransmitters. Hormones can only produce reactions in certain target cells, that have appropriate receptor sites for these specific hormones. The hormone adrenaline secreted by the adrenal gland and is responsible for arousal and the “fight or flight” response, it increases the heart rate, blood pressure and respiration. Cortisol is also secreted by the adrenal gland and is responsible for controlling blood sugar levels, metabolic regulation and its levels rise during periods of stress.

Psychologists believe that the stress hormone adrenaline plays a role in the creation of emotional memories. Adrenaline is responsible for stimulating the sympathetic nervous system. Cahill and McGaugh conducted a lab experiment in which there were two groups of participants. The first group was shown 12 slides accompanied by a rather boring story about a boy that was visiting his father in a hospital. The second group was shown the same 12 slides but told a traumatic story about a boy that was in a car accident in which his legs were severed.  After the story, the participants were asked to rate their level of emotion. Two weeks later, the participants were asked to come back to answer a set of questions regarding the stories they were told. They had three options for each question to choose as an answer. The researchers did a follow-up study in which they repeated the procedure but injected the group exposed to the “traumatic” story with a beta-blocker, propranolol. Propranolol interferes with the release of adrenaline and prevents the activation of the amygdala to prevent the formation of emotional memories.

In this first study, the group exposed to the “traumatic” story had better accuracy in terms of remembering details. They were also more capable of remembering details from the slides compared to the group exposed to the uninteresting story. In the follow-up study, the group that was injected with beta-blockers and exposed to the “traumatic” story performed no better than the group exposed to the non-emotional story. This suggests that the prevention of the release of adrenaline caused the inability to recall the “emotional” story.

By carrying out a highly controlled lab experiment Cahill and McGaugh were able to establish a cause and effect relationship between adrenaline’s interaction within the amygdala and the formation of emotional memories. As well this experiment was highly standardised, therefore it is easy to replicate. As it is easy to replicate, similar results would increase the reliability of the results.

One limitation of this experiment was its artificiality. The experiment was highly-controlled and took place in a lab setting, questioning its ecological validity. Instead of experiencing the event themselves they were told a story accompanied by 12 images in a lab environment. In addition, the participants self-reported their emotional state, there was no objective measure.

In an experiment conducted by Newcomer et al, the effect of levels of cortisol on verbal declarative memory was tested.  The participants were matched to one of three conditions based on age and gender. In the first condition, the participants were given a 160 mg tablet of cortisol daily during the four-day experiment. These tablets produced a level of cortisol that one would experience during a major stress event. The second condition had the participants take a 40 mg tablet of cortisol per day. This level of cortisol replicates the levels of cortisol experienced by someone during a low-stress event.  The last condition had participants take placebo tablets. The function of this was to provide a control group that eliminated the effect of taking a pill in itself. Each participant had to listen to a prose paragraph and then recall it in over a period of four days. This was done in order to test their verbal declarative memory.

The participants in the high-cortisol condition performed the worst in the verbal declarative memory task. This suggests significant negative effects on verbal declarative memory. On the other hand, the low levels cortisol condition showed better recall than the placebo group. These findings suggest that low levels of cortisol actually may enhance verbal declarative memory.

As the researchers manipulate the independent variable, a cause and effect relationship was established. Particularly the effect of cortisol levels on one’s verbal declarative memory. This experiment was highly standardised, therefore easily replicable. Replicability suggests high reliability of the experiment’s findings. This was a double-blind laboratory experiment. This meant that neither the experimenter nor the participant knew which group was receiving the cortisol pills or placebo pills. This eliminated demand characteristics such as the expectancy effect in which the participant acts the way they think they should act in order to produce data that aligns with the hypothesis. The participants weren’t aware of the dose of cortisol they were given, therefore couldn’t try to produce any desirable results.

Given that the experiment was conducted over a period of four days, extraneous variables from the participants’ daily lives were not controlled, suggesting low internal validity. Depending on the events of the participants’ day, the levels of cortisol could have fluctuated and influenced the findings.

Both Cahill & McGaugh’s, as well as Newcomer et al’s research, suggest that a strong relationship is present between the release of hormones and the consolidation and recall of memory.

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