Rogers and Kesner (2003)

Rogers and Kesner (2003)

Aim: To investigate the role of acetylcholine on memory encoding and memory retrieval.

Method: It was a laboratory experiment using rats. Rats were trained to learn a simple maze, but before the memories could be learned well-enough to be transferred from short-term memory to long-term memory, the rats were divided into groups and injected with drugs:

• Group 1 was injected with scopolamine, which is known to block the reception of acetylcholine by the post-synaptic neurons. This means that acetylcholine, a neurotransmitter expected to help form memories, cannot travel from one neuron to another. This was the no acetylcholine condition.
• Group 2 was injected with physostigmine, a drug that blocks cholinesterase, which is what cleans up the acetylcholine from receptor proteins on the post-synaptic neurons, returning the neurons to their resting potential, where no nerve impulse is being sent. Therefore the acetylcholine continued to act. This was the high acetylcholine condition.
• Group 3 was the placebo group, and was injected with an inert saline solution that had no effect on acetylcholine. This was the control condition.

Rats were then placed back in the maze and ran multiple trials over two days. Their learning and memory was measured by comparing the number of mistakes they made while completing the maze. The difference between the first five and the last five trials on day one was taken as a measurement of encoding, while the difference between the last five trials on day one and the first five trials on day two was used to measure retrieval.

Results: The no acetylcholine condition showed a deficit in encoding (but not retrieval), making relatively more mistakes during the last five trials on the first day. The high acetylcholine condition made relatively fewer mistakes during the last five trials on the first day and showed no deficit in encoding. However, the high acetylcholine condition did show a deficit in retrieval.

Conclusion: This suggests that acetylcholine plays an important role in memory encoding, because the rats with low acetylcholine levels wandered around the maze as though lost, even though they had learned it previously. At the same time, while acetylcholine may be necessary for memory encoding, the physostigmine condition suggests that too much acetylcholine may interfere with memory encoding and retrieval.

Strengths: This experimental design allows for cause-and-effect conclusions based on the isolation of variable in three experimental conditions.

Limitations: It’s difficult to generalize results from animal studies to humans, because the results may not be wholly applicable. However, the biochemical correlates of memory suggest that acetylcholine impact memory in humans too. The effects of neurotransmitters are difficult to isolate, because the alteration of one neurotransmitter may cause changes in other neurotransmitters too.

Application: The results suggest that drugs targeting the acetylcholine system, like physostigmine, may have applications in the treatment of memory disorders, like Alzheimer’s disease, assuming that acetylcholine plays a role in memory formation.