Antonova (2011)- Acetylcholine- scopolamine- antagonist

Aim

Aim

To see if scopolamine affected hippocampal activity in the creation of spatial memory.

participants

The researchers used a sample of 20 healthy males with a mean age of 28.

Method

The study used a double blind procedure and the participants were randomly allocated to one of 2 conditions. They were injected with either Scopolamine or a placebo 70-90 minutes before taking part in the experimental task.

The participants were then put into an fMRI where they were scanned playing the ‘Arena task’ ( a complex VR game, in which the researchers are observing how well the participants can create spatial memories.

The goal is for the participants to navigate around an ‘arena’ to reach a pole. After they have learned where the pole is located, the screen would go blank for 30 seconds. During this time, the participants were asked to rehearse how to get to the pole in the arena. When the arena reappeared, the participant was now a new starting point in the arena. The participants would have to use their spatial memory to determine how to get to the location of the pole.

The participants were first trained in the game to make sure they were comfortable with the use of the joystick and that they understood the rules of the game. After they were trained they took part in the experiment. The participants’ brain activity was measured for 6 trials.

The participants returned between 3-4 weeks and redid the test- receiving the opposite treatment (repeated measures design).

Results

The researchers found that when the participants were injected with scopolamine, they demonstrated a significant reduction in the activation of the hippocampus compared to when they received a placebo. It appears acetylcholine (which was inhibited by the antagonist scopolamine) could play a key role in the encoding of spatial memory in humans.

conclusion+link: antagonist

The findings support the idea that scopolamine inhibits acetylcholine, hence affecting the formation of spatial memory, as less hippocampus activity was demonstrated by participants infected by scopolamine compared to the placebo group.

Scopolamine is though to inhibit acetylcholine by attaching to post-synaptic rmembrane receptors, thus blocking acetylcholine from binding and allowing the message to convert back into an electric signal so that it can continue to be transmitted.

The hippocampus is an area of the brain with a high concentration of acetylcholine receptors and is also associated with the consolidation of spatial memories.

Thus, the findings not only show that scopolamine indeed inhibits acetylcholine, but it also supports the idea that the antagonist scopolamine may potentially prevent spatial memory formation, and hence affecting subsequent human behaviour.

Conclusion: AGONIST, SYNAPSE, NEUROTRANSMITTERS (EXCITATORY, INHIBITORY)

The findings support the idea that acetylcholine is an agonist/neurotransmitter, as when acetylcholine was inhibted by the antagonist scopolamine, less hippocampus activity was observed.

When acetylcholine is released by the presynaptic neuron into the synapse it should bind to the acetylcholine receptor on the postsynaptic membrane but had been blocked by the scopolamine, not allowing the signal to be transmitted. The hippocampus is an area of the brain with a high concentration of acetylcholine receptors so this explains why its activation was reduced.

The hippocampus is also an area associated with the creation of spatial memories, and this explains impairing accuracy of memory compared to when participants receive a placebo.

Therfore, this study suggests that acetylcholine is a neurotransmitter/agonist that could play a key role in the encoding of spatial memories in humans

Evaluation

Although there was a higher rate of error in the scopolamine group, it was not a significant difference. THe difference in the activity in the hippocampus, however, is significant. This means the tasks designed may not have been the best for showing performance difference; without the use of fMRI, there would be no way to know that at the biological level, there were significant differences in the two conditions.

The study was a repeated measures design- eliminating the effects of participant variability. In addition the study was counter balanced- that is some of the participants did the scopolamine condition first and other the placebo first. This is controlled for practice effect.

The study was double blind/ done blindly to control researcher bias.

During the debreifing several participants expressed that they felt stress, either as a result of the injection of an unfamiliar drug, or being enclosed in the fMRI. This may affect the working of the hippocampus as we know stress interferes with memory encoding.

The sample size was small. The study needs to be replicated to decide whether the results are reliable.