Paper 1 - Biological Approach - The Brain and Behavior - Neurotransmitters

Neurons

nerve cells that process and transmit messages through electrical chemical signals (see diagram)

neurotransmitters

brain chemicals released from synaptic vesicles that relay signals across the synapse from one neuron to another.

- can be divided into those which perform an excitatory function and those that perform an inhibitory function.

acetylcholine (ACh)

a neurotransmitter which has been linked to synaptic plasticity in the hippocampus and has a role in memory and learning, particularly when encoding new memories.

- It is an excitatory neurotransmitter which plays a role in the consolidation of memory in the hippocampus.

- Acetylcholine release in the hippocampus (brain area involved in the formation of new memories) enhances the encoding of new info and promotes the formation of LTM.

- It also enhances synaptic plasticity (the brain's ability to change and adapt to new experiences). This strengthens the connections between neurons and improve the storage and retrieval of memories.

(use Antonova's study for SAQs about acetylcholine/excitatory neurotransmitters)

GABA (gamma-aminobutyric acid)

a neurotransmitter that reduces neuronal excitability and induces relaxation by blocking specific signals in the CNS. Plays a role in memory formation.

- GABA is an inhibitory neurotransmitter which plays a key role in memory formation. It inhibits neural activity in both the hippocampus and frontal lobe, to allow us to inc our cognitive load and how we are able to use our working memory.

- When GABA levels are low, intrustive thoughts may make it harder to concentrate and lay down new memories.

(use Prevot's study for SAQ's about GABA/inhibitory neurotransmitters).

Synaptic transmission

the process by which neighboring neurons communicate w/ each other by sending chemical messages across the synapse that separates them.

- when the electrical impulse (action potential) reaches the end of the neuron (presynaptic terminal), it triggers the release of neurotransmitters from synaptic vesicles.

- the neurotransmitter than diffuses across the synapse to the next neuron in the neural network an dis taking up by a postsynaptic receptor site on the dendrites of that neuron (axons take signals to the synapse, dendrites take signals away).

- Here, the chemical message is converted back into an electrical impulse (action potential), and synaptic transmission occurs again in this neuron.

excitation

when a neurotransmitter increases the positive charge of the post-synaptic neuron, increasing the likelihood of it passing on the electrical impulse

inhibition

when a neurotransmitter inc the negative charge of the postsynaptic neuron, dec the likelihood of it passing on the electrical impulse.

summation

if the net effect is excitatory, neuron more likely to fire. if inhibitory, less likely to fire.

Antagonist

a molecule that binds to the synaptic receptor to dec the effect of a neurotransmitter.

agonist

a molecule that binds to a synaptic receptor and activates it to promote a reaction.

Agonists and Antagonists (use Antonova's study for both)

Neurotransmitters are affected by chemicals that bind to the receptor site. These chemicals are either agonists or antagonists.

Agonists inc the neurotransmitter effect, making the excitation or inhibition stronger.

- All neurotransmitters are agonists for receptor sites. They are endogenous agonists since they are biologically part of our nervous system.

- Acetylcholine is an agonist for ACh for ACh receptor sites.

- Exogenous agonists are external to our system. This includes drugs (e.g. nicotine, an agonist for ACh receptor sites, and in the short term, has positive effects on memory).

Antagonists reduce the neurotransmitter effect, making the excitation or inhibition weaker.

- These are drugs that fit into a receptor site and blocks the action of a neurotransmitter, so no action potential is sent down the neuron.

- For example, scopolamine is an antagonist for ACh, which reduces it's ability to carry out it's role in the formation of memory.

prevot et al aim

to investigate whether the manipulation of GABA levels could have a positive influence on impaired memory function in an animal model

hypothesis -> using an agonist (an imidazobenzodiazepine) which activates the a5-GABA receptor site in the hippocampus would inc the inhibition of neural activity, improving memory function.

prevot et al method

sample of mice that suffered memory impairment due to chronic stress, and older mice w/ memory impairment.

used a double-blind experiment with a pre-test/post-test design. the mice were either allocated to the placebo condition (control group) or the drug condition.

mice were placed alone in a y-shape maze to test their spatial working memory. mice w/ healthy working memory can alternate between the 2 arms of the 'y' when continually placed back to the start of the maze. mice that have impaired working memory are more likely to explore the same arm of the 'y' they had just explored.

prevot results

the drug treatment group performed almost as well as the mice that had not been chronically stressed.

older mice treated w/ the drug showed significantly higher levels of performance on the task than those given the placebo.

after the study, the mice were sacrificed and the researchers found the mice w/ the drug treatment showed new hippocampal cell growth, reversing the effects of stress and ageing.

prevot conclusion

GABA agonist led to an improved spatial working memory in mice w/ chronic stress and old age. This supports the theory of neurotransmitters as it shows how GABA is involved in memory formation.

This could be applied to human behavior as it demonstrates how neurotransmitters like GABA are involved in cognitive functions like memory formation.

prevot evaluation

- the study uses an animal model. this means the result of this study can only be cautionally generalized to humans, despite the similarities in the role of GABA in memory in humans. Therefore, the drug will have to go through human testing to determine if the findings are generalizable to a human sample.

+ although the study is recent (2019), it is based on an established theory - there's a body of research that has similar results, based on the assumption of GABA's role in memory. For example, this study confirms some of the findings of Koh et al (2017). Therefore, there is other research that supports this study, increasing it's reliability.

antonova aim

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

scopolamine antagonizes the acetylcholine receptors in the central nervous system and throughout the body, inhibiting it's ability to carry out it's role in memory.

antonova method

Sample of 20 health male adults, w/ a mean age of 28 years. Used a double blind procedure and ppts were randomly allocate to one of 2 conditions. They were injected w/ either scopolamine or placebo 70-90 mins before the experimental task.

The ppts were then put into an fMRI where they were scanned while playing the 'arena task' a complex virtual reality game in which the researchers observed how well the ppts were able to create spatial memories.

The goal was for ppts to navigate around an 'arena' w/ the goal of reaching a pole. After the locate the pole, the screen would go blank for 30s. During this, ppts were told to actively rehearse how to get to the pole. When the arena reappeared, ppts were at a new starting point. They would have to use their new spatial memory to find the pole.

ppts were trained in the game prior to the experiment. The ppts memory was measured for 6 hours.

Repeated measures design - ppts returned 3-4 weeks later, receiving the opposite treatment to the original study.

antonova results

When ppts were injected w/ scopolamine, they demonstrate a significant reduction in hippocampus activation compared to when they received a placebo (they took longer to find the pole).

antonova conclusion

It appears that acetylcholine could play a key role in encoding spatial memory, as the hippocampus, associated w/ moving STM to LTM has more activation in the placebo condition where acetylcholine levels were normal.- fMRI was used because there was no significant difference in the number of error made in both groups. w/o knowing the brain activity in the hippocampus, the conclusion that acetylcholine doesn't effect memory could have been reached.

antonova eval

+ the study used a repeated measures design, eliminate the effect of ppt variability. Furthermore, the study was counter-balanced as some ppts did the scopolamine condition first, and the others did the placebo condition first. This controls for order effects (e.g. practice and fatigue effect).

- Although there was a higher rate of error in the scopolamine group, it was not a significant diff. The diff. in hippocampus activity was, however, significant. This means the task as designed may not have been the best for showing performance differences; w/o the use of the fMRI, there would have been no way to know that at the biological level, there was significant different in the 2 conditions.

Evaluation of theory of neurotransmitters

+ neurotransmitter theories have practical applications. They have led to successful treatments for certain behaviors, and drug treatments for psychological theories. Therefore, neurotransmitters have positive uses in medicine and psychiatry.

- the argument that neurotransmitters are the cause of behavior is reductionist. Although the theory may b e good for research into memory as it could lead to positive strategies for helping people w/ memory impairment, explaining a complex behavior like 'falling in love' as a 'neurochemical cocktail' it an over simplification of human behavior. Therefore, these theories only explain behavior on a biological level and are reductionist.