‘Psychology Sorted’ Book 1 second edition (including all the new additions) out now on Amazon!

Laura and I have been working hard to get the second edition of ‘Psychology Sorted’ Book 1, Core Approaches out – and here it is! This second edition includes key study summaries for all of the new additions to the Core Approaches – yes, those pesky topics that could come up on Paper 1, Section A. So, if you have been wondering about which study to use for agonists, antagonists, excitatory/inhibitory synapses, neural pruning etc. (I mention the Biological topics as these are the ones that seem to have caused us all so much grief!) then do not fear, we have them here!

You can order the book here

And if you love it please leave a review to say that you do!

Neurotransmitters – keys in locks


All neurotransmitters are agonists – chemicals that bind to receptor neurons and activate them to respond. They act like keys in post-synaptic receptor neuron ‘locks.’ They fit into their own receptor neuron and bind to it to produce a voltage change called an action potential. When they do this they are having an excitatory effect in the synapse. An example of a neurotransmitter that does this is acetylcholine, which binds with receptors, especially in the hippocampal area, to improve encoding in memory. Kihara and Shimohama (2004; 2018) – found that a decrease in acetylcholine receptors has a leading role in the development of Alzheimer’s disease

Some drugs are also agonists, and bind to or mimic the effect of the neurotransmitter, provoking the same response in the receptor neuron. Alcohol does this for dopamine – activating dopamine receptors in the nucleus accumbens area of the brain.

However, although they are all agonists, not all neurotransmitters have an excitatory effect in the synapse. Sometimes they make it less likely for the receptor neuron to fire an action potential. GABA and serotonin both do this, decreasing the receptor neuron activity and having an inhibitory effect in the synapse.

Several neurotransmitters can have either excitatory or inhibitory effects, depending where in the brain  they are acting and with which receptor neurons they are interacting. This Youtube video is very informative regarding neurons and neurotransmitters https://tinyurl.com/qo8yqxp

Planning your course effectively – the biological approach and development

Overlaps Dev_Bio green

The biological approach to children’s cognitive development is well-established, as it seems obvious that learning must be directly related to neurogenesis (growth of new synapses connecting neurons) and neural pruning (‘cutting back’ of synapses no longer needed).  But of course this development through neuroplasticity requires not only good nutrition and nurturing to prevent injury, but also social stimulation, so a lot of research has looked at how trauma and deprivation may affect the cognitive development of the child, by delaying or preventing brain development in crucial areas like the hippocampus and amygdala.

The techniques used to study the brain and neuroplasticity topics under the biological approach can be successfully taught using material from the developing as a learner and the influences on social and cognitive development topics within the developmental psychology option. Recommended studies are Chugani’s (1998) PET scans of children from birth to late adolescence; Gotgay et al’s (2004) longitudinal study mapping brain development using MRI scanning; Luby et al’s (2013) research into the effects of poverty on the brain and the mediating effect of caregiving.

More help with planning is coming in the following weeks!

References (summaries of these studies can be found in Psychology Sorted Book 2):

Chugani, H. T. (1998). A critical period of brain development: studies of cerebral glucose utilization with PET. Preventive Medicine, 27(2), pp. 184-188.

Gotgay, G., Giedd, J., Lusk, L., Hayashi, K., Greenstein, D.et al. (2004). Dynamic Mapping of Human CorticalDevelopment During Childhood Through Early Adulthood. Proceedings of the National Academy of Sciences, 101(21), pp. 8174-8179.

Luby, J., Belden, A., Botteron, K., Marrus, N., Harms, M. P., Babb, C.,et al. (2013). The effects of poverty on childhood brain development: the mediating effect of caregiving and stressful life events. JAMA Pediatrics, 167(12), pp. 1135-1142.


Planning your course effectively – exploiting the overlaps

Bio_HR Image - green

Here is some support when planning for the new school year. This is one of the most useful exercises I have ever done before teaching a course on psychology. Using a table, or a simple Venn diagram, as above, identify the overlaps between the core approaches and the options. Putting these posters around your class, sharing them with students, and using them for your own planning can clarify and structure your thinking and theirs. This is so useful when it comes to revision.

For example, as we can see, the biological approach to human relationships comprises mainly evolutionary psychology arguments. The same overlaps mapped between biology and abnormal psychology would identify brain neurochemistry as a key conceptual argument. The biological approach to childhood development looks at brain development and neuronal networking.

Doing this helps immensely with understanding the big picture, and also minimising the studies one needs to cover. If teaching the human relationships option later in your course, when students are learning about evolutionary psychology in the biological approach earlier in your course – here are their examples.

I will be mapping more of these over the following weeks, so watch out for them before term starts!

Ethics of animal research

monkey-3512996_1280A few months ago, we posted about how we could use animals for research.  Today we are looking at the ethics surrounding the decision to conduct research using nonhuman animals. Most students can reel off the ethics involved in conducting research on humans (informed consent, lack of harm, right to withdraw, privacy, etc.) but when we talk about the ethics of conducting research using nonhuman animals as proxies for humans, they are less clear. Often the argument gets stuck at the level of “It’s OK for medical research, but not for cosmetics.”  This is not good enough for an understanding of the complexities (nor for an exam answer).  For students that wish to argue that conducting research on nonhuman animals in order to avoid causing pain or distress to humans can never be ethical, point out that this is a worthy philosophical question, and could even be a counter-argument in a psychology debate on the topic, but again, it cannot constitute the main argument of an exam essay on ethics.

The APA,  BPS and Australian government publish guidelines for conducting nonhuman animal research ethically. What emerges from the guidelines are the ‘3 Rs’ of animal research:

  • Replace animals with other alternatives – such as computer simulations, use of lesser species (such as single‐cell amoebae and nematode worms),  use micro-dosing, CRISPR DNA editing, or human cell cultures – known more colloquially as ‘patient in a dish’ or ‘body on a chip’.  But animals are used to generate new hypotheses, so CRISPR editing was tried out on animals first, as was stem cell research. 
  • Reduce the number of individual animals used, by using data from other researchers, or by repeated micros-sampling on one animal in a repeated measures design.
  • Refine procedures to minimise suffering, by using appropriate anaesthetics and painkillers, and training animals to cooperate with procedures to minimise any distress. Imaginative research, where faecal matter is analysed to investigate stress levels, rather than drawing blood from an obviously stressed animal, has a part to play here.

In Psychology Sorted Book 1, we provide summaries of studies by Xu et al. (2015) and Stanton et al. (2015) which show how nonhuman animals may be used more ethically, to contrast with others such as Barr et al. (2004) and Weaver et al. (2004) which cause more stress to the animals used. These will help to keep your students more closely focused on the complexities of whether and how we should use nonhuman animals in psychological research.

Antagonists – what do they do?

dementia-3761172_640Antagonists are any chemicals that fit into receptor sites on the post-synaptic neuron, inhibiting the neuron from firing. Well-known antagonists for serotonin, which we looked at in the previous blog post, are anti-psychotic drugs like Clozapine, which acts on the HT2A serotonin receptors to decrease the effects of serotonin in the brain. Many ant-psychotic drugs also act as antagonists for dopamine, as an excess of both dopamine and serotonin has been associated with schizophrenia.

However, easy-to-understand studies referencing this effect of Clozapine are difficult to come by, so while this is useful knowledge for students on how anti-psychotic medication works, when teaching about antagonists there is more available research on the effects of scopolamine on acetylcholine, and hence on memory.  (And incidentally on motion sickness, as scopolamine is excellent at preventing nausea and vomiting!)

Scopolamine acts by blocking the acetylcholine receptors, specifically the muscarinic receptors (see the link below). Atri et al (2004)  reported how blocking the muscarinic acetylcholine receptors (mAChRs), by injecting scopolamine impairs learning of paired words.

As an age-related deterioration in cognitive function is thought to be predominantly related to a decline in cholinergic neurotransmission (relating to nerve cells in which acetylcholine acts as a neurotransmitter), scopolamine administration has often been used to model dementia. Scopolamine has therefore been extensively used for preclinical and clinical testing of treatments for cognitive impairment.  For example, Tröster et al (2013) found that scopolamine negatively affected anterograde short-term memory and verbal and nonverbal learning in middle-aged men.

Agonists – what are they?


Biological psychology has come to the fore over the past years.  The mapping of the human genome combined with improved brain-scanning techniques has meant that the biological correlation to psychological conditions is more easily identifiable, and it is clear that many mental disorders like major depressive disorder, anxiety disorders and schizophrenia are explainable through a gene x environment interaction.  This usually means that an inherited genetic pre-disposition to a disorder, or a certain behaviour or addiction is triggered environmentally.

Talking of genes takes us to neurotransmitters.  How? Genes make proteins which make neurotransmitters and genes also transport neurotransmitters across the synapse. (See Caspi et al._2003 and the 5HTTR serotonin transporter gene).  Neurotransmitters are agonists –they bind with receptor sites on the post-synaptic neuron and cause an action potential.  Drugs are also agonists that act in the same way, but they are not natural in our nervous system.  Neurotransmitters are known as endogenous agonists (internal agonists); drugs, or any chemicals taken into the body, to deliberately stimulate a certain neurotransmitter or group of neurotransmitters, are exogenous agonists (external agonists).

An exogenous agonist for serotonin is MDMA (Ecstasy).  It works by binding with the serotonin transporter genes and also with the receptor sites, temporarily increasing the serotonin in the synapse in the neocortex (part of the cerebral cortex), the amygdala, hippocampus and hypothalamus, affecting cognitions such as memory and perceptions, as well as mood. We party!

However, studies have suggested that there is a rebound effect, whereby damage to the serotonin transporters after several doses of MDMA over a period of a few days has resulted in an ultimate decrease of serotonin in the brain, and memory and mood impairment, leading to theories that this might be linked to a motivation to take more and eventually to possible addiction. (See McCann et al MDMA and memory).

Of course, the opposite to an agonist is…an antagonist, which will be the subject of the next blog post.