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?

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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.

Child Poverty

cry-2764843_640Psychology comes right up to date with the study of the effects of child poverty on cognitive and social development.  In Psychology Sorted we make the link between child poverty, brain imaging technology and child development.  We could just as easily have also added in an abnormal psychology link to mental health, for as child poverty rates in the US and UK soar, so does the number of children in poor mental health.  (For a further cross-cultural perspective, the same is also true of Australia and New Zealand).

Luby et al. (2013) uses MRI scans to investigate the relationship between child poverty and brain development in pre-school and early school age children, and found that it was associated with less white and cortical grey brain matter and reduces hippocampal and amygdala volumes. The effects of poverty on the volume of the hippocampus were mediated by a close relationship with a good caregiver, but increased by stress and hostility. The effects on the cognitive development and  mental health of young people have been well documented.

While some subjects studied in schools may not always seem relevant to the world outside the classroom, psychology will never be one of them.

We’re all just animals, aren’t we?

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The question of when to use non-human animal studies as evidence for human behaviour is a tricky one. Because it remains unethical to lesion the brain of a live human to look for a correlation between brain damage and behaviour (at the moment!), animal studies are used in large numbers at the biological approach. However, many people are becoming more disturbed by this than previously as over the years we have come to realise that animals also suffer pain, fear and anxiety as we do, and maybe other ways should be sought to conduct animal studies.

In Psychology Sorted, this is part of the Biological extension: the British Psychological guidelines for working with animals (2012) state that researchers should: Replace animals with other alternatives. Reduce the number of animals used. Refine procedures to minimise suffering.  But isn’t how they are used a large part of the problem?  After all, observation under natural conditions should be no problem.  Xu et al. (2015) researched naturally-occurring depression in macaque monkeys by observing monkeys living at a research base in China in environmental conditions that closely resembled what they would experience in the wild, for nearly 3 years.  The monkeys were housed in colonies, usually of two males and 16-22 females, with offspring of under six months.

Instead of unnaturally separating baby chimpanzees from their mothers, as Bowlby and others have done, causing distress,  Stanton et al. (2015) ‘picked up poo’: they investigated the effect of maternal stress on the glucocorticoid levels of infant chimpanzees by examining and measuring faecal glucocorticoid metabolite (FGM) concentrations of mothers and babies in the wild.  Much less stress for the monkeys, though maybe not for the researchers! 

Bearing in mind that we are animals too, it is time empathy stretched to our non-human cousins, and these methods seem to be a first step on the way.  See Psychology Sorted for more examples of ethical animal research.

 

Research from Psychology Sorted: Poverty and childhood cognitive development – a biological approach.

This is the first in a series of posts using research directly from our new bookpoverty3349068_640 Psychology Sorted.  The study we’re looking at today is Luby et al. (2013) on how children’s brain development and therefore their cognitive development are affected by poverty. The researchers found that exposure to poverty in early childhood impacts cognitive development by school age. However, the effect is mediated positively by good caregiving and negatively by stressful life events.

This is highly relevant in light of reports from the UK, USA and  South-East Asia of the large, and in some cases growing, number of children living in poverty.  This research can be used as an example of both localization and neuroplasticity within the Biological Approach,  and to illustrate the influence of poverty/socio-economic status on cognitive development, for those studying the Developmental Psychology option.

This was a longitudinal study of 145 children from a sample of children already enrolled in a 10-year study of preschool depression who, prior to being scanned by MRI,  had undergone regular testing.  Once a year (for a duration of 3-6 years) the children had taken part in a series of tests aimed at measuring their cognitive, emotional and social aptitudes. The involvement of significant adults in their lives was also recorded (e.g. how close they were to their caregivers) as well as the occurrence of any negative and stressful events in their lives. Once this collection of information had been amassed, each child underwent two MRI scans – one of the whole brain and one of the hippocampus and amygdala only. This study can therefore also act as an example of the use of brain-imaging technology as a technique used to study the brain in relation to behaviour.

Both the hippocampus and the amygdala showed less white and grey matter in the MRI scans of the poorer children in this study, with a positive correlation between income/needs being met and brain volume. While both the hippocampus and amygdala showed less development in poverty-affected children the researchers found that in cases where the child experienced positive care there was less negative effect on the hippocampus. Difficult and stressful life events only affected the left hippocampus.

Of course, students and teachers need to evaluate the use of this research as well: how valid is the study as an illustration of both localization and neuroplasticity? This was a relatively small sample of pre-schoolchildren from the USA who exhibited symptoms of depression.  Moreover, attempting to measure complex variables (e.g. the nature of caregiving and behavioural responses) is beset with difficulties as these variables are not exact and may lack construct validity.  Nonetheless, there was triangulation of methods, with the background data from cognitive testing providing a rich backdrop for the results of the scans, and this research is supported by other studies, such as that by Duval et al. (2017). 

Encourage your student to find and read media and academic examples of evidence and counter-evidence, and to engage in critical thinking and evaluation. For example, some poor families often cannot afford pre-school kindergartens for their children, who may be raised to some extent in isolation as well as in poverty.  This could be a confounding variable. Are there others? The student who is thinking like this is well on the way to writing a good argumentative essay on the effects of poverty on childhood cognitive development.

Pheromones – are we looking the the wrong place?

pheromonesA pheromone is a chemical substance released  by a non-human mammal or an insect which affects the behaviour or physiology of others of its species. Most of the search for human pheromones has focused on their role in attracting members of the opposite sex, even though in animals and insects they have also been shown to affect the feeding behaviour of ants and baby rabbits are known to begin nursing when exposed to a specific pheromone from a lactating mother rabbit.  If you search for ‘pheromones’ on the web, it is quite likely that a picture like the one above will pop up, and you will be encouraged to buy ‘X perfume spray, which contains the highest possible concentrate of known human pheromones, to make you irresistible to the opposite sex.’ Wow!

Of course this statement is probably true, as the total numbers of known human pheromones is exactly zero. There are no known human pheromones, and Tristram Wyatt is one researcher who says that scientists are looking in the wrong place for them.  In his TED talk he points out that rather than thinking about sex, we should be thinking about breast feeding  and the secretions from those tiny little white bumps in the areolae around the nipples of both men and women. It is over nine years since the secretion from these glands in lactating women was shown to act on newborn babies, causing them to wake and suckle.  Research by Doucet et al. (2009) shows that this is true of  any newborn and any woman, which means, like a pheromone, this is action at species level, rather than individual level.

So, while the perfume spray may attract one or two members of the opposite sex, it is not because of the human pheromones in there. In fact this is not where the real action is at all. In his most recent article, Wyatt argues that we should go back to the beginning and focus on a possible human mammary pheromone, rather than wasting any more time thinking about attracting others through chemical secretions. Sounds like a plan!

Lifelong learning – old dogs and new tricks

dog-2183114_640You can’t teach an old dog new tricks – or so the saying goes.  Developmental psychologists like Piaget tended to assume that cognition and the corresponding brain development were complete by the age of about twenty.  However, recent research into brain neuroplasticity shows that adults, even older adults, can continue to learn throughout their lives, and improve their brains in the process.  Lisa Pauwels and her colleagues published a paper this month, describing the structural and functional brain changes that occur with practice of a new task.  They found that older adults may be a little slower than younger ones in attaining new skills, but they were equally capable of learning, and intensive practice led to modulation of GABA (gamma-amino butyric acid, the main inhibitory neurotransmitter) and an increase in neurons and connections  (neurogenesis) in the corresponding brain regions.

The brain doesn’t only respond to learning, as Sandrine Thuret describes in her TED talk (below).  When you eat and what you eat, exercise and sleep all increase neurogenesis in adults.

So, if some days you are struggling with your studies, remember,  it is never too late to grow some more brain!