Monday article #36: biological, emotional, and cognitive effects of maternal deprivation

Deprivation is defined as the severed bond from the primary attachment figure, usually the mother. This can be either long term deprivation (for instance, through death) or short term (for example, being placed in day-care). If a child undergoes privation, they have never created a bond. In this instance, children are unable to access basic needs. This is usually the case with feral children such as Genie. Much of the research into deprivation focuses on the social, cognitive, and emotional effects on an individual. However, this essay will focus on the biological effects of deprivation, specifically the effects on brain structure and hormones and in turn, the effects on human behaviour. Attachment theory

Bowlby’s Maternal Deprivation theory

Maternal deprivation is the separation of the mother from the infant. Bowlby’s theory suggests that attachment behaviour is used to strengthen the bond between the mother and infant. The child will remain distressed until the primary caregiver is present, leading the accumulation of anxiety that would cause deeper problems during physical, cognitive and emotional development. Bowlby went on to suggest that infants have an innate and inborn capacity to attach to a single attachment figure. He believed that the quality of the bond with different people differs, there had to be one bond, usually with the mother, that was stronger than other bonds with other people. Bowlby claims that there is a critical period when nurturing an infant, a broken or not forming an attachment during the first 2.5 years or life could result in permanent negative consequences. Therefore, a continuous care is needed to avoid being socially, cognitively and emotionally impaired. Long term consequences resulting from maternal deprivation includes not having the ability to form attachments in the future with their significant others, affectionless psychopathy, juvenile delinquency, increased aggression and reduced intelligence. (McCrory et al, 2010) In Bowlby’s 44 thieves’ study, he found that the majority of the juvenile thieves had experienced separation from their mothers for as long as 6 months during their critical period. Amongst the thieves, 85% of them had affectionless psychopathy, the inability to feel affectionate towards others. From this, we can conclude that deprivation during the critical period for a long period of time results in an irreversible emotional damage. (Bowlby, 1944) Further evidence for this comes from Harlow et al (1971). The researchers aimed to study how being separated from or neglected by their mother can affect development in the later years of life using rhesus monkeys. The monkeys were taken away from their biological mother within 6-12 hours of their lives. He found that, although equal amount of food was given to the baby monkeys, after a period of time, the baby monkeys that was nourished by the wired mother with cloth were more emotionally attached compared to the sample of baby monkeys that were brought up by the wired monkey. However, both group of monkeys developed aggressive antisocial behaviours, many were aggressive towards their own offspring in some cases killing their young. Suggesting that deprivation leads to physical and social impairments on behaviour, in this case, aggression. (Harlow et al, 1971) Neurobiology of cognition and behaviour

Neuroplasticity & the biological stress system Moving away from psychological theories such as Bowbly, it can be suggested that the effects from suffering from deprivation mirrors the symptoms of stress. Sufferers are likely to experience anxiety, depression, and in some cases can lead to illnesses such as schizophrenia (Janetsian-Fritz, 2018). This is a result of alterations in brain size and how the brain itself functions, this can extend to affecting our genetic makeup.

When we experience stress, the hypothalamus pituitary adrenal (HPA) axis is tiggered which in turn triggers a reaction in the endocrine glands found in the brain and our kidneys. Together these will secrete an excess amount of the hormone cortisol (glucocorticoids), a hormone linked to the physiological and psychological events of stress by increase blood sugar levels and plays a role in the fight-or-flight system, which will then trigger symptoms mentioned earlier (anxiety, depression etc) (Smith et al, 2006). Further to this, due to the limbic system’s close relation with the HPA axis, the amygdala and hippocampus, and the prefrontal cortex are the most vulnerable to the early life stress that maternal deprivation creates. The excess cortisol will impact the effectiveness of the limbic system in the brain, resulting in an inability to control our emotions (e.g. mood swings) and an inability to process and remember information effectively. Many if these symptoms have been identified in research into the effects of deprivation, where sufferers again have experienced cognitive impairment (Smith et al, 2006). Pathological outcomes to brain regions such as the hippocampus could be a result of glucocorticoids negative feedback. Psychopathological outcomes such as, but not limited to, depression, anxiety disorders may also be a consequence due to the increasing levels of stress hormones that have the potential to impact behavioural and cognitive processes because of the cortisol’s ability to access the brain and bind to corticosteroid receptors (Dhikav et al, 2012). Additional effects of experiencing chronic stress, has led to epigenetic changes where the modification of the gene has occurred. This has been evident in rat studies that included separating mother and pup, and the epigenetic changes were passed down many generations. This was shown that the epigenetic changes present int the mother rat were passed down through many generations, thus making the results inheritable (Murgia, 2015). However, studies have shown that there are many ways to reverse the adverse effects of chronic stress, including exercising and meditations (Sosa et al, 2019). Kennards Principle suggests an immature brain, similar to the ones found in babies, are more able to recover from a brain injury compared to a more developed brain. From this we can imply that an infant’s brain is much more plastic and more prone to the negative changes caused by the environment. Plasticity is the capability of a system to change in response to the alteration occurring internally or externally by adapting the appropriate phenotypes or reinstate older phenotypes. In response to the environment, our brains have the ability to adapt and alter in order to support us in learning and development. Undesirable psychosocial experiences may have an impact on the human brain as it is vulnerable to the negative effects it produces; early childhood maltreatment is an example (Dennis, 2010). Though, it also suggests that through intervention, such as adopting at an early age, individuals have the potential to recover from the effects induced by deprivation (Anderson et al, 2011). The autonomic nervous system produces fast response to potential threats on an individual’s well-being or survival. It uses the sympathetic nervous system and parasympathetic systems, releasing hormones that relaxes the mind while slowing down the bodily functions which are then overactive. The sympathetic nervous system triggers the regulation of the HPA-axis, causing the secretion of hormone cortisol, and a continuous activation of the nervous system can become problematic, resulting in the problems previously stated (anxiety, depression) (American psychological association, 2018). Negative feedback

Humans undergo allostasis, the process of maintaining homeostasis by changing the organism’s internal environment to meet the demands from the body, in order to balance the level of mediators depending of the individual's body to stabilise the physiological system through change however, many would mistake this for homeostasis. So, what is the difference between allostasis and homeostasis? Homeostasis is a process that regulates the body’s systems such as blood pH level, whereas allostatic processes is involved with altering physiology to counter the environmental obstacles. McEwen and Wingfield (2010) suggested that allostasis is an important process that allows us to adjust to new environments that are predictable and unpredictable. Allostatic overload is a stage in allostasis which could potentially cause pathophysiology. There are two types of allostatic overload: type 1 occurs when energy demanded exceeds supply. It directs the organism from normal life to survival mode, normal life cycle resumes when the feeling of anxiety or mental uneasiness passes. Type 2 occurs when there is an excess consumption of energy accompanied by social disagreements. If load is chronically high, then pathologies develop. Type 2 allostatic load does not trigger an escape but can be overcome through learning and changes in the social structure.

The allostatic load is often used as a structure to explain the biological consequences of exposure to chronic stress, which can be induced by deprivation, in patients with psychotic disorders, and is found to be highly correlated with depressive symptoms and working memory impairments (Misiak, 2020).

Figure 2: The allostatic load explaining the biological consequences of

exposure to chronic stress



How maternal deprivation affects the Brain and limbic system, and how it alters behaviour, cognition and

emotions Neuropeptide Y

Widely expressed in the central and peripheral nervous system, the neuropeptide Y (NPY) is a protein that contributes to countless physiological processes, one of which is emphasised in this review: modulating stress response and emotions. According to rodents’ studies, the NPY regulates stress and emotional behaviours and is mainly expressed in the brain’s limbic and stem areas. It is involved in the mechanism of anxiety and depression, the most common effects of being deprived, and research on rodents have been done that supports this (Sah, 2012). Rodents were utilised to test the effect maternal deprivation has on emotional behaviour of rats of both genders, who was deprived at postnatal day 3 (DEP3) and postnatal day 11 (DEP11). It was found that maternally deprived rats had shown increased anxiety- and depressive-like behaviours in a number of behavioural tests (Suchecki et al, 2018). This is said to be linked to the decreased expression of NPY in emotion related organs such as the amygdala and hippocampus. From the results of the experiment, we can infer that the maternal deprivation at an earlier age impacts behaviour more, such that during the tests the rats did, DEP3 rats showed more anxiety symptoms compared to the control group, non-deprived rats, and DEP11. Although both sets of deprived rats were affected negatively, DEP3 was affected more than DEP11, this can be shown through the adrenal weight found in DEP3 rats as they were heaviest in both male and female, indicating that adolescents may be experiencing chronic stress. The study also found that reduced NPY expressions in brain areas in charge of emotions in rats that were maternally deprived at a younger age lead to impaired cognition, fear and alcohol addiction to name a few. Therefore, the effects maternal deprivation has on different ages could, to some extent, be used to explain behaviour in young adult rats. The neuropeptide Y not only plays a role in developing disorders, but it also is potentially therapeutic for stress-triggered disorders. A study (Federation of American Societies for Experimental Biology, 2013) delivered NPY to rats through intranasal infusion 30 mins before or immediately after being exposed to singly prolonged stress (SPS), intranasal infusion is a non-invasive method to avoid the blood brain barrier. Behaviour were analysed 1 to 3 weeks after exposed to SPS and compared to the control group, the group which was not treated with NPY. In animals that were exposed to intranasal NPY, their anxiety, depressive-like and hyperarousal behaviours reduced significantly. Studies have concluded Figure 3 – functions of Neuropeptide Y in different areas of the brain, suggesting the different impairments depending on the area which has a lower NPY expression that an immediate delivery of NPY intranasally could promote resilience and enhance PTSD symptoms. However, these studies do not take sex differences into account and mainly uses male rats in experiments, assuming it would be generalisable to females. Due to the excessive evidence for a lower expression of NPY in females compared to males when exposed to prolonged stress made scientist wonder if delivery of NPY the same effect in females have as it did in males. 600µg dose of NPY had prevented the impairment of social interaction mediated by SPS, whereas there was a dose-response effect of intranasal NPY when delivered with 1200 µg, successfully reducing symptoms of depressive like behaviours. Though a combination of 600µg of intranasal NPY and dipeptidyl peptidase IV inhibitor, which is an NPY protease, has a greater effect of improving depressive-like behaviours on the forced swim test, as they become more mobile. Concluding that intranasal NPY is therapeutic for both males and females, though females may need a higher dose (Nahvi, 2021). Suggesting that reducing symptoms induced by maternal deprivation requires an activity that would increase NPY expressions, a classic example would be to have a healthy diet or intermittent fasting (Cao, 2021). Intermittent fasting contributes to the increase hippocampal NPY expressions, and a one-month intermittent fasting promotes the prevention of cognitive dysfunction induced by deprivation. Risk of developing psychiatric disorders Risk of depression and anxiety is not only concerned with maternal deprivation, development of schizophrenia is also a potential threat (Janetsian-Fritz, 2018). Alteration in cognition and brain functioning occurs as a result of being maternally deprived. This effect was experimented on rodents who were maternally deprived on postnatal day 9. A series of tests were done to find the following: their ability to recognise previously occurred events, also known as recognition memory, expression of catechol-o-methyltransferase (COMT) in the medial prefrontal cortex, ventral striatum and temporal cortex and how sensory gating is affected by maternal deprivation. COMT is an enzyme that is involved in the deterioration of catecholamine neurotransmitters, which responds to the body’s stress symptoms triggering either a fight or a flight, thus holding a potential threat to cognitive flexibility, switching behavioural responses depending on situations, impulse control, abstract thought and difficulty in obeying. Sensory gating is when an individual filters irrelevant stimulus from the environment in the brain, and sensory gating deficit is known to be a marker for schizophrenia. Deprived animals displayed impaired recognition task and lower expression of COMT in the medial prefrontal cortex and temporal. Not only were bioelectric noises observed on the EGG at each recording site of deprived animals, there was also an alteration in the stimulus encoding. Data obtained suggests that neurodevelopmental perturbation produces permanent alterations in cognition and brain function and have been applied to research done on humans that establishes a relationship between the genetic differences in COMT and bioelectrical noise. Current studies have suggested that the low protein expressions play a role in ensuring that information flows through brain regions smoothly, resulting in unusual combination of sensory information which could potentially cause a mild impairment in cognition. The maternal deprivation caused modifications lead to a change in shared information between cognitive and primary sensory processing areas, which provides an understanding to how trauma experienced during early life leads to a change in neural functions and increase the risk of developing psychopathology.

Autism spectrum disorder, nowadays described as a group of complicated neurodevelopment disorders characterised by the lack of ability to interact and communicate with society, is also developed through traumatic stress events experienced in early life. Although the molecular mechanisms of the increased risk of psychiatric disorders as a result of neonatal maternal deprivation remains questionable, there are researches that observed the involvement of oxytocin receptor signalling in the medial prefrontal cortex in autistic- like behaviour induced by early life stress. Development of brain plasticity in the neonatal period is crucial, as there is an increased risk of picking up a psychiatric disorder in juveniles and adults (Wei et al, 2020). Rats that had went through 4 hours of neonatal maternal separation during postnatal 1 – 20 had displayed symptoms of autism, however no learning or memory impairments. In an attempt to study the mechanism molecularly, oxytocin receptors were found to be downregulated in the medial prefrontal cortex, especially in the neurons, relative to the control group. Erk/MAPK signalling plays a role in transmitting extracellular signals, which regulates the interaction between unicellular organisms and fundamental regulators that affect development and is also used to signal the downstream coupling of oxytocin receptors (OTXR). The signalling was found to be prevented in juvenile rats. Due to the fact that this research had also found that medicines containing the inhibitor of H3K4 demethylase, regulation of gene expression, reduced abnormal behaviour and increased OTXR expressions in the medial prefrontal cortex in neonatal maternally separated rats, it shows that social deficits induced had an epigenetic mechanism. Suggesting that interruptions in mother-infant interactions influences the later signs on typical social behaviours and also OXTR expression could be adapted and passed down through generation. Effects of age and gender Stress hyporesponsive period (SHRP) is a period where there is a relatively inactive stress response system, therefore exposure deprivation to SHRP promotes reduced abnormal social and cognitive behaviours. As a consequence of maternal separation, oxidative stress is created, damaging brain cells and increasing the risk of Parkinson’s disease (Sampson, 2019). The study (Uysal et al, 2005) decided to test the effects of deprivation during and after this period. During the SHRP in rats, the endocrinological response to stress were absent during postnatal 4 and 14 th days. This study experimented on age-dependent effects of maternal deprivation and examined the oxidative stress in the hippocampus, prefrontal cortex and striatum regions of the brain in rats after SHRP and during SHRP. Being maternally deprived during the SHRP showed an increase in antioxidant enzyme activities and a reduction of peroxidised lipids in the brains of infant rats. On the other hand, being deprived after the SHRP had lowered enzyme activities and increase in lipid peroxidation. Antioxidant enzyme are capable of stabilising and deactivating free radicals before it attacks cellular components and lead to pathological outcomes such as Alzheimer’s disease. Lower levels of lipid peroxidation are desirable as excess an of peroxidised lipids lead to cell damage because electrons from the lipids are transferred to the free radicals. Predictions have been made that the brain is being protected in SHRP from the oxidative stress produced by maternal deprivation, reducing the immediate development of impairments, though anxiety related behaviours will be displayed later in life (Schiavone et al, 2013). Males and females are different in many aspects, including how they respond to stress in the environment and their vulnerability as well differs. In an experiment to research to possible role of the endocannabinoid system in maternal deprivation (Llorente et al, 2008), it was found that the cellular and biochemical effects of maternal deprivation were gender dependant. Despite the body’s endocannabinoid system playing a role in neuroprotection, plasticity and aspects of memory, it is also part of the hypothalamic function which responses to stress. The cortisol levels induced by maternal deprivation were found to have been reduced in both genders, though in males astrocytes, a type of glia cell which has access to 2 million synapses, in CA1, a region located near the hippocampus and in charge of encoding spatial awareness, and CA3, an area which encodes episodic memories and is susceptible to neurodegeneration, increased along with the hippocampal variation of endocannabinoid, 2-arachidonoylglycerol, which can have a disruptive effect on both memory and learning. The cannabinoid compounds reversed the endocrine and cellular effects of maternal deprivation, providing evidence that cellular and biochemical effects of maternal deprivation on developmental hippocampus and alteration in the endocannabinoid system is gender dependent. Reducing the adverse effects of & resilience towards maternal deprivation Susceptibility to chronic stress induced by maternal deprivation can be reduced through acute aerobic exercise (Sosa et al, 2019), improving cognition and consolidating memory. Although the effects of chronic exercise on cognition is well understood, the influence of acute aerobic exercise on cognition lacks evidence. Studying on male rats, they split the group into deprived and non-deprived, both groups were to undergo an object recognition training. A certain number of rats were submitted to perform aerobic exercises immediately after the test, using the retention test, memory consolidation and persistence was analysed 24 hours, 7 days, 14 days and 21 days after the object recognition trainin

Results showed that with one session of physical exercise was sufficient enough to regulate learning by encouraging memory consolidation and persistence in rats that had cognitive deficits induced by maternal deprivation. Using the high-performance liquid chromatography method, dopamine levels in the hippocampus was measurable and found to not have changed before and after the object recognition training. Dopamine released into the hippocampus promotes attention, episodic memory, spatial learning and synaptic plasticity. On the contrary, promotion of norepinephrine in non-deprived rats increased after object recognition training whereas, no increase was found in maternally deprived rats, despite performing exercise or not, even though norepinephrine plays a key role in enhancing memory. Predicting that exercise does enhance memory in deprived individuals, but the effect is not long-term. Impaired social behaviour, emotions and behaviours are generally associated with maternal deprivation, though some individuals who experienced childhood maltreatment may have functioned better despite being exposed to chronic stress. Resilient, however, is not due to one resilient gene, instead is due to multiple complex processes from polygenetic influences on supportive social influences (Ioannidis et al, 2020), although the molecular mechanism is not fully understood. Other than the NPY that was mentioned previously, serotonin transporter gene also suggests the gene-environment interactions can have a resilient impact on genes. A study (Stein et al, 2009) that investigated the association between genetic variation in a repeated polymorphic (5-HTTLPR) region in the serotonin transporter gene and emotional resilience found that variation in 5-HTTLPR does have an influence in how individuals respond and withstand events that exhibit stress like maternal deprivation, providing an explanation for the constant interaction between 5-HTTLPR and life stressors when predicting mental health. Therefore, variations of 5-HTTLPR gene could justify why some individuals are not affected by the adverse effects of maternal deprivation. Conclusion Since maternal deprivation can negatively impact infants due to the plasticity of their brain relative to adult brains, the evidence presented in this essay has outlined some of the molecular mechanisms underlying the development of social, emotional and cognition impairments and how some individuals are not affected by the adversity. The research presented here has investigated the relationships between the paternal carer and infant rats/mice, very few have used the mother, unless they are investigating for gender differences. This calls into question the generalisability to not only the effects of mother-infant interactions in mice/rats, but also, more importantly the application to human mother-infant interactions and effects on deprivation. Humans are more complex as is the relationship between mother and infant, and so this weakens the validity of the studies. Furthermore, considering we differ in terms of our organ systems and the human brain is far more complex to study. Nevertheless, summing up, the regulation of the HPA axis leads to altering gene expressions and hormone secretion, potentially causing the development of undesirable psychiatric disorders such as schizophrenia and autism spectrum disorder. References:

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This article was prepared by Fatini Khadrishah

 










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