Neuroplasticity and its relation to depression
Neuroplasticity is the term given to the physical changes occurring in the brain over one’s lifetime. In the past, it was believed that the brain stayed the same size and shape all one’s life, but now that modern technology has given us the ability to view the brain visually and observe its changes, we have seen evidence of the brain’s natural ability to change its shape, structure and density. Neuroplasticity occurs in small scales over time, but can also change in response to injury, behaviour, environmental stimuli, thought, and emotions. This is significant in relation to learning, memory, development, and recovery from brain damage (Pascual-Leone et al, 2005). Neuroplasticity occurs when new
…show more content…
connections are made between neurons in the brain in response to stimulation from the environment. This reorganisation subsequently leads to a change in brain shape or weight (Fuchs et al., 2004). Due to advancements in imaging technology over the past few decades, researchers have been able to note a relationship between Major Depressive Disorder (MDD) and neuroplasticity, by observing structural changes across limbic and nonlimbic circuits of the brain.
Patients with MDD have been recorded as possessing lighter and less dense grey matter than patients without, which is taken as evidence of a reduction in neural plasticity. This impairment of plasticity also helps to explain the symptoms of depression that are to do with learning and memory, as these are functions that are affected in the case of reduced plasticity.
The structural plasticity theory of depression has gained traction in recent years, and it is viewed by many scientists to be a more feasible explanation of the pathophysiology of depression rather than the traditional monoamine theory. As more and more evidence is uncovered to support the plasticity and neurogenesis hypothesis of depression, it
…show more content…
becomes The notion that depression is related to impairments of structural plasticity is supported not only by imaging technology, but also by post-mortem morphometric studies of patients suffering from MDD. These studies have shown reduced metabolism and volume in the prefrontal cingulate cortex, as well as atrophy in the hippocampus. This lack of volume is associated with a lack of neuroplasticity. Various animal models have also been used to test this theory, through applying stress (such as forced swims, maternal deprivation, and foot shocks) onto test animals to observe the subsequent change in brain plasticity (Fuchs et al., 2004). Despite this, however, there is still far more research needed to investigate the link between impaired plasticity and MDD. It is still unknown the true extent of this link, as well as what is causing it. Brain Derived Neurotrophic Factor The Brain Derived Neurotrophic Factor (BDNF) is a neurotrophin – a group of proteins that work to regulate neuronal function and assist neurogenesis: the creation of new neurons. Without new neurons being created, when old neurons die they will not be replaced, which results in overall brain cell atrophy. When the neurotrophic factor system is altered, or BDNF levels decrease, issues in neural maintenance and regeneration arise, leading to structural abnormalities in the brain and potential reduction of neural plasticity. This can then impair the individual’s ability to adapt to a crisis situation. An inability to adapt to a crisis can be a major trigger leading to the development of depression (Dwivedi, 2009). Neurotrophins work by binding to the appropriate tyrosine kinase receptor in the brain (BDNF to TrkB) (Figure 1). This binding results in the dimerization and transphosphorylation of tyrosine residues in the cells of the Trk receptors, which results in the activation of cytoplasmic signalling pathways (Dwivedi, 2009). Repeated activation of signalling pathways over time leads to a change in brain shape, and increased neuroplasticity. With less BDNF, less signalling pathways will be activated, and so there will be a reduction in brain plasticity. This expression of BDNF is regulated by neuronal activity, so with reduced activity there will be a reduction in BDNF. Coordinated BDNF release and expression of TrkB receptors is important for synaptic response (Ibid, 2009), meaning that for the brain to function correctly, high levels of BDNF are required, and therefore increased neuroplasticity occurs. This shows a link between the brain derived neurotrophic factor, brain plasticity, and depression. There are many clinical and pre-clinical studies which provide direct evidence suggesting that changes in the levels and expression of BDNF could be involved in behaviour phenomenon associated with depression (Ibid, 2009). Stress and depression is associated with a decreased expression of BDNF, and antidepressants have been shown to increase BDNF levels in the brain. Post-mortem studies of patients suffering from MDD have shown decreased levels of BDNF in the cerebral cortex (Lanfumey et al., 2012), as well as a compromise in synaptic and structural plasticity associated with depression. Extensive studies in both humans and animal models have suggested that monoamines (serotonin, dopamine, and noradrenaline), produce their effects through signalling pathways that regulate neuroplasticity and cell survival, including the BDNF pathway (Lanfumey et al., 2012).
This provides a strong link between the traditional monoamine theory of depression and the BDNF and neuroplasticity theories. This evidence could provide basis for belief that with reduced expression of BDNF, there are fewer pathways for monoamines, leading to a decreased level in these monoamines. It has also been established that BDNF is required for the proper development and continued survival of dopaminergic and serotonergic neurons (Autry and Monteggia, 2012). This could have implications for the etiology of depression to be not in the lack of monoamines, but in neuroplasticity and
BDNF. Furthermore, indirect evidence shows that antidepressants regulate the expression of BDNF and TrkB, and that BDNF itself shows antidepressant-like effects. When given to healthy rodents, several classes of antidepressants all increase the expression of BDNF in the brain (Dwivedi, 2009). Additionally, different classes of antidepressant drugs increase BDNF expression in the hippocampus, an area of the brain closely linked to depression. Post-mortem studies of humans who suffered from depression but had not been treated with antidepressants showed decreased expression of BDNF, while similar studies of patients who had been treated were found with greater BDNF expression in the brain. (Lee & Kim, 2010) However, there have been inconsistent findings in studies researching the link between neurotrophic factors and the onset of depression. Although clinical studies show us that there is a link between decreased BDNF activity and major depression, animal knockout studies have demonstrated that a decline or lack of BDNF can not cause or produce depression or depressive symptoms and behaviour. This suggests that insufficient BDNF does not cause major depression, but is rather a side effect of it. However, it may also be that a decrease in BDNF expression is in fact due to impaired brain plasticity, and that depression and a lack of neurotrophins are both being caused by this decline of neuroplasticity.
Major Depressive Disorder, which is also referred to as Clinical Depression, is a disorder caused when low serotonin levels, that suppress pain perception and are often found in the pineal gland at the center of the brain, promote low levels of norepinephrine, a monoamine neurotransmitter that controls cognitive ability. This disabling disorder interferes with a person’s daily life as it prevents one from performing normal functions, such as eating, sleeping, interacting, or enjoying once pleasurable activities. According to the National Institute of Mental Health, the common symptoms of Major Depressive Disorder are continued feelings of anxiety, worthlessne...
Rupke, S., Blecke, D., & Renfrow, M. (2006, January 1). Cognitive therapy for depression. National Center for Biotechnology Information. Retrieved March 10, 2014, from http://www.ncbi.nlm.nih.gov/pubmed/16417069?dopt=Abstract
Through my extensive research on depression I have learned a lot of new things. I have learned about the many forms of depression and treatment for depression. I have also learned a little about what is believed to go on chemically in the brain of a clinically depressed person. I was also able to partially determine what sort of role genetics, chemicals and personal influences in the brain. Though I was unable to determine exactly how environmental and personal stress can cause a chemical imbalance in a person, I was even able to speculate about this issue and determine some theories of my own on why and how this may happen.
Since the discovery of monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants in the 1950s and its affect on depressives, Schildkraut first proposed the Monoamine Theory. The theory states that depression is caused by an imbalance of monoamine transmitters (neurotransmitters) in certain areas of the brain, such as noradrenaline, serotonin and dopamine (Schildkraut, 1965). This led to the introduction of antidepressant medication in the treatment of depression, known as pharmacotherapy. However, ongoing research suggests that the theory is “inadequate, as it does not provide a complete explanation for the actions of antidepressants, and the pathophysiology of depression itself remains unknown.”(Hirschfeld, 2000) A few of the main reasons for this inadequacy are because it is difficult to measure the level of neurotransmitters in an individual’s brain (P. L. Delgado, 2000) and that evidence is indirect on whether monoamine function is impaired in individuals with depression as the causes of depression appear to be more complex than simply a reduction in levels of monoamine or diminished function in these systems. (P. Delgado & Moreno, 1999)
Neurogenesis, the production of new nerve cells, has been a revolutionary finding as nerve formation has always been thought to end with adulthood. It has not been until recently that such dogma has been contradicted as research findings report that neurogenesis continues in the hippocampus throughout most of the adult life of mammals and primates (1). Recent correlations have been further made between neurogenesis and depression as the latter depletes neuron cells in the brain while antidepressive drugs have demonstrated to increase neuronal growth
Depression is a mental illness, which affects millions of Americans each year. Currently there are many prescription drugs, called anti-depressants that have been proven to successfully treat it. The causes of depression are somewhat of a medical enigma, however, it is known that depression is associated with a change in the brains chemistry involving the function of neurotransmitters (Reichert). This chemical change occurs in healthy brain’s, which experience sadness, but ends after the unpleasant stimulus is removed. In people suffering from depression this chemical change does not correspond to any particular stimulus. Symptoms of depression are often incapacitating and include severe and extended sadness, feelings of worthlessness, feelings of emptiness, irritability and anxiety (Reichert, Spake).
Although historically depression has been considered a character condition, evidence has accumulated suggesting the role of a biological substrate, namely serotonin, in subgroups of depressed patients. This accumulated evidence supports the indoleamine hypothesis of depression, which suggests that major depression results from a deficiency of available serotonin or inefficient serotonin. (16). We see that depletions of serotonin from certain regions of the brain such as the hypothalamus, amygdala, and cortical areas involved in cognition and other high processes, can have a great impact in contributing to depression.
Out of the numerous fascinating concepts covered in this course I found that neural plasticity and memory were two of the most interesting and personally relevant topics. Neural plasticity involves the brains ability to reorganize neural circuits to better adapt to physical or environmental changes. This course primarily covered plasticity with regards to recovering from physical damage to the brain as well as the initial development of the brain and how environmental factors influence this process. With brain damaged victims, neural recovery is almost always apparent; this occurs through either the growth of new axons and dendrites if the cell body remains intact, or a heightened sensitivity of surviving neurons. When axons cannot regrow
It delves into the specific sections of the brains, and how depression can impact the production of the hormone, cortisol. This plays a large part of how the brain is negatively impacted by this disorder. Even though the article states which parts of the brain change from depression, I wish the article explained how the other sections of the brain are affected by the increase of cortisol levels, even if they do not play a major role in regards to depression. I would pose the question of why the other parts of the brain do not influence depression in anyway, to give the reader more context of the other structures of brain development. However, this information is not provided in the text, and this may require further research from revised medical journals or published print. Regarding cortisol levels and depression, I am curious to find if are there are any benefits of neutral effects on the brain and it’s development. In neuroscience, is it known that most mood or mental disorders have absolutely no positive impact on our physical development, but I would like to learn more information related to that. In the future, I may have to look into other functions of the brain influenced from MDD. Another question I would ask is how other disorders or detrimental feelings like suicidal thoughts can influence the brain’s structure as a result of
The biologic basis of Clinical Depression originates in the brain. Your brain is made up of a complex network of nerve cells, called neurons and of brain chemicals, called neurotransmitters. Neurotransmitters transmit messages from one neuron to another. Two of these neurotransmitters are not produced in sufficient quantities in a depressed person’s brain. Because of this lack, too few messages get transmitted between neurons and the symptoms of depression occur. In Clinical depression the chemicals in the brain are out-of-balance. New technology allows researchers to take pictures of the brain that show activity levels in the brain. These imaging techniques such as f-MRI and PET scan actually create images of how active different parts of the brain are. Some studies with these kinds of techniques have suggested that the patterns of activation in the brains of depressed people are different than those who are not. These tests can help doctors and researchers learn more about depression and other mental illnesses. Since this research is fairly new, it is not yet used to diagnose clinical depression.
Neuroplasticity Neuroplasticity refers to the brain’s ability to remap itself in response to experience. The theory was first proposed by Psychologist William James who stated “Organic matter, especially nervous tissue, seems endowed with a very extraordinary degree of plasticity". Simply put, the brain has the ability to change. He used the word plasticity to identify the degree of difficulty involved in the process of change. He defined plasticity as ".the possession of a structure weak enough to yield to an influence, but strong enough not to yield all at once" (James, 1890).
...owell, E. R., Thompson, P. M., & Toga, A. W. (2004). Mapping changes in the human cortex
Recurrent brief depression is caused by a combination of factors including biological, social, sociocultural, and psychological dimensions (Sue and Sue 2013). The different interactions of these dimensions can result in depression. The biological dimension is inherited from our parents and could potentially be traced back to the beginning of one’s lineage. It includes our genetics, brain anatomy, biochemical imbalances, central nervous system function and autonomic nervous system reactivity (Sue and Sue 2013). Depression has a strong hereditary component, so if someone in your family suffers from depression, then you are at a higher risk of getting it (Cohen-Woods, Craig, and McGuffin 2013). There is not one gene that leads to depression; instead there are multiple genes that interact with each other and the environment that can lead to the vulnerability of developing of depression (El Hage, Powell, Surguladze, and McGuffin 2013).
As the human body goes through different experiences, the brain grows, develops, and changes according to the environmental situations it has been exposed to. Some of these factors include drugs, stress, hormones, diets, and sensory stimuli. [1] Neuroplasticity can be defined as the ability of the nervous system to respond to natural and abnormal stimuli experienced by the human body. The nervous system then reorganizes the brain’s structure and changes some of its function to theoretically repair itself by forming new neurons. [2] Neuroplasticity can occur during and in response to many different situations that occur throughout life. Some examples of these situations are learning, diseases, and going through therapy after an injury.
"Patterns of activity in small, more primitive areas of the brain are recapitulated in larger, more advanced parts," Sutton says. "This means that nature did not have to develop new rules of operation for different levels of the brain from small clusters of cells to large systems."