The Neurobiological Factors Associated with Depression Essay

Depressive disorders do not cause just a momentary feeling of sadness, but instead initiate a long-term persistence of feeling upset or worthless. A patient having this disorder will lose interest in their former hobbies and will often spend time in a more secluded environment. Anxiety disorders are described as causing fear, worry, and uneasiness in individuals. Patients with these disorders feel a more unreasonable amount of fear in daily, or common situations. Adverse situations early in life triggers depression. There are noted abnormalities in the hypothalamo-pituitary -adrenal axis (HPA) with raised cortisol concentrations and dexamethasone nonsuppression in depressed patients. Depressed subjects with a history of child abuse show have

People who experience depression can often find relief in taking antidepressants. An antidepressant affects the way the brain passes neurotransmitters, which include, serotonin, dopamine, and norepinephrine, to the different nerve cells in the brain. A study published in Current Biology found that antidepressants change the way the brain cells communicate with one another in as little as a day. It's common, however, for it to take weeks before patients notice a difference in their depression symptoms. Understanding the different ways that antidepressants affect the neurotransmitters can help patients get the relief they need.

Neurotransmitters are chemical messengers that carry messages between neurons and affect behaviour, mood and thought. Two of the neurotransmitters that play a role in depression are norepinephrine and serotonin (Shives 2005). In depression, neurons don’t produce enough neurotransmitters. Shives (2005) states as a result, membrane channels don’t open, nerve messages are not communicated, and areas of the brain affecting emotion may not receive stimulation (Shives 2005). The hormonal system known as the hypothalamic-pituitary-adrenal axis, that regulates the body’s response to stress, is overactive in many people with depression. The hypothalamus increases production of corticotrophin releasing factor when a person’s physical or psychological well-being is threatened (Shives 2005). Elevated levels of corticotrophin releasing factor lean to an increase in hormone secretion by the piturity and adrenal glands which prepares the body for defensive action (Shives 2005). The chronic overactivity of the hypothalamic-pituitary-adrenal axis may occur following a traumatic experience this may contribute to the onset of depression (Shives 2005).

TCAs, SSRIs, SNRIs, SRMs, MAOIs and Lithium Salts) providing a variable range of options that help in considering patients’ preferences along with overcoming antidepressants tolerance and resistance issues. Nevertheless, despite the availability of more than two dozens different antidepressants, these treatments often yield inadequate results, for instance; up to 70% of patients with MDD (Major Depressive Disorder) do not reach remission with an adequate course of one antidepressant and experience poorer long-term outcomes (Fava 2003).The failures and shortcomings of classical antidepressants are usually rationalized through illustrating the hypothesis of their

Neurotransmitter Systems. The study of monoamines in relation to MDD has been at the forefront for the majority of the time that the subject itself has been under research. With a particular focus on serotonin (but also norepinephrine and dopamine), these studies find that the rate of serotonin synthesis is often low in depressed patients (Rosa-Neto et al., 2004). Interpretation of serotonin levels may however become problematic, because it can be concluded that: depression may cause a low synthesis of serotonin; a low synthesis of serotonin may cause depression; or that another third process may cause both a low synthesis of serotonin and depression simultaneously. There is little doubt that a decrease in serotonin plays a key role in MDD but the notion of whether the neurotransmitter’s absence is a mechanism that is uniquely responsible, or merely a

The first antidepressant, a MAOI called Iproniazid, was used in the 1950’s, where it was accidentally discovered whilst treating patients with tuberculosis. It was found that a side effect was that the patients experienced heightened mood and euphoria. It was these side effects that led clinicians to trial the drug on patients suffering with depression, where it was found that 70% showed an improvement. The first antidepressants paved the way for the development of newer drugs which targeted specific receptors, namely SSRIs and SNRIs (Ramachandraih. C,

According to The Diagnostic and Statistical Manual of Mental Disorders (also known as DSM-IV), depression is named as Major Depressive Disorder (Unipolar Depression) and is included in the Mood Disorders group of mental illness (2000). This mental illness is characterized by the following symptoms: “depressed mood, reduced interest in activities that used to

Research has determined that depression is identified by an individual's failure to concentrate, biases seem to be implying that this comes from a negative set of memories and experiences that make up a persons’ beliefs. This mind set results in a deeply thoughtful style described by a lack of logical thinking which leads to depressed emotions and behaviours. The neurobiology behind depression shows that changes in the brain system are commonly linked to this theoretical way of thinking. This similarity proves the cognitive process behind the theory of depression and it also shows the noticeable features of a depressed brain described by neurobiologists

Serotonin, also known as 5-HT, is one of many brain chemicals that transmit messages between brain cells. Serotonin primarily influences feelings of happiness, optimism, and positivity. It also is in responsible for regulating the body’s sleep-wake cycle or internal clock. Normally, serotonin circulates in the brain and then absorbs into the bloodstream. Depression is linked with low levels of serotonin, as well as low levels of dopamine, norepinephrine, and other neurotransmitters (Delgado, 2000). Dopamine, another neurotransmitter, produces feelings of excitement, pleasure, euphoria, and creates motivation and drive. Too little dopamine can result in a variety of symptoms, including depression, anxiety, fatigue, apathy, slowed thinking, memory impairment, the inability to feel enthusiastic about anything, lack of motivation, excessive sleep, etc. (Delgado, 2000). Dopamine is also responsible for reward-seeking behavior. People with abnormally

In studies that examine serotonin and norepinephrine (NE) it is observed that the concentrations of these chemicals are lower than normal in depressive states. This may point to a deficiency in the concentration of monoamines, which are the chemical precursors to neurotransmitters. Enzymes that control the synthesis and breakdown of neurotransmitters may also play a role in depression. For example, the inhibition of tyrosine hydroxylase, which synthesizes NE, leads to decreased concentrations of NE in the synapse. Furthermore, decreased levels of monoamines and enzyme deficiencies, defects in neurotransmitter receptors on post-synaptic membranes may lead to depression. The signal-cascade pathway that occurs after a neurotransmitter binds to its receptor may be affected at the G-proteins on the surface of the neuron, the cAMP pathway, and protein

Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter in the brain that has an enormous influence over many brain functions. It is synthesized, from the amino acid L-tryptophan, in brain neurons and stored in vesicles. Serotonin is found in three main areas of the body: the intestinal wall; large constricted blood vessels; and the central nervous system. The most widely studied effects have been those on the central nervous system. The functions of serotonin are numerous and appear to involve control of appetite, sleep, memory and learning, temperature regulation, mood, behavior (including sexual and hallucinogenic behavior), cardiovascular function, muscle contraction, endocrine regulation, and

Synaptic activity is vital for the passage of information throughout the nervous system, as it allows for electrical impulses to be passed from one neuron to another. Electrical impulses in the form of action potentials are passed through the axon of a neuron towards the axon terminal. This information is then passed across the synaptic cleft to receptors present on the postsynaptic membrane via the process of neurotransmission. Drugs can interrupt this specific process in a variety of ways such as through affecting the production, storage and release of neurotransmitters, the presynaptic and postsynaptic receptors as well as the reuptake and destruction of neurotransmitters (Carlson, 2014). Selective Serotonin Reuptake Inhibitors (SSRIs) and Monoamine Oxidase Inhibitors (MAOIs) are just two types of drugs which can affect different pathways in this process of neurotransmission. In doing so, the neurotransmitter serotonin is made more available within the central nervous system (CNS), a neurotransmitter believed to be central to the affective disorder of depression, which is caused by a deficiency of serotonin.

Clinical and preclinical trials point to a disruption in central nervous system serotonin activity as an important influence. Norepinephrine, dopamine, glutamate, and brain-derived neurotrophic factor are other neurotransmitters included. However, medications that cause only an acute rise in neurotransmitter availability, such as cocaine or amphetamines, do not have the effectiveness over time that antidepressants do.

Most licensed psychologists agree that the controlled use of drugs to alleviate certain mental disorder symptoms is necessary. However, the Big Pharma industry has pushed hard to promote the use of medication for solving every type of mental disorder through psychoactive agents. As a result, antipsychotics have become equally ubiquitous as antidepressants, which are most widely prescribed medication today. This will always be an ongoing debate surrounding the excessive use of stimulants to treat

In today’s society it isn’t uncommon for most people to know someone who has been diagnosed with depression or been diagnosed personally. Over time it has been proven that depression isn’t just ‘a way of thinking or a weakness in ones character. It has been linked not only to genetics but also chemical imbalances that occur within the brain. Based upon the severity of the depression it can have a significant impact on a person’s ability to function and their overall quality of life. There are many treatments currently available for depression. Most of these treatments are in the form of medications that work by inhibiting the reuptake of neurotransmitters such as serotonin, dopamine, and norepinephrine from within the synapses of the brain.