Implications Of The Thesis : How Flx Affect Neural Development

The cerebral cortex directs functions like speech, behavior, reactions, movement, thinking, and learning. In fact, some research suggests that bipolar disorder originates with problems with the thalamus, which links sensory input to good and bad feelings. The hippocampus also affects depression. It, like the amygdala, is part of the limbic system. It is vital in processing long-term memory. This section of the brain registers recurring fear. In people with clinical depression, the hippocampus is much smaller. Research suggests, even, that ongoing exposure to stress impairs the growth of nerve cells in this part of the brain. One of the most important jobs of the brain is to process senses, through neurons. Neurotransmitters are specific substances that help relay information to the brain. Scientists have identified many neurotransmitters that affect depression. A lack or excess of the neurotransmitters acetylcholine, serotonin, norepinephrine, dopamine, glutamate, lithium carbonate and gamma-aminobutyric acid are thought to contribute to depression. Acetylcholine is involved in learning and enhances memory. Serotonin helps regulate sleep, appetite, and mood, and inhibits pain. Research shows the idea that many depressed people have reduced levels of serotonin. Low levels of a byproduct of serotonin have been linked to a high risk for suicide. Norepinephrine is a neurotransmitter which constricts blood vessels and raises blood pressure. An excess in

In addition to allowing us to feel good, serotonin also affects growth of synapses in the brain, aiding in deciding the proper response to situations, during brain developmental years. Use of SSRIs at this time could permanently alter connections in the brain, damaging a person’s ability to react in appropriate ways. It was previously thought that the brain ceased development at the age of 12, but recent studies show that the brain continues its development well into one’s mid-20’s, and perhaps even beyond. This new information concerned

Selective serotonin reuptake inhibitors are utilized for their ability to reversibly block the reuptake of serotonin in the synaptic cleft. In order to understand the importance of these drugs, it is crucial to review the various regions of the brains that are influenced by serotonin and the implications of impaired functioning. A dysfunction in the hypothalamus region of the brain might lead to weight or appetite changes. Sleep disturbances are characterized by a dysfunction in the hypothalamus as well, along with the thalamus, basal forebrain, and prefrontal cortex. Thoughts of suicide and perceived feelings of guilt or worthlessness are associated with a dysfunction in the brain regions connected to our emotional well-being, including the amygdala, ventromedial prefrontal cortex, and orbitofrontal cortex. Psychomotor agitation is linked

Drugs like Prozac are SSRI’s (Selective Serotonin Reuptake Inhibitors) and allow serotonin to remain in the synaptic cleft of the neurons for a longer period of time. The only drawback of such drugs is that it takes weeks for them to have any significant effect on the patient. Ketamine, on the other hand is one of the fastest acting anti-depressants. However, there are many concerns regarding the impact ketamine may have on the neurocognitive functioning of the brain. Therefore, despite the instantaneous anti-depressant effects, ability to erase suicidal thoughts and use as a general anesthetic, the long term effects of ketamine may be irreversible and detrimental to the neuro-cognitive functioning of an organism. These effects have been studied in various species; mice, kittens and humans and this topic is of growing importance as many

Selective Serotonin Reuptake Inhibitors (SSRIs) are currently one of the most controversial groups of medicines, with fluoxetine, more commonly known by its brand name Prozac, at the head of the controversy. Opponents of the use of SSRI medications as a successful and safe method for treating depression and related disorders assert that the actions of the drug are an unnatural and a dangerous form of tampering with our neurochemistry. Not only are these medications incredibly safe in almost all cases, they are actually an unnatural method of modifying an already disordered, natural sequence of chemicals in the brain, and therefore are not a form of tampering, but are a method for fixing

It is metabolised by different subtypes of CYP450 enzymes, and converted to active metabolites, n-demethylation metabolite (norfluoxetine). Both fluoxetine and norfluoxetine converted to p-trifluoromethylphenol by o-dealkylation, and to hippuric acid for excretion (3). The elimination half-life of fluoxetine for single dose is one to four days, for multiple doses is four to six days; half-life of norfluoxetine is seven to ten days (5). As well as the serotonin receptor, it also interact with channel ions (Na+, K+, and Ca2+), and monoamine oxidases A and B (6). Both fluoxetine and norfluoxetine show highest tissue concentration in lung, moderate in brain, heart, kidney, and liver, and low in embryonic/fetal tissue, amniotic fluid, and maternal plasma of rat (7,

Monoamine oxidases (MAOs) are FAD depending enzymes and exists in two forms, namely MAO-A and MAO-B. MAOs are responsible for the regulation and metabolism of major monoamine neurotransmitters such as 5-hydroxytryptamine (5-HT), norepinephrine (NE), and dopamine (DA). MAO-A preferentially oxidizes serotonin. Human MAO-A inhibitors are antidepressants and antianxiety agents [1].

The physiological and behavioral effects of early life stress (ELS) on the developing and adult brain are a subject of great interest in the field of neuroscience today. The ability to delineate the mechanisms and structures that are affected during postnatal exposure to chronic stress has the potential to provide invaluable insight into the development of a multitude of neuropsychiatric disorders. While we have come to understand a few of the mechanisms involved in many of these illnesses – such as the significance of the serotonin (5-hydroxytryptamine, 5-HT) neurotransmitter in many depression cases – the complex nature of these disorders and our ability to effectively treat them remains elusive. Such an understanding of how the brain adapts and differentially develops as a result of chronic stress, particularly in early life, may also be able to broaden our understanding of the way in which the brain codes and responds to a variety of emotional triggers.

A deficiency in both serotonin and norepinephrine neurotransmitters specifically in the locus coeruleus, and the dorsal raphe nucleus, which both are important in relations to serotonin receptors can cause depression in AD. Individuals who had both AD and depression showed fewer neurons in the two locations when compared to non-demented individuals (Modrego, 2010 as cited by Zubenk, Moossy & Knopp, 1990). The use of animal shows the links of depressive behavior and AD. Ledo et al. (2016) used a mouse model to show an association of amyloid beta oligomers (AβOs) and depressive like behavior. It was hypothesized that AβOs induced depressive behavior in AD by causing an inflammatory response, which was triggered by activation of microglial cells. Ledo et al. (2016) found that AβOs decreased serotonin levels in the mice. This suggest that the decrease levels in the brains are leading to abnormalities in the AβOs, which then causes cognitive impairments.

Serotonin is a neurotransmitter in the brain that has an immense effect over many functions of the brain. “Cells that make serotonin use tryptophan hydroxylase, a chemical reactor which, when combined with tryptophan, forms 5-hydroxytryptamine”. Serotonin can be discovered three key parts of the body. However, the main location of serotonin lies within the intestinal walls. It is also located within large blood vessels throughout the body and the central nervous system. The most commonly studied area of the body when it comes to serotonin, is how this neurotransmitter effects the central nervous system. The functions of serotonin are abundant and can include the regulation of many important attributes of the human body such as appetite, sleep, mood, behavior, endocrine regulation, and depression.

The 2011 article “Selective p38α MAPK Deletion in Serotonergic Neurons Produces Stress Resilience in Models of Depression and Addiction” is by Michael R. Land et al. The article is about the use of p38α MAPK deletion in model of depression behavior. It also goes into detail about how the use of combination of conditional p38α MAPK null alleles might have an influence in the deletion of p38α MAPK. The research in this article can be used to advance drug that counter at depression and control behavior. It helps to understand what exactly is causing the depression chemically.

In vitro: Fluvoxamine was effective in inhibiting 5-ht uptake by blood platelets and brain synaptosomes [1].Fluvoxamine (10 mg/kg) increased [5-HT]ex levels in all brain areas, and also increased [DA]ex levels in the striatum. Fluvoxamine (10 mg/kg) in combination with of quetiapine (10 mg/kg) increased [DA]ex and [5-HT]ex levels in all brain areas compared with baseline. The combination produced a significant increase of [DA]ex levels in the prefrontal cortex and thalamus whereas

Hollrigel GS, Chen K, Baram TZ, Soltesz I (1998). The pro-convulsant actions of corticotropin-releasing hormone in the hippocampus of infant rats. Neuroscience. 84: 71?9.

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

The purpose of this study was to determine whether or not inhibiting the medial prefrontal cortex (mPFC) reduced positive emotion-triggered cataplexy and to study the brain sites activated during positive emotion-triggered cataplexy. The researchers used chocolate as the cataplexy trigger, as mice have a strong positive emotional reaction to it. Cataplexy is characterized by an instant loss of muscle tone via efferent shunting usually found in narcolepsy. The efferent shunting can reduce muscle tone anywhere from select areas of the body to the entire body. High bursts of positive emotions can cause bouts of cataplexy and is a phenomenon that has been observed for more than 100 years. Despite how long this has been observed, (Oishi et al.) insist that little to nothing is understood about the circuits that are responsible for this phenomena. To examine a model for cataplexy in mice, the team had to examine orexin knock-out mice. These mice had their genetic codes for the