Dopamine Replacement Therapy Research Paper

epinephrine and dopamine, will have an average HR higher than the average HR of stimulants when administered separately. For daphnia 2, it can be concluded from the data that 1mM epinephrine administration resulted in average of 256 BPM, an almost 10% increase from base average BPM of 210 BPM. Administration of 1mM dopamine resulted in average BPM of 212 BPM, similar to the base average BPM of 210 BPM. Lastly, the daphnia was subjected to a combined epinephrine and dopamine solution. From the data, it can be concluded that the combined solution caused the average BPM to increase almost 4%, that is average 218 BPM, in comparison to baseline BPM of the second daphnia. From the second daphnia results: epinephrine and dopamine combined solution didn’t have any drastic increase, almost no effect, when compared to stimulants being administered separately. Hence, this hypothesis is also rejected by the data. Previous research by Barrazo has shown that stimulation of dopamine signaling pathways leads to “decreased movement with different time-courses of

Parkinson’s disease is a “neurodegenerative disorder of the basal nuclei due to insufficient secretion of the neurotransmitter dopamine” (Marieb & Hoehn, 2013, p. G-17). The cause of Parkinson’s disease is unknown, but many factors play a role in the development of Parkinson’s disease. One factor that has been found in an individual who has Parkinson’s disease causes over activity of targeted dopamine-deprived basal nuclei. This over activity is caused by the breakdown of neurons that release dopamine in the substantia nigra (Marieb & Hoehn, 2013). Another factor that is present in a person who has Parkinson’s disease, is the presence of lewy bodies in the brain stem ("What is lbd?," 2014). Lewy bodies are unusual

The major support and refutation of the dopamine hypothesis has come from the examination of dopamine receptors in these regions of the brain. There are two main types of dopamine receptors, D1 and D2. However, within the category of D2 receptors, there are three subtypes, D2, D3, and D4. (5) Through PET scan analysis of dopamine usage in the brain and post-mordum molecular analysis of brain tissue, researcher were able to determine relative levels of dopamine receptors in patients with schizophrenia compared to non-schizophrenics. Overall analysis of dopamine

After attaining the seminar about new treatment L-Dopa and seeing astounding results on Lowe (patient) awakening completely from his catatonic state by using L-Dopa, Dr. Sayer believed that drug might help others as well. He ran trial for his own group. Later, they found out that this treatment is just a temporary triumph. The situation

In Parkinson's Disease and Huntington's disease the nigra-striatum neural communication assemblage is severely hampered. PD results from a depletion in the amount of dopamine produced by the brain. At the onset of the disease, dopamine-secreting cells of the substania nigra, either because of genetic factors or environmental toxins, experience mass cell death. Thus, the nigra cells are unable to form synapses through which they secrete and relay dopamine to the striatum in a neural circuit within the basal ganglia (18).

Some dopaminergic (i.e., dopamine-releasing) neurons run from the substantia nigra to the corpus striatum; their loss gives rise to the clinical manifestations of Parkinson's Disease (Korczyn 1994); others, involved in the rewarding effects of drugs and natural stimuli, run from the mesencephalon to the nucleunucleus accumbens.

Furthermore Parkinson’s disease, which is associated with a depletion of dopamine display behaviours characteristic of schizophrenia when given too much L-DOPA, a dopamine stimulant (Gershon, Angrist, and Shopsin, 1977 as cited in Kalat, 1992). In addition if schizophrenics are given drugs such as L-DOPA their symptoms are heightened. (Kalat, 1992).

The results of these earlier studies were expounded on by research that suggested increased striatal dopamine

In the research presented by Howes and Kapur (2009), they have pointed out a possible concern to invalidate the dopamine hypothesis in schizophrenia as current PET studies did not holding a firm position in measure the dopamine level, they were more to a postulation of a generated estimation from the data. Furthermore, Howes and Kapur (2009) also stressed that the role of dopamine could be circumvented by using the antipsychotic drugs which effectively to the psychotic symptoms but neutral to the dopamine system, thus the role of dopamine will be less critical in schizophrenia. This is because most of the recent antipsychotic researches only prove that dopamine merely contributed in providing a solution in alleviating the psychosis-liked-symptoms but those symptoms are not the symptoms only existed in schizophrenia.

The key function of antipsychotic drugs as recognised by various researchers, is the significant interference with brain dopamine function. This is underpinned by the hypothesis that symptoms of schizophrenia are produced from increased activity of the neurotransmitter dopamine. This essay, therefore discusses and examines the function and mode of action of these antipsychotics drugs with a view to critically identifying whether schizophrenia is a disorder of dopamine function.

Dopamine is a brain chemical/Neurotransmitter that work as messenger signal between the Substantia Nigra to the next relay station of the brain, the corpus striatum which helps to produce smooth coordinate movement and also plays a major role to help control muscle’s movement. With Parkinson’s disease, the brain cells that produce dopamine slowly die, which lead to decrease production of Dopamine. The loss of dopamine causes abnormal nerve firing with brain and the cells that control muscle’s movement by sending the messages to the muscles; due to this it becomes really hard to control muscles movement and cause tremors and various other symptoms such as rigidity and difficulty walking and performing daily tasks. Dopamine is not the only neurotransmitter involved in Parkinson’s Disease. Norepinephrine is very relatively close to dopamine and is also involved in Parkinson’s Disease. Individuals with Parkinson’s Disease have loss of nerve ending that produce norepinephrine. Norepinephrine is a major neurotransmitter for sympathetic nervous system, which control many autonomic functions of our body; it causes increase in blood pressure and heart rate. Loss of norepinephrine can help us explain the non-motor symptoms associated with Parkinson’s Disease such as fatigue, decrease in gastric stability and disruption in cognition. Parkinson’s Disease can be hereditary

The Dopamine Hypothesis theorizes that the symptoms portrayed in Schizophrenia is can be explained by abnormal function of dopamine in the brain. There have been three versions of the Dopamine Hypothesis. The first version of the hypothesis focuses on the dopamine receptors. Antipsychotic drugs that impact the metabolization and reabsorption of dopamine where found to be effective in treating the symptoms. It was theorized that if the symptoms of a Schizophrenic episode can be treated by the use of dopamine

Parkinson’s disease is affected by the degeneration of dopaminergic neurons which is responsible to produce dopamine. Dopaminergic neurons have their cell bodies in substantia nigra pars compacta (SNpc) in basal ganglia (O’Sullivan and Schmitz, 2007). Basal ganglia are a collection of interconnected gray matter nuclear masses deep within the brain”. These gray matter masses are caudate, putamen, globus pallidus, subthalamic nucleus and the substantia nigra. Basal ganglia receive its input through striatum (O’Sullivan and Schmitz, 2007).

Attempts to cure or slow down the progression of Parkinson’s disease have largely failed; researchers in this paper maintain this is obviously a direct result of the lack of insight into the pathogenesis of the disease. Parkinson’s disease is the product of the deaths of a number of dopaminergic (dopamine-secreting) neurons in the substantia nigra pars compacta region (SNc) of the brain. But what causes these deaths? In the paper “‘Rejuvenation’ protects neurons in mouse models of Parkinson’s disease,” Chen and researchers find that older neurons in the SNc are unusually reliant on calcium channels and that after blocking these channels, the cells are “rejuvenated” and begin acting like their juvenile counterparts; as a

Parkinson disease (PD) is a progressive neurodegenerative disorder characterized mainly by physical and psychological disabilities. This disorder was named after James Parkinson, an English physician who first described it as shaking palsy in 1817 (Goetz, Factr, and Weiner, 2002). Jean- Martin Charcot, who was a French neurologist, then progressed and further refined the description of the disease and identified other clinical features of PD (Goetz, Factr, and Weiner, 2002). PD involves the loss of cells that produce the neurotransmitter dopamine in a part of the brain stem called the substansia nigra, which results in several signs and symptoms (Byrd, Marks, and Starr, 2000). It is manifested clinically by tremor,