Dopaminergic Observation

How is the attention related to the the quantity of dopamine in each persons, and how it influenced their behavior.

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.

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.

PD is the second most common neurodegenerative disease featured pathologically by the progressive loss of dopaminergic neurons in the substantia nigra. The typical symptoms of PD include slowness of movements (bradykinesia), muscle stiffness (rigidity), tremor, and balance disturbance. Etiopathologically, PD is considered to be caused by the significant loss of dopaminergic neurons in the substantia nigra pars compacta and the subsequent dopamine depletion at the striatum. To date, there are only symptomatic treatments available for PD, particularly in the early stages of the disease. No therapy has been found that can cure or halt the progression of the disease.

Focus Statement: Levodopa (L-DOPA) is a drug which enters the brain and changes its composition to dopamine, a neurotransmitter that is low in Parkinson's disease.It is a most popular treatment to control the symptoms of Parkinson’s disease.

Schizophrenia is a Psychological disorder that impacts the person 's ability to process thoughts, emotions and action. Schizophrenia symptoms are categorized as cognitive, positive and negative symptoms. There has yet to be a confirmed singular cause of schizophrenia. The dopamine hypothesis is a theory that attributes the cause of schizophrenia to an increase in dopamine levels. The antipsychotic medication mentioned in this theory is beneficial in the treatment of the symptoms of schizophrenia. Although the medication that treats increased dopamine levels it does not affect other

It has been demonstrated that altered activity of pallidal neurons evoke irregular signaling patterns of dopaminergic neurons, which in turn may cause a shift in signaling rates to the stiatum and its activating role of the indirect pathway (7). Interestingly, axonal collaterals from the substantia nigra pars compacta also provide innervation to the globus pallidus through dopaminergic signaling (5,1,13). The literature suggests that activation of dopamionergic receptors in the globus pallidus play an important regulatory role of GABAergic activity. Therefore, stimulation of dopaminergic receptors is also involved in the modulation of pallidal firing. The depletion of dopaminergic stimulation in the pallidus suggests a potential role in PD motor deficits and correlation with symptoms such as tremors and dyskenisia (1,2) .Interestingly, experiments conducted in non-human primates have demonstrated that a decrease in dopaminergic inputs to the globus pallidus, due to degeneration of dopaminergic neurons in the substantia nigra pars compacta, triggered irregular firing patterns (1,4); however, the precise role of these dopaminergic projections that cross and directly innervate the GP in parkinsonian physiopathology is not clear

PD pathology results from a degenerative process which reduces the function of dopaminergic substantia nigra (SN) neurons below a certain threshold until it manifests as clinical symptoms17. It should be noted that degeneration of the SN is not the sole location of degeneration – regions such as the locus coeruleus, raphe nuclei, basal forebrain, and frontal cortex undergo a similar process17. The pathology is still not fully understood, but the degenerative process has been found to stem from the glossopharyngeal, vagal, and olfactory cranial nerve nuclei and then ascend upwards through the brainstem18. The degeneration of these origin structures have been theorized to be responsible for the non-motor symptoms presented in PD18.

Dopamine is a neurotransmitter that controls brain reward and pleasure centers. It regulates body movement and your own emotional responses, and it enables people not only to see rewards, but to take action to move toward them, How dopamine makes us human, by Emily Deans M.D (2011). Unfortunately, dopamine deficiency can result in Parkinson’s Disease. Although dopamine is not used in treating Parkinson’s because the normal variant of dopamine does not cross blood to brain barrier, which is like a border that only allows certain substances to transfer from the blood into the brain. Instead scientists use Levodopa; which is a precursor 0f dopamine that can cross blood to brain barrier and converted to dopamine. People with low dopamine activity are more susceptible to addiction. The presence of one type of dopamine receptor is associated to sensation-seeking people, for example, adrenaline junkies.

When I’m talking to my friends or other residents of Augusta, they often tell me how much they dislike living here. When I question them, they usually tell me the reason for this viewpoint is because there’s “nothing to do here” or “it’s an unexciting place to live”. The ones who say these things often have never scoped out the city or made an attempt to find the extraordinary in the mundane. These people are also often unhappy or look to the future for happiness instead of making an attempt to find some now. They don’t know this, but the greatest parts of Augusta are its nature areas like the canal, the lake, Riverwalk, or one of the many nature trails. The residents of Augusta should make more of an attempt to get out in nature and explore

Examined the neuro protective effect of cigarette smoke and nicotine on a MPTP- induced in mouse model of PD. Chronic nicotine treatment resulted in a significant reduction in the loss of dopaminergic neurons in the substantia nigra. These authors suggested that nicotine and low exposure to cigarette smoke may have a neuroprotective effect on the dopaminergic nigrostriatal system(37).

Arguably one of the most famous neurotransmitters, dopamine is better known for its role and impact on reward-motivated behaviour in humans. However, dopamine The human brain contains these dopaminergic pathways which produce and transmit the neurotransmitter between certain areas of the brain, the mesolimbic pathway being one of them which is responsible for reward-related cognition. Other dopaminergic pathways have functions such as memory and associative learning, which alongside reward-related cognition, encourages the formation of an addiction. Addictions are developed as the brain learns to associate the feelings of pleasure created by a release of dopamine with the dopamine-inducing action, and is able to remember this learned association over a period of time. Actions such as engaging in exercise or eating can trigger a sudden release of dopamine that increases brain activity in the dopaminergic pathways.

It is a strong neurotoxin that was identified in 1979 and 1983 when it was administered by accident to heroin addicts and it developed Parkinsonism. By detailed study of the neuropathology by MPTP induced PD in humans, it showed severe neurodegeneration in the substantia nigra and Lewy bodies' absence. Lewy bodies' absence may reflect the patient's age and the duration of MPTP exposure. L- DOPA shows good effects on MPTP induced PD cases in primates.

Hypothesis that the positive symptoms are caused by excessive dopamine in the brain or an overreaction of the dopamine receptor sites

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).