Dopaminergic Observation

Outline The importance of a neurotransmitter denominated dopamine to regulate emotion and behavior. How is the attention related to the the quantity of dopamine in each persons, and how it influenced their behavior.

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).

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.

Neurotransmitters can also produce their effects by modulating the production of other 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.

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).

The Dopamine and Glutamate Hypothesis and other Influencing Factors in the cause of Schizophrenia Michele P. Bryant Antelope Valley College Abstract 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

5. In the dopamine reward system, there is a stimulus that is given to change the behavior of certain things. The dopamine is present in food, sex, and drugs. Dopamine can be blocked off by the drug pimozide. Pimozide causes the reinforcer (drugs for example) to no longer be reinforcing.

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

The diagnosis of PD is based off of a physical exam and patient history. If someone experiences bradykinesia, rigidity, postural instability, or tremors at rest, they will be considered to have PD. Just one of these symptoms needs to be present for a diagnosis, although they can occur simultaneously. About 10-25% of PD diagnosis are misdiagnosed so it is important to extensively observe a patient’s symptoms before diagnosis. The patient’s history is observed to see if they present symptoms that are associated with other disorders. This allows for similar disorders to be ruled out, increasing the accuracy of the diagnosis. Dopaminergic therapy can be administered and if there is a lasting, significant response, it is likely that the person has PD. If they do not have a response from this treatment, it is an indication of a disease other than Parkinson’s (Savitt, Dawson, & Dawson, 2006).

Patients who are suspected of having The pathology behind PDD is a dopaminergic neuronal loss in the substantia nigra and the presence of Lewy bodies made up of α-synuclein in the cell bodies and processes of the neurons that are left over (Rongve, Dauer). The dopaminergic neurons in the substantia nigra are being lost or inhibited by the production of the misfolded proteins resulting in the lewy bodies. The neurons of the substantia nigra are thought to make up the nigrostriatal pathway, thus their destruction would result in loss of dopamine up to the striatum, made up of the caudate nucleus and putamen. This loss of sufficient dopamine to the striatum of the basal ganglia is what is causing most of the motor movement symptoms seen in PD patients (Dauer). My grandpa used to be a police officer, and I have always perceived him as this big tough guy who could take on anything. After he got older and his PD developed, his movements got much slower and I saw him become this timid man who was unsure

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.

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.

Pathophysiology: 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).

1. Dopamine Replacement Therapy Reverses Abnormal Synchronization of Pallidal Neurons in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Primate Model of Parkinsonism. (J. Neurosci., September 15, 2002, 22(18):7850–7855) GaliHeimer, Izhar Bar-Gad, Joshua A. Goldberg, and Hagai Bergman In the basal ganglia, one of the crucial neuro modulator is dopamine. It

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