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Parkinson's disease and action of drugs on movement

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Parkinson's disease and action of drugs on movement Introduction: Parkinson's disease is a neurological disorder that seriously impairs motor function, with people afflicted with this condition exhibiting akinesia, muscle rigidity and having a tremor at rest. It is accepted that the loss of motor function is brought upon by the progressive degeneration of nigrostriatal dopamine neurons, which leads to a corresponding loss of dopamine in the caudate/putamen part of the basal ganglia, which is accepted as the main receiving area in motor circuits. Information coming to it from the cortex and thalamus is processed and channeled to the pallidum and to the substantia nigra reticular. ...read more.


This enzyme has a much higher activity in comparison to tyrosine hydroxylase so under normal conditions there is little or no endogenous DOPA found in most cells. The first line of treatment for a patient is to replenish their dopamine stores, which have diminished due to loss of dopaminergic neurones. As dopamine cannot cross the blood-brain barrier it is of no use to simply administer dopamine, instead its precursor L-DOPA is given. This is able to cross the blood-brain barrier upon which it is then converted to dopamine by aromatic amino acid decarboxylase. However L-DOPA can also be converted to dopamine in the periphery, which can cause unwanted effects and so to prevent this a decarboxylase inhibitor is given. ...read more.


Once dopamine is released from the neuron, it is removed from the synaptic extracellular space by a transporter protein located in the presynaptic membrane. This transporter helps to control the extracellular concentration of dopamine. However, amphetamines can disrupt this process as they are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters. They are also capable of diffusing through the neural membrane directly. Once inside the presynaptic neuron, amphetamines force the dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse. This results in a large concentration of dopamine in the cytoplasm. ...read more.

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