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How does dopaminergic receptor agonists and antagonist treatment affect neurons that arise from the subthalamic nucleus...

How does dopaminergic receptor agonists and antagonist treatment affect neurons that arise from the subthalamic nucleus and Substantia Nigra?

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Expert Solution

The subthalamic nucleus and the (STN) of the substantia nigra pars compact The dopaminergic innervation of the office receives the projection considered more frontal. To do this, we use immuno, terrestrial languages ​​D1, D2, and D5 dopamine receptors on the STN martial terrestrial macaque pieces and have studied the effects of the electrophysiological activity of D1, and D2 like normal and I receptors. - phenyl methyl 4 . D1 D2 receptors and a key part of the vinous presynaptically in preterminal axons and gabaergic glutamatergic terminal assumptions and even more significant postsynaptic D5 receptors expressed in STN neurons of the dendritic network. The electrical activity of STN firing neurons, memory, with the standard memory of extracellular forms that are learned before, during and after administration of intra-STN dopamine D1 and D2 as the SKF82958 receptor agonist, as the receptor agonist quinpyrol or artificial cerebrospinal fluid (government injections). In normal animals, things like burning spring: But SKF82958 administration significantly increased the reduced rate of intraburst firing and the fall slowed them down. Quinpyrol only increased the very notion of such a delay, the normal explosion in monkeys, the series of neurons in the STN. In the chat treated with MPTP and D1, entered as a receptor agonist reduced the delay rate increased in a burst sequence, while D2, as the receptor agonist, chose not to change any of the descriptors for burning the pattern of STN neurons. Receptor activation can directly modulate the electrical activity of neurons in the pre and postsynaptic mechanisms of STN and in normal and parkinsonian states, especially through the activation of D1 receptors. The disease (PD) and STN receives gabaergic projections from outside the pale globe segment (GPE) and glutamatergic inputs to the cerebral cortex, thalamus, and brain stem, which traditionally cause activity changes associated with PD as a result of STN degeneration. Dopaminergic route as a result of loss of striatal dopamine. However, small STN primates and rodents receive aminergic innervation of the compact substantia nigra (CNS).


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