A monoamine neurotransmitter that plays a key role in the communication between nerve cells and muscle cells, between neurons in the brain, and in the autonomic nervous system. When the brain sends out a signal, for example, to make a voluntary muscle movement, the message travels along a network of nerves until it reaches the nerves that are in contact with the muscle group. When the neurons at the end of the line, the terminal neurons, receive the signal it triggers the release of acetylcholine into the synapse (the space between the nerve terminal and the muscle cells). The acetylcholine then serves as a chemical messenger, traveling across the synapse to activate receptors on the muscle cells, causing them to contract.
dopamine, norepinephrine, and serotonin are other monoamine neurotransmitters in the brain. In health, these neurotransmitters exist in balance. When disease causes one of them to exist either in excess or deficit, this balance shifts and alters the brain’s function. Dopamine becomes increasingly deficient in Parkinson’s disease, allowing excess levels of acetylcholine to accumulate. This, researchers believe, is what accounts for the tremors and dyskinesias that are characteristic of Parkinson’s disease. Medications called anticholin-ergics block the action of cholinergic neurons, thereby reducing the amount of acetylcholine they release. For a time, this reduction relieves many of the motor symptoms. As Parkinson’s disease progresses, however, the imbalance increases and the symptoms return.
Acetylcholine plays a significant role in the processes of cognitive function, as well, and is deficient in dementias such as Alzheimer’s disease. Researchers are exploring whether anti-cholinergic medications used to treat the motor symptoms of Parkinson’s disease might contribute to cognitive function losses and dementia that develop in some, but not all, people with Parkinson’s disease. glutamate antagonist medications are sometimes successful in offsetting this effect. There does not seem to be a direct correlation between acetylcholine levels and Parkinson’s disease.
The relative paucity of norepinephrine and dopamine, combined with the relative overabundance of cholinergic activity, also may account for the autonomic nervous system dysfunction commonly seen with Parkinson’s disease. The sympathetic nervous system, which constricts vascular smooth muscle to raise blood pressure, depends on norepinephrine as its neurotransmitter, while the antagonist parasympathetic nervous system, which utilizes acetylcholine, relaxes blood vessels, lowering blood pressure. Hence the relative adrenergic deficit and cholinergic excess can lead to lowering of blood pressure, particularly with postural changes like standing.
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