1. why is it important to remove or degrade a neurotransmitter in the synaptic s
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Question
1. why is it important to remove or degrade a neurotransmitter in the synaptic space after it has bound itself to a receptor on the post-synaptic neuron?
2. what is actually happening at the synapse that causes alcohol to exert its sedative effect? And which agonist is a neurotransmitter?
3. why do people with diabetes have a greater incidence of cataracts than the general public?
4. why do patients with Parkinson's disease experience tremors and trouble moving? Discuss the brain region and neurotransmitter associated with this disease?
5. Why do the sensation of smell fade (chemoreceptors), and the sensation of motion stays (mechanoreceptors)?
Please guys help me with these questions.. Thank you
Explanation / Answer
1. Once a neurotransmitter has activated its receptors, it must be removed or destroyed rapidly in order to permit transmission of subsequent signals. Some neurotransmitters, regardless of type, simply diffuse from the synaptic cleft. Small-molecule neurotransmitters are also taken back up by presynaptic and postsynaptic neurons and by neighbouring cells. One neurotransmitter, acetylcholine (ACh), is broken down rapidly by a membrane-bound enzyme in the region of the synapse. Neuroactive peptides are eliminated only by diffusion from the synaptic cleft and by proteolysis (degradation) by extracellular enzymes; thus they tend to have more sustained effects than small-molecule neurotransmitters.
2. Alcohol directly affects brain chemistry by altering levels of neurotransmitters -- the chemical messengers that transmit the signals throughout the body that control thought processes, behaviour and emotion. Alcohol affects both "excitatory" neurotransmitters and "inhibitory" neurotransmitters. An example of an excitatory neurotransmitter is glutamate, which would normally increase brain activity and energy levels. Alcohol suppresses the release of glutamate, resulting in a slowdown along your brain's highways. An example of an inhibitory neurotransmitter is GABA (Gamma-amino Butyric acid), which reduces energy levels and calms everything down. Alcohol suppresses the excitatory neurotransmitter glutamate and increases the inhibitory neurotransmitter GABA. What this means for you is that your thought, speech and movements are slowed down, and the more you drink the more of these effects you'll feel (hence the stumbling around, falling over chairs and other clumsy things drunk people do).
3. In galactosemia (diabetes), high galactose concentrations are found in blood and urine. Affected individuals develop cataracts, caused by deposition of the galactose metabolite galactitol in the lens.
4. Parkinson’s disease (PD) is a degenerative, progressive disorder that affects nerve cells in deep parts of the brain called the basal ganglia and the substantia nigra. Nerve cells in the substantia nigra produce the neurotransmitter dopamine and are responsible for relaying messages that plan and control body movement. For reasons not yet understood, the dopamine-producing nerve cells of the substantia nigra begin to die off in some individuals. When 80 percent of dopamine is lost, PD symptoms such as tremor, slowness of movement, stiffness, and balance problems occur.
Body movement is controlled by a complex chain of decisions involving inter-connected groups of nerve cells called ganglia. Information comes to a central area of the brain called the striatum, which works with the substantia nigra to send impulses back and forth from the spinal cord to the brain. The basal ganglia and cerebellum are responsible for ensuring that movement is carried out in a smooth, fluid manner. These impulses are passed from neuron to neuron, moving quickly from the brain to the spinal cord and, finally, to the muscles. When dopamine receptors in the striatum are not adequately stimulated, parts of the basal ganglia are either under- or over-stimulated. In particular, the subthalamic nucleus (STN) becomes overactive and acts as a brake on the globus pallidus interna (GPi), causing shutdown of motion and rigidity. When the GPi is overstimulated, it has an over-inhibitory effect on the thalamus, which in turn decreases thalamus output and causes tremor.
The action of dopamine is opposed by another neurotransmitter called acetylcholine. In PD the nerve cells that produce dopamine are dying. The PD symptoms of tremor and stiffness occur when the nerve cells fire and there isn't enough dopamine to transmit messages. High levels of glutamate, another neurotransmitter, also appear in PD as the body tries to compensate for the lack of dopamine.
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