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Topic 1:
Phenytoin (sodium channel blocker) and ethosuximide (calcium channel blocker) are anti-seizure drugs that stop seizures from happening. These drugs work by inhibiting electrical impulses (action potentials) from occurring. Explain the importance of sodium and calcium channels on a neuron and and the reasons why action potentials do not occur when these channels are inhibited. Be sure to include the phases of an action potential, the channels involved, and the importance of an action potential.
Be detailed in your explanation and support your answer with facts from your textbook, research, and articles from scholarly journals. In addition, remember to add references in APA format to your posts to avoid plagiarism.
Topic 2:
The hormone leptin regulates food intake and body weight. It can cross the blood-brain barrier. Search PubMed () for blood-brain barrier and leptin and select two original research articles about leptin. Summarize the results of these articles. Which proprieties of leptin allow it to cross the blood-brain barrier? How does leptin regulate energy balance?
Be detailed in your explanation and support your answer with facts from your textbook, research, and articles from scholarly journals. In addition, remember to add references in APA format to your posts to avoid plagiarism.
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Seizure is a sudden burst of uncontrolled electrical activity in the brain that occurs when neuron becomes excessively active. Seizure is a result of an imbalance between inhibitory and excitatory process in the brain that produces either too little inhibition or too much excitation. The main form of communication among neuron occurs through the action potential which is the travelling wave of electrical excitation. Action potential causes of opening and closing the ion channel. It started when voltage-gated sodium channel open allowing positively charged ions rush into the cell making the membrane depolarize. Membrane depolarization leads to the opening of high voltage activated calcium channel causing positively charged calcium ions enter the neuron which triggers the release of glutamate from the vesicle into the synaptic cleft. Then, glutamate will bind to two postsynaptic neurons: AMPA- permits the entry of sodium ions, then NMDA-permits the entry of calcium ions. All this influx of positive ions leads to depolarization and propagation of action potential. The next phase of AP is repolarization it causes of efflux of potassium ions into the cell through the opening of potassium channel, the membrane returns to resting membrane potential. The last phase is hyperpolarization, the potassium channel in this stage remains open until resting potential is met and returns to normal membrane potential.
When there is too much glutamate around the neuron, it becomes hyperexcitable that results to seizure. Phenytoin and ethosuximide drugs lower the neuron excitability and enhance neural inhibition. The way, the drugs may prevent excessive firing of action potential in neurons by blocking the sodium and calcium channel thereby reducing the amount of sodium and calcium that enter into the neuron. When these two channels are blocked, there is no depolarization, no action potential, with that said no neurotransmitter being release and transmission of electrical impulses.
Reference:
Antiepileptics, acting predominantly as sodium-channel blockers. (n.d.). Retrieved from .
Silverthorn, D. U., Johnson, B. R., Ober, W. C., Ober, C. E., Impagliazzo, A., & Silverthorn, A. C. (2019). Human physiology: an integrated approach. New York: Pearson Education, Inc.