BIO 526 Assignment 6.1: Organization and Control of Neural Function Case Study 

BIO 526 Assignment 6.1: Organization and Control of Neural Function Case Study

BIO 526 Assignment 6.1: Organization and Control of Neural Function Case Study

Riku Case Study

Riku is a 19-year-old college student. One morning, after a long night of studying, Riku woke up and made himself a hot cup of coffee and toast. Much to his surprise, when he brought the cup to his mouth to drink, the coffee spilt onto the table. Riku went to the bathroom mirror and noticed the left side of his face seemed to droop. He quickly got dressed and ran to the medical clinic on the college campus. As he ran, his left eye began to feel scratchy and dry, but he could not blink in response. The physician at the clinic listened to Riku’s story and then did a careful cranial nerve examination. She concluded that Riku had Bell palsy, an inflammatory condition of the facial nerve most likely caused by a virus.

ORDER A PLAGIARISM-FREE PAPER HERE ON;BIO 526 Assignment 6.1: Organization and Control of Neural Function Case Study

1. What are an afferent neuron and an efferent neuron? What are the efferent components of the facial nerve and their actions?

Afferent neurons transport impulses or signals from a sensory organ to the brain or the central nervous system (CNS), where they interpret data from both the outside world and the body itself (Schneider et al., 2021). Efferent neurons are regarded as motor neurons since they transmit signals from the brain to the body’s sensory organs. They have a crucial role in the regulation of endocrine and exocrine glands, as well as muscle fibers. The cranial nerve VII (CN VII) is a mixed nerve that has both efferent and afferent components in normal physiology (Berntson & Khalsa, 2021). The medulla and pons junction serves as the origin of the facial nerve’s efferent components. The nerves for the palate’s taste and nasopharynx are supplied by the nervus intermedius and general visceral efferent neurons. The anterior 2/3 of the tongues, the lacrimal glands, the mucous membranes of the nose, the sublingual and the submandibular salivary glands, and the mouth roof are also all innervated. The muscles on a single side of the face are under the direction of the efferent cranial nerve. Additionally, it regulates actions on the face including smiling, shutting the eyes, and blinking. Moreover, it sends signals to the muscles of the tiny bone in the middle ear as well as the tear and salivary glands.

A deficit of CN VII can cause eye dryness, which increases the chance of blindness and corneal scarring (Tereshenko et al., 2022). The facial nerve’s pharyngeal efferent motor neurons provide sensory input to the muscles that govern facial expressions like frowning and smiling. Muscles on one side of the face become paralyzed due to a lack of facial nerve function. The name of this ailment is Bell palsy. Bell palsy is a transient, idiopathic facial weakness or paralysis that affects one side of the face. One-sided facial droop, difficulty making facial expressions, drooling, jaw or dorsal ear discomfort, unilaterally enhanced sensitivity to sound, migraine, loss of taste, and alterations in tear and saliva secretion are only a few of the symptoms that come from cranial nerve VII malfunctionings. Bell palsy can affect both sides of the face and can range from little weakness to total paralysis, causing observable facial deformation. It often only affects one side of the face. Bell palsy’s precise etiology is uncertain. However, many scientists think it arises from the reactivation of a latent virus that results in CN VII swelling and inflammation.

1. Under certain circumstances, axons in the peripheral nervous system can regenerate after sustaining damage. Why is axonal regeneration in the central nervous system much less likely?

The presence of the endoneurial sheath makes axonal regeneration in the CNS considerably less likely to take place. Peripheral nerve regeneration depends on a tissue called the endoneurial sheath (Tereshenko et al., 2022). This explains why damaged axons in the PNS may regenerate. A regenerated axon can once more reach its original destination through the collagen tube provided by the endoneurial sheath. The endoneurial sheath, nevertheless, does not enter the CNS during axonal regeneration (CNS). As a result, axonal regeneration in CNS nerves is less than in PNS. Because a stroke leaves a person permanently disabled, the capacity of the neuron to repair itself is essential for the CNS to regain its normal function. It is believed that growth-inhibitory elements connected to the CNS myelin in contrast to the PNS myelin are the cause of the absence of axonal regeneration. Specific growth-inhibitory substances derived from glial scar tissue around injured regions that hinder axon regeneration include the myelin-associated glycoprotein (MAG),  oligodendrocyte myelin glycoprotein, Nogo proteins, and chondroitin sulfate proteoglycans (CSPGs).

Due to the endoneurial sheath, the PNS nerves are also more robust and resilient than those in the CNS. The connective tissue sheaths that encase the nerve fibers in the nerves are present (Varadarajan et al., 2022). The medium-sized to big nerves are encased in the epineurium, an outer fibrous sheath. Each bundle of nerve fibers is encased in a sheath called the perineurium. Each nerve fiber is protected by a thin sheath of connective tissue called the endoneurium inside each bundle. Schwann cells (SC) that process the myelin sheath covering the peripheral nerves are found inside these endoneurial sheaths. Each SC mostly myelinates the axon it covers, but occasionally other axon segments as well. Therefore, a lengthy line of SCs must participate in the myelination of a complete axon.

Myelinating and non-myelinating SC undergo substantial reprogramming during axonal damage, which aids and guides axonal healing. SCs become repair phenotypes after losing touch with and demyelinating the distal axon stump (Au et al., 2022). Numerous pro-myelinating genes have been downregulated as a result of this phenotypic change. Repair SCs may be recognized by a distinctive quality that makes the regeneration process possible. Several genes are upregulated during SC reprogramming, and numerous transcriptional pathways are involved. To provide a favorable environment for regeneration to occur at the wounded spot, repair SCs are involved in the breakdown and elimination of damaged axon debris. Myelin debris clearance entails engaging and activating a large number of macrophages as well as digesting both intrinsic and extrinsic myelin pieces through a process known as myelinophagy and phagocytosis. Furthermore, SCs release trophic substances to aid in the survival of injured neurons and encourage axon regeneration. Axon regrowth returning to innervate its original target is facilitated by repair and SCs, which also project lengthy parallel processes and align in tracts known as bands of Bungner. Finally, SCs multiply, activate promyelinating genes, transform into myelinating SCs, and remyelinate the regenerating axon

1. At a healthy myoneural junction, acetylcholine is responsible for stimulating muscle activity. What mechanisms are in place to prevent the continuous stimulation of a muscle fiber after the neurotransmitter is released from the presynaptic membrane?

The neurotransmitter signal follows a process in healthy muscle fibers. Typically, chemical synapses and the utilization of neurotransmitters are used by neurons to interact with one another. Three distinct processes are dependent upon this communication: the presynaptic neuron’s production and release of the neurotransmitter; the neurotransmitters attachment to the postsynaptic neuron’s receptors; and the neurotransmitters release from the receptor site (Bittner & Martyn, 2019). To maintain precise control, the neurotransmitter is rapidly withdrawn from the muscle fiber after it has had its effects on the postsynaptic membrane. The neurotransmitter, however, goes through one of three stages once it is released to stop the muscle fiber from being stimulated continuously:

• Enzymes can convert them into inactive compounds. For instance, the enzyme acetylcholinesterase (AChE) attaches to the plasma membrane through a glycerophospholipid anchor (Debarshi Kar Mahapatra & Sanjay Kumar Bharti, 2023). The asymmetric A12 does, however, have a collagen tail in the neuromuscular junction that connects to the synaptic basal lamina. ACh receptors are grouped at the neuromuscular junction, and this localization necessitates a close interaction with extracellular matrix proteins. AChE’s localization to this specific location links neurotransmitter release and breakdown, helping to regulate.
• It is capable of reuptake, in which case it is returned to the presynaptic neuron. Acetylcholine’s breakdown into choline and acetic acid is one instance of this. In this mechanism, choline is taken up again by presynaptic neurons and regenerated into acetylcholine via the Na+ gradient across the cell membrane. Cl- is involved and is in charge of returning the catecholamines to the neuron in an unmodified state so they may be utilized once more (Bittner & Martyn, 2019). The extracellular transmitter must be removed from the synaptic cleft for this neurotransmitter reuptake to be effective in terminating the signal.
• Until its concentration is too low to affect postsynaptic excitability, it can spread into the intercellular fluid (Debarshi Kar Mahapatra & Sanjay Kumar Bharti, 2023). The enzyme that produces acetylcholine, acetylcholinesterase, is localized to the neuromuscular receptor sites, which promotes breakdown with neurotransmitter release. Additionally, perlecan and dystroglycan, two extracellular matrix proteins, are strongly adhered to by acetylcholine during localization. Catecholamines are also broken down by enzymes in the synaptic gap or nerve terminals, allowing for their degradation and distribution into the intracellular compartment. These are actions that help govern the release and regulation of neurotransmitters.

References

Au, N. P. B., Chand, R., Kumar, G., Asthana, P., Tam, W. Y., Tang, K. M., Ko, C.-C., & Ma, C. H. E. (2022). A small molecule M1 promotes optic nerve regeneration to restore target-specific neural activity and visual function. Proceedings of the National Academy of Sciences, 119(44). https://doi.org/10.1073/pnas.2121273119

Berntson, G. G., & Khalsa, S. S. (2021). Neural Circuits of Interoception. Trends in Neurosciences, 44(1), 17–28. https://doi.org/10.1016/j.tins.2020.09.011

Bittner, E. A., & Martyn, J. A. J. (2019, January 1). 21 – Neuromuscular Physiology and Pharmacology (H. C. Hemmings & T. D. Egan, Eds.). ScienceDirect; Elsevier. https://www.sciencedirect.com/science/article/pii/B9780323481106000211

Debarshi Kar Mahapatra, & Sanjay Kumar Bharti. (2023). Biologically Active Small Molecules. CRC Press.

Schneider, G. T., Lee, C., Sinha, A. K., Jordan, P. M., & Holt, J. C. (2021). The mammalian efferent vestibular system utilizes cholinergic mechanisms to excite primary vestibular afferents. Scientific Reports, 11(1). https://doi.org/10.1038/s41598-020-80367-1

Tereshenko, V., Maierhofer, U., Dotzauer, D. C., Laengle, G., Schmoll, M., Festin, C., Luft, M., Carrero Rojas, G., Politikou, O., Hruby, L. A., Klein, H. J., Eisenhardt, S. U., Farina, D., Blumer, R., Bergmeister, K. D., & Aszmann, O. C. (2022). Newly identified axon types of the facial nerve unveil supplemental neural pathways in the innervation of the face. Journal of Advanced Research. https://doi.org/10.1016/j.jare.2022.04.009

Varadarajan, S. G., Hunyara, J. L., Hamilton, N. R., Kolodkin, A. L., & Huberman, A. D. (2022). Central nervous system regeneration. Cell, 185(1), 77–94. https://doi.org/10.1016/j.cell.2021.10.029

BUY A CUSTOM-PAPER HERE ON;‌BIO 526 Assignment 6.1: Organization and Control of Neural Function Case Study

Introduction
Complete the Riku Case Study

Links to an external site..

Riku Case Study Alternative Version

Riku Case Study
Riku is a 19-year-old college student. One morning, after a long night of studying, Riku woke up and made himself a hot cup of coffee and toast. Much to his surprise, when he brought the cup to his mouth to drink, the coffee spilt onto the table. Riku went to the bathroom mirror and noticed the left side of his face seemed to droop. He quickly got dressed and ran to the medical clinic on the college campus. As he ran, his left eye began to feel scratchy and dry, but he could not blink in response. The physician at the clinic listened to Riku’s story and then did a careful cranial nerve examination. She concluded that Riku had Bell palsy, an inflammatory condition of the facial nerve most likely caused by a virus.

Student Name:

What are an afferent neuron and efferent neuron? What are efferent components of the facial nerve and their actions?
Under certain circumstances, axons in the peripheral nervous system can regenerate after sustaining damage. Why is axonal regeneration in the central nervous system much less likely?
At a healthy myoneural junction, acetylcholine is responsible for stimulating muscle activity. What mechanisms are in place to prevent the continuous stimulation of a muscle fiber after the neurotransmitter is released from the presynaptic membrane?

Assignment Guidelines
You may also submit your completed work using the Riku Case Study (Word) document. Please make sure to include your name on your case study submission.

Turnitin
This assignment will be scanned using Turnitin software. Turnitin is an online service that highlights matching text in written work. It indexes Internet sources, databases of subscription services, and written work submitted through its website. Assignments sent through Turnitin are scanned against all of its sources and a report is generated that summarizes and highlights matching text and where it was found. It is up to instructors and students to interpret the report to determine if plagiarism occurred.

You may submit your assignment to Turnitin prior to its due date to assess your work against Turnitin’s database. You may use the Originality Report’s results to address any originality concerns in your work, and then resubmit your assignment for grading. You may resubmit until the assignment’s due date. Any work that has been submitted at the time the assignment is due will be considered your final submission, and this will be the submission used for grading.

Visit the Bradley University Turnitin student page for tips and resources, including a video tutorial on how to submit an assignment using Turnitin.

Submission
Submit your assignment and review full grading criteria on the Assignment 6.1: Organization and Control of Neural Function Case Study page.