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Riku Organization and Control of Neural Function Case Study
Riku Organization and Control of Neural Function 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. Riku Organization and Control of Neural Function Case Study What mechanisms are in place to prevent the continuous stimulation of a muscle fiber after the neurotransmitter is released from the presynaptic membrane?
The case study involves a 19-year-old college student who woke up with the left side of his face drooping after a long night of studying. On his way to the medical clinic, his left eye began to feel scratchy and dry, and he could not blink. The physician conducted a cranial nerve examination and found that the patient had bell palsy, which presents with weaknesses or paralysis of facial muscle mainly caused by a virus leading to inflammation or damage of the cranial nerve VII (facial nerve). This paper will discuss differences between afferent and efferent neurons, efferent components of the facial nerve, axonal degeneration in the central nervous system, and mechanisms preventing continuous muscle fiber stimulation at a healthy myoneural junction.
Afferent Neuron and Efferent Neuron
Afferent neurons transmit sensory information from sensory organs like skin, eyes, and ears to the central nervous system (CNS) (Aragona et al., 2022). They detect stimuli like touch, pain, and temperature and transmit these signals to the brain and spinal cord for processing. As the patient was on his way to the medical clinic, his temperature rose, and he encountered some light detected by the sensory neutrons converting these stimuli into nerve impulses that the CNS, which, after processing, he could not blink. Afferent neurons help us perceive and become aware of our external environment and internal bodily conditions Riku Organization and Control of Neural Function Case Study.
Efferent neurons transmit signals from the central nervous system (CNS) to effector organs, such as muscles (Yam et al.,2018). These neurons initiate and control muscle contractions and glandular secretions. Efferent neurons are responsible for carrying out motor commands, including voluntary movements. They carry out commands and instructions from the CNS to initiate specific actions. Efferent neurons control voluntary muscle movements, involuntary muscle actions like heart rate and digestion, and the release of hormones and other substances by glands (Norris & Lalchandani, 2018). They execute the body’s responses to sensory input and maintain various physiological functions.
Efferent Components of the Facial Nerve and Their Actions
The facial nerve (cranial nerve VII) has several efferent components that control various facial muscles responsible for facial expressions and some glands. The facial nerve controls the muscles responsible for facial expressions, including the orbicularis oculi, which closes the eyelids; the orbicularis iris, responsible for closing the lips; and other facial muscles involved in smiling, frowning, and other expressions (Norris & Lalchandani, 2018). His orbicularis oculi were affected since he could not blink. Salivary Glands also innervate the submandibular and sublingual salivary glands, stimulating saliva production.
Axonal Regeneration in the Peripheral vs. Central Nervous System
Due to several factors, axonal regeneration is much more likely in the peripheral nervous system (PNS) than in the central nervous system (CNS) (Norris & Lalchandani, 2018). The environment within the CNS is inhibitory to axonal regeneration. After an injury, glial cells called oligodendrocytes in the CNS release inhibitory molecules like myelin-associated glycoproteins and chondroitin sulfate proteoglycans, which create physical and chemical barriers that impede axon growth (Norris & Lalchandani, 2018). In the PNS, Schwann cells are crucial in supporting axonal regeneration. They provide physical guidance for regenerating axons and release growth-promoting factors. The equivalent glial cells in the CNS are oligodendrocytes, which do not have the same regenerative properties as Schwann cells. Neurons in the CNS generally have a lower intrinsic regenerative capacity than those in the PNS. This intrinsic regenerative capacity refers to the neuron’s ability to initiate and sustain axonal growth.
In response to CNS injury, astrocytes in the CNS tend to form scar tissue. This glial scar further inhibits axonal regeneration by creating a physical barrier and releasing inhibitory factors. The CNS contains highly complex neural circuits with precise connections. Even if axonal regeneration were possible, ensuring that regenerated axons connect correctly and functionally reestablish the lost neural pathways would be challenging. This level of precision is much more challenging in the CNS than in the simpler PNS. The CNS has a limited neuronal plasticity and reorganization capacity compared to the PNS. This means that even if axons can regenerate, the CNS may not be able to adapt and rewire effectively to restore lost functions. The window of opportunity for successful axonal regeneration in the CNS is often limited. After injury, the damaged tissue undergoes significant changes, making it increasingly difficult for axons to regenerate effectively (Norris & Lalchandani, 2018).
Preventing Continuous Stimulation of Muscle Fibers at Myoneural Junction
Several mechanisms in a healthy myoneural junction, also known as a neuromuscular junction, prevent muscle fibers’ continuous stimulation after acetylcholine (ACh) is released from the presynaptic membrane (Norris & Lalchandani, 2018). This is crucial to ensure that muscle contractions are precisely controlled and do not become uncontrollable Riku Organization and Control of Neural Function Case Study.
Acetylcholinesterase, an enzyme in the synaptic cleft (the gap between the motor neuron’s presynaptic membrane and the muscle fiber’s postsynaptic membrane), rapidly breaks down acetylcholine into its constituent parts, acetic acid and choline (Kaur et al., 2019). This breakdown process is highly efficient and occurs within milliseconds of ACh release. By degrading ACh, acetylcholinesterase ensures that ACh’s stimulatory effect on the muscle fiber is short-lived. After acetylcholinesterase breaks down ACh into choline and acetic acid, choline is actively transported back into the presynaptic neuron. This process helps recycle choline for the synthesis of new acetylcholine molecules. This recycling limits the availability of choline for ACh synthesis and release, contributing to the termination of muscle stimulation.
The postsynaptic membrane of the muscle fiber contains ACh receptors. When ACh binds to these receptors, it triggers muscle fiber depolarization and contraction (Norris & Lalchandani, 2018). However, with continuous ACh binding, these receptors undergo desensitization. This means that they become less responsive to ACh stimulation, reducing the effectiveness of ACh in stimulating the muscle fiber. The action potential (electrical signal) that travels along the motor neuron has a limited duration. Once the action potential ends, ACh release from the presynaptic membrane also ceases. This ensures that the stimulus for muscle contraction is transient and does not persist indefinitely.
Calcium ions play a crucial role in muscle contraction. The release of ACh from the motor neuron causes an influx of calcium ions into the muscle fiber’s cytoplasm. However, the sarcolemma, muscle cell membrane, and the sarcoplasmic reticulum, an organelle within muscle cells, actively regulate calcium levels (Norris & Lalchandani, 2018). Once the stimulus ends, the sarcoplasmic reticulum takes up calcium ions, reducing their concentration in the cytoplasm and allowing the muscle fiber to relax.
Aragona, M., Porcino, C., Guerrera, M. C., Montalbano, G., Laurà, R., Cometa, M., … & Germanà, A. (2022). The BDNF/TrkB neurotrophin system in the sensory organs of zebrafish. International Journal of Molecular Sciences, 23(5), 2621. https://doi.org/10.3390/ijms23052621
Kaur, A., Anand, C., Singh, T. G., Dhiman, S., & Babbar, R. (2019). Acetylcholinesterase inhibitors: A milestone to treat neurological disorders. Plant Arch, 19, 1347-1359.
Norris, T. L., & Lalchandani, R. (2018). Porth’s pathophysiology: Concepts of altered health states. Lippincott Williams & Wilkins Riku Organization and Control of Neural Function Case Study.
Yam, M. F., Loh, Y. C., Tan, C. S., Khadijah Adam, S., Abdul Manan, N., & Basir, R. (2018). General pathways of pain sensation and the major neurotransmitters involved in pain regulation. International Journal of Molecular Sciences, 19(8), 2164. https://doi.org/10.3390%2Fijms19082164

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