Neurology Week 2 Saq Study Guide Questions

NEUROLOGY WEEK 2 SAQ STUDY GUIDE QUESTIONS 129. Describe the role of astrocyte in the removal excess neurotransmitters using glutamate as an example. (2 marks) Answer: • When the glutamatergic neuron release glutamate, after a while it will saturate in the in synaptic cleft. • Astrocytes have channel that uptake glutamate. In the cell it converts glutamate into glutamine via glutamine synthase. • Glutamine then gets re-up taken into glutamine neurons or GABAergic neurons for recycling to be made into glutamate once again. 130. Compare and contrast Shawn and oligodendrocytes and name ONE disease that affects each. (4 marks) Answer: • Shawn cells: - Myelinate the peripheral nervous system including cranial nerves II to XII. - If damaged, can regenerate and repair themselves. - One cell myelinates only some parts of one axon. - Can be affected by G.B.S. • Oligodendrocytes - Myelinate the central nervous system and cranial nerve II. - If damaged cannot regenerate and repair. - Once cell myelinates 30 to 60 axons. - Can be affected by multiple sclerosis. 131. Explain the pathogenesis of pain in response to: a. Trauma b. Inflammation c. Temperature (with reference to cool, and the different types of warm temperatures. d. Explain the difference between primary and secondary hyperalgesia. e. Define allodynia. Answer: a. Trauma such as being stabbed, activated mechanically gated Na+ and Ca2+ channels, which cause depolarisation to the nociceptors, and thus activate it and cause the sensation of pain. b. In inflammation there is increase H+, K, serotonin and prostaglandins which stimulate nociceptors. There is also substance P release which stimulates mast cells to make histamine. These activate C fibres of nociceptors and cause itchy pain sensations. c. Temperature: - Cold temperature -> TRPM-8 - Moderate temp -> TRPV-R - Temperature over 52 -> TRPV-2 - Temperature over 41 -> TRPV-1 - Warm temperatures 22 – 40 -> TPRV3 - These will cause the activation of nociceptors. d. Hyperalgesia refers to increased sensitivity to pain. - Primary hyperalgesia: refers to increase pain sensitivity within the area of damage. Secondary hyperalgesia: refers to increased pain sensitivity in the surrounding damaged after, 20 minutes after injury. e. Allodynia refers to a pain after a small stimulus, that usually does not cause pain. 132. Cortical plasticity refers to the concept of cortical reorganisation. (13 marks) a. Describe the importance of repetitive spacing for learning. (8 marks) b. Describe the concept of ocular dominance, with reference to what happens to the treatment of amblyopia. (4 marks) c. In patient with impaired hearing in one ear, explain the changes that occur as a result. (1 mark) Answer: a. In response to a learning experience: 1. An action potential will pass through the axon of a glutamatergic neuron, which will stimulate voltage gated Na+ ion channels, allowing an influx of Na+. 2. This will increase the resting membrane potential closer to the threshold potential and will also stimulate the opening of Ca2+ channels, allowing Ca2+ influx. 3. The Ca2+ will bind on SV2aR receptors on glutamate vesicles, that will cause the linkage of snare proteins on the vesicle with those of the membrane. 4. cleft. This will cause the release of glutamate from the presynaptic neuron into the synaptic 5. Glutamate will bind on AMPA and NMDA receptors on the membrane of the dendrites of the post synaptic neuron. Na+ will flow in through the AMPA channels, due to their opening. A bit will also flow through the NMDA. Once enough Na+ enters and the action potential rises, it will cause the Mg2+ that blocks some of NMDA, to come off, which will allow even more Na+ to flow through the NMDA channels, in a similar amount to the AMPA. 6. This will also allow Ca2+ to enter through the NMDA channels, causing Ca2 build up in the cytoplasm. 7. Ca2+ will bind to calmodulin, causing a confirmational change in calmodulin. The confirmational change will expose the hydrophobic receptors on it to allow the binding of PKC and CAMKII causing their activation. i. PKC and CAMKII will cause the translocation of already made NMDA and AMPA, into the presynaptic membrane, and thus upregulating their expression. ii. CAMKII, will phosphorylate itself, so that even after cytosolic Ca2+ levels are back to resting levels, it remains active and continue to perform its’ function. 8. The above enhances LTPs, so that the next time, even mor Ca2+ enters, and thus allow for a better stimulus, more glutamate release and thus better LTPs. 9. The next time the additional Ca2+ entry in addition to the dopamine stimulate a g coupled stimulatory protein -> AC -> conversion of ATP to cAMP -> PKA -> activate CREB genes which causes: i. More BDNF -> increased growth factors -> increased synapse formation -> synaptogenesis. ii. More AMPA and NMDA channels expression, to allow more ion flow and thus for a stronger signal generation and better memory. b. Ocular dominance refers to a columnar organisation in the visual cortex, that is done according to which column gets more visual stimuli from one eye compared to the other. A column that is numbered 1 it means it exclusively responds to the opposite eye, 7 gets exclusively from the same 1, 4 responds equally to both eyes. Treating the lazy eye, can involve covering the healthy eye. This will cause re-organisation of the visual cortex of that lazy eye, so that it becomes stronger. c. When there is one ear that is impaired, the auditory cortex on the opposite hemisphere, will undergo regeneration so that the healthy ear, starts taking more duties of the other ear.