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Intro to Movement Neuroscience Tutorial Notes

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Health Sciences
HLSC 2400U
Dr.Kevin Power

Neuroscience Tutorial One Notes Sept. 26 th 2011 Multiple Choice Answers Spinal cord does not extend from the Medulla to the Sacrum Cerebellum contains about 50% of the total neurons The shallow grooves separating the Gyri are called Sulci Basal Ganglia are responsible for smooth movement. One of the functions of Cerebellum is coordination of equilibrium. The latin word for “Little Brain” is Cerebellum The spinal cord is not the site where sensations are felt. The somatosensory center is. The spinal cord connects periphery information to the brain and also functions to process information A tract is a bundle of nerve fibers inside the CNS Sensory neurons are also known as “Afferent” neurons. They are located on the Dorsal side. Motor neurons are located on the Ventral side. A stroke affecting the medial portion of the post central gyrus of the right hemisphere is most likely to result in symptoms such as:  Loss of sensation in the left foot Primary Motor Cortex is also known as Pre – Central Gyrus which is responsible for motor output. Post - Central Gyrus is the Somatosensory area which is responsible for sensation interpretation Central Sulcus seperates the Pre- and Post- Central Gyri The sensory pathway into the Spinal Cord is afferent. The motor pathway from the ventral horn is Efferent and is on the ventral side Neuroscience Tutorial Two Notes Oct. 3 rd 2011 Group Questions 1. Membrane potential is created because the Leak channels are active at rest and more K+ ions can leave than Na+ because of the concentration cell. Since there are more potassium leak channels than sodium leak channels, the membrane is more permeable to K+. Since the cell becomes more positive on the outside relative to the outside, there is the gradient. Since the cell wants to reach equilibrium, Na+ ions will try to move in, but can’t. The K+ ions moving out take negative ions with them to prevent even more K+ ions leaving the cell. Results in a -70 mv membrane potential. Sodium potential is +50mv and Potassium potential is -90mv. Membrane potential is -70mv as a combination of the two. 2. Definitions Depolarization: Decrease in potential of the membrane of the cell. Shifts the cell to less negative or more positive by increasing Na+ Hyperpolarization: Increase in polarity of membrane potential. Shifts the cell to more negative or less positive by increasing K+ Conc. Gradient: The difference in concentration on both sides of the membrane. Unequal distribution of ions across a cell membrane. Electrochemical Gradient: 3. Linkage channels during Resting membrane potential are open. Due to the concentration gradient, more K+ will be able to leave and will make inside of cell more negative. This results in the cell undergoing hyperpolarization. 4. Due to medication, Na+ would not be able to move towards equilibrium and wouldn’t be able to move inside the cell. If the positive charge cant come in, the cell is becoming more negative and is also undergoing Hyperpolarization. Tutorial Four Notes Oct. 24 th2011 Question One Describe 7 Steps of Synaptic Transmission i. Action potential reaches the Presynaptic Terminal ii. Presynaptic Terminal becomes depolarized iii. Calcium enters through voltage gated channels iv. Calcium ions signal vesicles carrying neurotransmitters to move towards Presynaptic Terminal v. PT releases neurotransmitters vi. Neurotransmitters move across synaptic cleft and bind to receptors on Postsynaptic cell membrane vii. Postsynaptic membrane channels change shape and ions enter the cell Case Study 1 M.J, a 54 year old woman suffers from progressive muscle weakness. Medical evaluation determines that MJ’s weakness is related to a NMJ disorder consistent with Lambert – Eaton Syndrome. In this syndrome, the voltage gated Calcium channels in the axon terminals at the synapse between the motor neuron and the muscle are disrupted. Plasmapheresis: the process of removing blood from the body, centrifuging the blood to separate the plasma from the cells, then returning the blood cells and replacing the plasma with a plasma substitute. (Effectively reduces MJ’s symptoms) Questions i. The neurotransmitter released at the NMJ is ACh. Why would destruction of Calcium ion channels in the axon terminal disrupt the release of Acetylcholine from the axon terminal? o If there is a problem with the calcium channels, then the calcium ions cannot enter the presynaptic terminal. The calcium would then not be able to signal the vesicles carrying the acetylcholine to move towards the terminal for release. ii. Would physical therapy be beneficial for increasing MJ’s strength if the antibodies to the Calcium channels continue to circulate? Explain answer. o Physical therapy would be useless because if no acetylcholine is reaching the muscle, then the muscle will remain weak. Case Study Two A patient complains of muscle weakness – his eyelids seem to constantly droop and he cannot fully open his eyes. He feels his muscles are weaker elsewhere as well. The patient has an autoimmune disease that affects the number of Acetylcholine receptors at the NMJ. i. Based on what was discussed in class regarding the steps of transmission at the junction, what pharmacological approaches could be suggested to help alleviate the symptom of muscle weakness in this patient? Consider if and how the drug would affect the terminal potential and ion channels or the postsynaptic muscle membrane potential. o We want to increase amount of ACH that is available. If we prescribe a drug that blocks Acetylcholinesterase, then the acetylcholine will stay for longer. o We could also prescribe a drug that increases the amount of calcium being released so that in turn, more acetylcholine will be released. Tutorial Five Notes November 7 th 2011 Tutorial #5: Sensory and Motor 1) A 25 year-old man sustained an incomplete spinal cord injury in an industrial accide
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