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
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.
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.
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
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
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)
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