Download Lectures 26-27 Study Guide

TA: Lauren Javier
FALL 2014
Discussion D10, D11, D12
Lectures 26-27 Study Guide
I have organized some terms and topics that I think are important. This does not mean that other topics
mentioned during lecture or in the book will not be tested. This guide is meant to clarify and emphasize certain
points, NOT to list everything you need to know. I will focus on tying things together across lectures, and giving
real-life examples of the biological principles that we are learning. Details that I include that I think will be
helpful, but that you don’t need to know, I will write in green. Questions to think about I will write in blue.
Lecture 26: Physiology, Membrane Potential
Neuron: Nerve cells that transfer information within the body. Neurons are elongated because they have to
transmit signals around the brain and body Remember from our first lecture: structure fits function! Also,
neurons are very specialized cells and as such, they cannot proliferate and cell division does not occur in these
cells. This means that the neurons we are born with are the only neurons we have for our lifetime! Any
damage to our neurons is irreversible and that is why our body has developed protective mechanisms to
protect them (ex: hard skull to encase the brain).
1. Two types of signals for communication:
a. Electrical signals: long distance
b. Chemical signals: short distances
2. The transmission of information depends on the path of neurons along which a signal travels.
a. Central nervous system (CNS): Neurons that carry out integration and the processing of
information. This includes the brain and spinal cord.
b. Peripheral nervous system (PNS): Neurons that carry information into and out of the CNS. Our
brain communicates to the rest of the body using the PNS.
3. The nervous system processes information in three stages and specialized population of neurons
handle each stage of information processing:
a. Sensory input: sensory neurons transmit information about external stimuli (i.e., light, touch,
smell, internal conditions etc.)
b. Integration: Neurons in the brain or ganglia integrate the sensory input. The vast majority of
neurons in the brain are interneurons, which form local circuits that connect neurons in the
brain.
c. Motor output: Neurons that extend out of the processing centers trigger an output in the form
of muscle or gland activity (i.e., motor neurons transmitting signals to muscle cells that cause
them to contract)
4. Structure of a neuron. Depending on its role in information processing, the shape of a neuron can vary
from simple to quite complex.
a. Cell body: contains most of the neuron’s organelles including the nucleus
b. Dendrites (“tree”): receives signals (information) from other neurons
c. Axon (joined to the neuron at the axon hillock): an extension that transmits signals to other
cells.
d. Synaptic Terminals: ends of the axons. This is where the axon passes information across the
synapse in the form of chemical messengers called neurotransmitters (NT).
i. Presynaptic cell (“before the synapse”): cell transmitting the information
ii. Postsynaptic cell: cell receiving the signal
By what process are NT released in the synapse?
5. Glial cells or glia: nourish neurons, insulate the axons of neurons, and regulate the extracellular fluid
surrounding neurons.
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TA: Lauren Javier
FALL 2014
Discussion D10, D11, D12
a.
b.
c.
d.
Astrocytes (“astron” or “star”): support neurons and form the blood-brain barrier (BBB)
Ependymal cells: promote circulation of cerebrospinal fluid
Microglia: immune cells in the CNS that protect against pathogens (similar to WBC)
Oligodendrocytes (CNS) and Schwann (PNS) cells: form the myelin sheaths around axons. This
increases the speed at which an action potential (AP) travels along the axon (more on this in
Lecture 27).
When comparing neurons and glia, which cell type do brain tumors arise from?
6. Ion channels and the Na/K pump maintain the resting potential of neurons.
a. Membrane potential: localized electrical gradient across the plasma membrane
b. Resting potential: membrane potential of a resting neuron- one that is not sending signals. Two
important things:
i. The inside of the neuron is slightly negative compared to the outside.
ii. Na+ has a high concentration outside the cell and K+ has a high concentration inside the
cell. This Na/K gradient is maintained by sodium-potassium pumps, which use the
energy of ATP hydrolysis to actively transport three Na+ out of the cell and two K+ into
the cell. Every time the pump works, we’re exporting a net positive charge! There are
also ion channels. There are many open K+ “leak” channels and very few open Na+
channels. Because Na+ (and other ions) cannot readily cross the membrane and enter
the cell, the K+ outflow leads to a net negative charge inside the cell. Thus, the Na/K
pump combined with the K+ leak channels contributes to the negative charge inside the
cell. The net flow of K+ out of the neuron proceeds until the chemical and electrical
forces are in balance.
7. Action potential (AP): this can travel long distances by regenerating itself along the axon. These are
characterized as an all-or-none event and can only travel in one direction towards the synaptic
terminals
a. Resting state: the gated Na+ and K+ channels are closed.
b. Depolarization: A stimulus opens some sodium channels causing Na+ to enter the cell causing
depolarization. If the depolarization reaches threshold, it triggers an action potential (this
makes it slightly more positive inside the cell)
c. Rising phase of the AP: depolarization opens most voltage-gated sodium channels while
voltage-gated potassium remain closed.
d. Falling phase of the AP: Most voltage-gated sodium channels become inactivated, blocking
sodium inflow. Most voltage-gated potassium channels open, permitting potassium outflow,
making the inside of the cell negative again (cell is trying to get back to its normal membrane
potential and it’s doing this be adding in back the negative “charge”)
e. Undershoot: The voltage-gated sodium channels close, but some voltage-gated potassium
channels are still open and take time to close. The membrane then returns back to its resting
state.
8. Refractory period: this is a result of the temporary inactivation of voltage-gated sodium channels.
During this time, a second action potential cannot be initiated and this ensures that all signals in an
axon travel in one direction from the cell body to the axon terminals.
Lecture 27: Organization, Plasticity
1. Properties that Affect Conduction Speed of Neurons
a. Axon Diameter: Larger diameter=faster AP. (Ex: Think of regular drinking straws vs. Boba straws.
It’s much easier to get more liquid from the larger diameter Boba straw than the normal straws.
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TA: Lauren Javier
FALL 2014
Discussion D10, D11, D12
This is due to less resistance).
b. Myelin Sheath: Formed by Schwann Cells (PNS) and oligodendrocytes (CNS). They look like flat
pancakes and wrap themselves around the axon forming insulation. Voltage-gated channels are
now restricted to gaps in the myelin sheath called Nodes of Ranvier. AP in myelinated axons
jump between nodes of Ranvier in a process called saltatory conduction (“to leap”).
2. Types of Synapses
a. Electrical: electrical current flows from one neuron to another at gap junctions.
b. Chemical: a chemical neurotransmitter (NT) carries information across the gap junction.
Majority of synapses are chemical synapses.
i. An action potential at the synaptic terminal depolarizes the membrane, opening voltagegated channels that allow Ca2+ to diffuse into the terminal. This triggers vesicles to fuse
with membrane and release NT. (Remember, the axon is full of VG-sodium and
potassium channels. The synapse contains VG-calcium channels).
ii. The NT diffuses across the synaptic cleft, bind to ligand-gated ion channels in the postsynaptic membrane, opening ion channels. This generates a postsynaptic potential.
1. NT can be excitatory (stimulate a second AP) or inhibitory (block the formation of
an AP)
3. Temporal vs. Spatial Summation: A single excitatory postsynaptic potential (EPSP) is not sufficient
enough to trigger an AP on the postsynaptic neuron! (EPSP=depolarization; IPSP=hyperpolarization 
You’ll need to understand this difference!)
a. Temporal Summation (think “timing”): If two EPSPs are produced in rapid succession, an effect
called temporal summation occurs.
b. Spatial Summation (think “space” so multiple neurons): EPSPs produced nearly simultaneously
by different synapses on the same postsynaptic neuron add together. If you get an IPSP and
EPSP, they cancel each other out.
c. The combination of EPSPs through spatial and temporal summation can trigger an AP if the
threshold potential is reached.
4. Neurotransmitter (NT): The same NT can produce different effects in different types of cells.
a. 5 classes
i. Acetylcholine
ii. Biogenic Amines (Norepinephrine, Dopamine, Serotonin)
iii. Amino Acids (Glutamate, GABA, Glycine)
iv. Neuropeptides
v. Gases (NO)
b. NT after an AP: As soon as the NT has done its business of binding to the postsynaptic cell, it
has to be gotten rid of. If this does not occur, the postsynaptic cell will continually bind to
receptors.
i. Diffuses out of the synaptic cleft
ii. Taken up by surrounding cells
iii. Degraded by enzymes
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