55-101 Study Guide - Midterm Guide: Ocular Dominance, Excitotoxicity, Tropomyosin Receptor Kinase A

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Neuro Midterm Review
Introduction to the Neuron
I. Morphology:
a. Neurons contain machinery for extremely active protein synthesis and packing,
like liver and pancreas cells. (Ribosomes in ER, Golgi complex, mitochondria).
b. Microtubules (of α and β tubulin and microtubule associated proteins [MAPs]) are
important for maintaining the shape.
i. Microtubules help transport vesicles and organelles to the axon terminals
via anterograde transport (kinesin motor), and bring stuff back via
retrograde transport (dynein motors).
c. Neurofilaments, neuronal intermediate filaments, are responsible for axon
diameter.
d. 99% of cytoplasm is in the axon.
e. Stacks of rough ER are called Nissl bodies in neurons.
f. Synapses onto the cell body itself are more often inhibitory, and very powerful.
g. Dendrites:
i. Dendritic fields allow neurons to selectively sample incoming messages.
ii. Most dendrites give off dendritic spines. The spines are areas of chemical
isolation.
iii. Usually excitatory synapses at the spines, and local changes in ion
concentration aren’t diluted by the whole dendrite, so spines remember
what’s happened to them for a long time.
h. Axons:
i. Single axon from each neuron, with integration of synaptic potentials
occurring at the axon hillock.
ii. Very high density of voltage-gated Na+ channels here.
iii. Axon collaterals are usually modulatory in nature.
iv. On average a single neuron gives off 1000’s of axon terminals.
II. Ion Channels:
a. All ion channels allow either positively OR negatively charged ions.
b. Channels can be ligand- or voltage-gated, but can also bind molecules (usually
cyclic nucleotides) on the inner surface of the neuron to hold them open or keep
them closed.
c. Great majority of cation channels exclude Ca2+ and allow Na+ or K+.
III. Synapses:
a. A.P. hits the axon terminal, and the depolarization from voltage-gated Na+
channels causes the opening of Ca2+ channels, which causes fusion of synaptic
vesicles and presynaptic membrane.
b. Tetrodotoxin (TTX) blocks voltage-gated Na channels, TEA blocks K channels.
Even with both these blocked, you can cause N.T. release from the synapse by
direct stimulation.
c. There are dendro-dendritic synapses that release n.t. even w/o an A.P.
d. Axo-axonic synapses can produce presynaptic inhibition by opening K+ channels.
e. Ca2+ is the key b/c removing external Ca or blocking Ca channels inhibits N.T.
release, you can see Ca flowing into terminals during N.T. release, and injecting
Ca evokes or augments N.T. release.
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i. Ca may interact directly with the vesicles or presynaptic membrane, via an
effector like calmodulin.
ii. We discovered N.T. was stored in vesicles b/c its release is quantal, not
continuously graded.
f. Post-synaptic receptors are most often ionotropic.
i. Acetylcholine is the transmitter of neuromuscular junctions. It opens a
channel permeable to both Na and K in the postsynaptic membrane, which
has an Erev of about 0 mV, so it depolarizes.
ii. Excitation is produced if the reversal potential is above the spike firing
threshold and inhibition if it’s below. It is NOT a factor of whether Erev is
more negative or positive than resting!
1. You can have inhibitory depolarizations, therefore!
g. Another large group of receptors activate GTP-binding proteins (G-proteins), and
are also called metabotropic receptors.
i. Slower-acting b/c they activate 2nd messengers, but stronger and longer-
lasting.
h. The location of the synapse is very important, b/c of λ. Axosomatic synapses are
generally more powerful than axo-dendritic or axo-spinous.
i. Most inhibitory synapses are on the cell bodies while most excitatory
synapses are on dendrites and spines, b/c the driving force for Cl- is zero
when the neuron is at -70 mV, so is most effective at the final segment.
i. Gap Junctions are formed by connexins combining to make connexons.
i. Largely confined to depolarizing signals, and are very simple.
Conduction of Decremental and Regenerative Signals
I. Cable properties of neurons are passive properties, flow w/o channels.
a. Time constant (τ) and length constant (λ) take into account membrane resistance,
axoplasm (internal) resistance, and the thinness of the membrane.
b. As diameter goes down resistance goes up and λ gets smaller.
a. λ = sqroot (rm/ri)
b. ri = Ri/πr2, and rm = Rm/2πr.
c. τ is the amount of time it takes to get to about 60% of starting value, so if you
make 5 mV of Na+ enter it’ll take 10 ms for the neuron to be depolarized by 3
mV, so τ = 10 ms. τ = RC, where R = internal resistance and C = capacitance.
ii. Capacitance is the build-up of stored charge, and the thinner the
separation, the higher the capacitance.
d. ΔVx = ΔVo e-x/λ, so ΔV falls off exponentially with distance from the source.
II. Ion stuff and Nernst Equation
a. Standard membrane potential is -70 mV.
b. Na+ equilibrium potential is +64 mV
c. K+ equilibrium potential is -86 mV.
d. Cl- equilibrium potential is -78 mV.
e. Ca2+ equilibrium potential is +116 mV.
iii. Because this is more negative than the AP threshold, Cl- channels are
therefore inhibitory.
j. For monovalent ions, Eion = 58 mV log(Ko/Ki).
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k. Iion = gion (Vm – Eion), where g is conductance.
l. WEIGHTED NERNST EQUATION:
i. Erev = (gNa/gK)(ENa) + EK / (gNa/gK) + 1
ii. So the reversal potential depends on the conductance of the channel to
both ions and the equilibrium potential of them both.
m. Dendrites don’t have the same positive feedback loop b/c they don’t have enough
voltage-gated Na+ channels.
e. Excitatory synapses far from the hillock will produce small depolarizations,
inputs on large-caliber dendrites have more of an effect, and inputs must be
triggered with appropriate delays to sum together.
f. Myelin both increases the length constant and reduces the time constant, by
increasing membrane resistance and decreasing C.
g. Action Potentials:
a. Total current flow across a membrane is Itotal = gNa (Vm-ENa) + gk(Vm-Ek).
i. The minimum Vm where Itotal becomes inward is the threshold.
b. A.P.s are terminated by voltage-gated Na channels becoming inactivated
after a few ms, and delayed rectifier K channels driving Vm back even
closer to Ek than at rest. Refractory period.
c. Studying the squid giant axon and either removing external Na or blocking
K channels with TEA allowed them to identify that the initial inward
current is Na and the delayed outward is K.
d. The increased density of Na channels in the axon allows propagation.
e. Conduction velocity of axons ranges between 0.5-150 m/sec.
h. Take homes:
a. Conduction of signals in dendrites is graded and decremental, while
conduction in axons is regenerative and all-or-none.
b. Passive spread of current is a factor in the speed of both dendritic and
axonal transmission, with the caliber of the process the biggest
determinant.
Glial Cells of the CNS and PNS
I. Astrocytes:
a. Facts:
i. Most numerous glial cells, outnumbering neurons 10:1.
ii. Inexcitable, high resting conductance to K+, R.P. of -90 mV.
1. Essentially only permeable to K+.
2. May allow them to remove K+ released during activity and
redistribute it, preventing extracellular accumulation.
3. Their gap junctions allow them to form a syncytium, so they can
move ions and metabolites between cells.
4. Bergmann glial cells perform the roles of astrocytes in the
cerebellum, and Müller glial cells do it in the retina.
b. During development, they secrete growth factors, guide neuronal migration, and
enhance synapse formation.
c. Remove ions and neurotransmitters that accumulate extracellularly.
i. They contain glutamine synthetase so they can convert glutamate to
glutamine, and the glutamate transporter GLAST/EAAT1.
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