NEUROSCI 101 Lecture Notes - Lecture 6: Camillo Golgi, Ependyma, Cranial Nerves

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17 May 2016
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Ch. 3: Neurophysiology + Ch. 4: Neurochemistry
Pre-Lecture Questions:
All spinal nerves are both sensory and motor T
All cranial nerves provide information to and from the head and neck only F
All brains have the same blueprint but elaborations on that blueprint lead to brains with
larger or smaller regions T
4 types of Glia: astrocytes, oligodendrocytes, Ependymal cells (Schwann cells in the
PNS), microglia
astrocyte - star shaped, takes up chemicals and releases them back to axons
The neuron doctrine was championed by Ramon y Cajal, and the reticular theory was
supported by Camillo Golgi.
Functions of glial cells:
microglia - phagocytosis, tries to digest parts of dead neurons during cell death
oligodendroglia - provide the myelin insulation to neurons in the CNS
Communication within Neurons:
resting potential - more + ions outside the axon cell, more - ions inside the cell
not expected b/c of principle of electrostatic attraction (opposite charges
attract, like charges repel) or diffusion (ions seek equal distribution)
forces at work that maintain resting potential of -60 mV:
diffusion/osmosis through the membrane
osmosis - completely permeable membrane, concentration
of ions equally distributed across both sides after moving
down concentration gradient
electrostatic pressure
intra/extracellular space contains IONS w/ +/- charges
passive resistance of semi-permeable membrane - axon
membranes are SEMI-permeable, letting ions in unequally
lipid bilayer w/ channels
neural membrane is 100x more permeable to K+ than Na+,
so K+ can escape from the cell to the outside
active transport for Na+/K+ pump, exchange throughout
membrane, requires a lot of energy (mitochondria), pump Na+ out
and K+ in
Resting Potential
maintaining resting potential:
passive factors that maintain equal distribution of ions across axon
membrane: diffusion/osmosis, ESP
factors that maintain unequal distribution of ions across axon membrane:
passive resistance, active transport
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if we stop the NA/K pump, we end up w/ axons that have no potential charge and
won’t be able to fire the action potential (since membrane is by nature
semipermeable and inside of the cell becomes more + rather than -, less sodium
inside and more outside)
resting potential allows cell to respond rapidly, polarizing the axon
Na+ wants to get inside membrane for 1) osmosis and 2) polarization
(positive ion attracted to negative intracellular area)
greater [ ] inside: K+, O-
greater [ ] outside: Na+, Cl-
Graded Potential
axon become depolarized if a + charge is given (SLIGHTLY LESS NEGATIVE)
ex. give small + charge of Na+ inside the cell via electrode at axon hillock
electricity decrements in charge the further you get from the stimulus charge
“charges diffuse across the membrane, becoming MORE NEGATIVE the
further you get from the point of stimulation” - graded potential
only way axons and cell bodies can communicate is via graded potentials
once graded potential fades as it moves away from the source, dynamic
equilibrium is restored, cell becomes depolarized (gets less negative,
moves towards 0 mV)
graded potential - small stimuli that results in minor electrical charge
across the membrane that are restored as the charge moves away from
its source, seen in axons/dendrites/cell bodies
Action Potential
complete depolarization occurs during action potential: inside of cell: +, outside of cell: -
for a brief moment, then goes back to resting potential
axn potential starts at axon hillock - depolarized to -40 mV, opens voltage-gated
Na+ channels (opens due to electrical stimulation only)
as soon as cells interior becomes + due to the inrush of Na+ ions, K+ diffuses
out of the cell and the axon repolarizes to become -
K+ goes out too fast, and cell becomes hyperpolarized
as inside of cell becomes more negative, K+ channels close
entire process takes 2-3 ms
What happens if we stimulate places other than the axon hillock?
each piece of membrane stimulates the next piece of membrane to spread the
charge to other areas of the body
nodes of Ranvier - areas where there are gaps in the myelin, responsible by graded
potential (don’t require ions to move downwards, since ions degrade the further they
move away from source of axn potential
new axn potential generated each time
graded potential is faster than axn potential b/c you don’t have to open/close any
Na/K channels
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vertebrates have myelin to speed up conduction, and don’t want to wait
for action potentials to regenerate to often
how does speed affect transmission of action potentials?
7 ms/m
invertebrate axons are unmyelinated and small in diameter, slow speed of conduction
the larger the width of the axon, the faster the speed of conduction
vertebrate axons are myelinated
2 micrometer myelinated axon > 5 m/s
20 micrometer myelinated axon > 120 m/s
50 micrometer unmyelinated axon > 50 m/s
Postsynaptic Potentials
postsynaptic potentials spread rapidly but do not regenerate
EPSPs depolarize the postsynaptic neuron
you’re attractive, you must be sending lots of excitatory postsynaptic potentials ;)
IPSPs hyperpolarize the postsynaptic neuron
sum of EPSPs + IPSPs need to reach threshold to fire axn
if < threshold, graded potential occurs
Types of Neuronal Information Processing
neurons integrate PSPs two ways
spatial summation - sums potentials from different locations
temporal summation - sums potentials across time
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