Download What neurons are

Neuronal
Communication
Honors Psychology
Outline
What neurons are
• How neurons communicate
• The Action Potential
• The Chemical Synapse
• Applications
• Drugs & Addiction
• Learning & Memory
•
The Neuron
Is Neural Information
Electrical or Chemical?
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Is the nervous system an electrical grid or a chemical plant?
Descartes and Sherrington thought it was electrical; Otto
Loewi thought it was chemical.
Is Neural Information Electrical or Chemical?
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Loewi repeatedly stimulated the vagus nerve to a
frog’s heart, thereby decreasing its heart rate.
When he collected the fluid from the heart and
transferred it to a second frog’s heart, the second heart
also decreased its rate of beating.
Is Neural Information Electrical or Chemical?
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In a similar experiment, Loewi stimulated the accelerator
nerve to the first frog’s heart, thereby increasing its heart rate.
When he transferred the fluid from the first heart to the
second, the second heart increased its beating.
Q: What gets
the chemicals
moving?
A: Changes in electric charges
across the neuron
Q: What gets
the chemicals
moving?
A: The propagation of an
ACTION POTENTIAL
The Resting Potential
• The neural membrane is specialized to control the exchange of
chemicals between the inside and outside of the cell and thereby
maintain an electrical gradient necessary for neural signaling.
• The inside of the neuron’s membrane has a slightly negative electrical
potential (-65 mV) with respect to the outside. This difference in
voltage is the resting potential.
The Resting Potential
• The neural membrane is specialized to control the exchange of
chemicals between the inside and outside of the cell and thereby
maintain an electrical gradient necessary for neural signaling.
• The inside of the neuron’s membrane has a slightly negative electrical
potential (-65 mV) with respect to the outside. This difference in
voltage is the resting potential.
No Rest for
the Resting Potential
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•
‘Resting potential’ is a bit of a misnomer
• the resting potential is maintained through
an active process of exporting sodium and
importing potassium
• this process spends costly ATP
Maintaining the resting potential is critical
• when the process is disrupted by channelblocking substances (such as the venom
TTX), all action potentials come to an end,
resulting in death
The Action Potential
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When there is a positive change in the cell membrane’s potential, an
action potential is initiated
An action potential is a neural impulse (shown in orange), an all-ornone electrical burst that begins at one end of the axon of a neuron
(shown in blue) and moves along to the other end.
It is “all-or-none” in the sense that the size and the shape of the
action potential are independent of the stimulus that initiated it--like
pulling a trigger.
•
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During the depolarization phase, the approaching action potential
triggers sodium channels to open, which allow sodium to pass into
the axon causing a depolarization.
During the repolarization phase, the membrane closes the sodium
in and lets the potassium out, thereby reestablishing the original
resting potential.
Depolarization to Repolarization
Speed Limits on
Action Potentials
•
Speed of the action potential is limited by axon
thickness: thicker axons present less electrical
resistance and result in faster action potentials.
•
The maximum speed is about 10 m/s. At that
speed, an impulse from a giraffe’s foot would take
about a second to reach the brain. Even for small
animals, that is too slow for the rapid adjustments
necessary to fly, jump, and swim.
•
Myelin sheaths speed up the action potential by
closing up the sodium channels everywhere
along the axon except at the nodes of Ranvier
(gaps between the sheaths). Thus the action
potential skips along the axon from node to node
at speeds up to 120 m/s. (Multiple scelrosis
destroys myelin sheaths.)
10
10
Synapses
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Once the action potential reaches the
end of the neuron, the neuron releases
chemicals (neurotransmitters) into a gap
between one neuron and another.
The gap is called the synapse
The neuron doing the releasing is called
the presynaptic neuron
The neuron on the other side is called
the postsynaptic neuron.
Chemical Events at Synapses
– 1. The neuron synthesizes
chemicals that serve as
neurotransmitters
– 2. The neuron transports these
chemicals to the axon
terminals
– 3. An action potential causes
the release of the
neurotransmitters from the
terminals
– 4. The released molecules
attach to receptors and alter
the activity of the postsynaptic
neuron
– 5. The molecules separate
from their receptors and (in
some cases) are converted into
inactive chemicals
– 6. In some cases,
neurotransmitter molecules
are taken back into the
presynaptic cell for recycling
– 7. In some cells, empty
vesicles return to the cell
body.
Drugs & the Synapse
•
Drugs can inhibit each step of
the events at a synapse. This
is a norepinephrine synapse.
– Reserpine causes leakage
from the vesicles that store
norepinephrine.
– Clonidine stimulates the
presynaptic receptors that
inhibit release of
norepinephrine.
– Tricyclic anidepressants
block reuptake. Prozac, for
example, blocks the reuptake
of serotonin. Cocaine and
Ritalin block the reuptake of
dopamine.
– MAO inhibitors block MAO,
an enzyme that breaks down
norepinephrine and similar
transmitters.
Drugs mock neurotransmitters
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Ecstasy opens serotonin channels, leading to a sense of
euphoria and hedonia.
Prozac prevents the reuptake of serotonin. Low levels of
serotonin are correlated with depression.
Cocaine blocks the reuptake of dopamine, which is
important in reward. Low levels of dopamine is thought to
be correlated with schizophrenia.
Nicotine works on acetylcholine, which is important for
wakefulness.
Ketamine is an NMDA-receptor antagonist. NMDA works
on glutamate, which is the major excitatory
neurotransmitter of the brain (learning affects glutamate
signaling)
Synapses and Personality
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In 1990, researchers identified the
gene that controls the development of
the D2 (dopamine type 2) receptor in
humans. A less common form of this
gene is commonly involved in
unrestrained pleasure-seeking
behaviors, including alcoholism, drug
abuse, obesity, and habitual
gambling. The theory is that people
with this gene have a “reward
deficiency syndrome.”
In 1996, researchers identified a gene
that controls the development of the
length of the human D4 receptor.
Those with the long-form tend to be
more impulsive, exploratory, and
quick-tempered.
D2-D4 may be a route by which
personality factors are partly
heritable.
The Synapse
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The synapse is not just a gap; it’s a
hub of chemical information
The properties of the synapse explain
how information from the
environment can be integrated to
produce behavior, learning, and
addiction
Properties of the Synapse
•
Based almost entirely on behavioral data,
Charles Sherrington (1906) deduced
almost all the properties of synapses we
know today through direct observation
Antagonistic muscles:
Flexor muscles draw legs
toward trunk; extensors move a
leg away. A pinch on the foot
will activate the flexors.
Properties of the Synapse
(1) Reflexes are slower than conduction
along an axon; therefore, there must be
some delay at the synapses.
Properties of the Synapse
(2) Several weak stimuli presented at slightly
different times or locations produce a stronger
reflex than a single stimulus does; therefore,
the synapse must be able to summate different
stimuli.
• For example, several synaptic inputs
originating from separate locations can exert a
cumulative effect on a neuron. So if you
pinch a dog lightly, it will yield no effect; but
two simultaneous light pinches, will--if they
connect at a common interneuron.
Properties of the Synapse
(3) When one muscle becomes excited, a different
set becomes relaxed; therefore synapses are
connected so that the excitation of one leads to the
decreased excitation (or inhibition) of another.
• Pinch a dog’s foot vigorously, and not only will the
flexor muscles of the leg contract, but so will the
extensor muscles of the other three legs. At the
same time, the dog will relax the extensor muscles
of the stimulated leg and the flexor muscles of the
other legs.
• Why? The pinch sends a message along a sensory
neuron to an interneuron in the spinal cord, which
in turn excites the motor neurons connected to the
flexor muscles of that leg. The same interneuron
also has inhibitory synapses on the motor neuron
connected to the extensor muscles. So the
interneuron puts the gas on the flexor muscles and
the brakes on the extensor muscles.
Excitation & Inhibition
Neural Basis of Learning
•
The chemical events at the synapse provide a powerful
explanation for how animals learn about their
environment
• Finding rewarding stimuli (food)
• Avoiding harmful stimuli (predators)
Neural Basis of Learning
Before Learning
Shock is
applied to tail
Gill
withdraws
Before
LightLearning
siphon touch
Gill doesn’t
withdraw
Learning
Light
siphon touch
Shock
is applied
to tail
Gill
withdraws
Learning
Light
siphon touch
Shock
is applied
to tail
Sensory
synapse
strengthens
Gill
withdraws
After
Learning
Light
siphon touch
Gill
withdraws
After Learning
Gill doesn’t
withdraw
Light
mantle touch
Learning
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This learning mechanism is called Hebbian learning or
long-term potentiation, and it explains a whole class of
learning called classical conditioning
The mechanism allows for adaptation to all kinds of
situations not encountered in our evolutionary past
Genetically-altered mice show enhanced long-term
potentiation, suggesting that evolution could select for
genes that make this kind of learning possible
Addiction is Learning
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Habituation: “liking” neurons in the limbic system adapt by
becoming less responsive to the drug as a result of decreases
in the number of receptors.
For this reason, a heroin addict needs higher (or more
frequent) doses to achieve an acceptable high.
Sensitization: dopaminergic “wanting” neurons adapt by
becoming more responsive to the drug context.
For example, a cocaine user becomes increasingly “jumpy”
and excitable in response to the presence cocaine.
Hormones
• Hormones and Neurotransmitters
– A hormone is a chemical that is secreted by a gland and conveyed by the
blood to other organs.
• Descartes’ pineal gland, for example, releases the hormone melatonin which
increases sleepiness.
– Like neurotransmitters, hormones such as adrenaline have an effect on the
mind and behavior.
– Neurotransmitters and hormones differ in that a neurotransmitter is
released next to the target cell, whereas a hormone is carried by the blood
to its target. Consequently, neurotransmitters work better at targeting very
small groups of cells, and hormones can organize many organs or brain
areas for a single function, such as reproduction or hibernation.
Neurotransmitters are like cell phones; hormones are like CB radios.
Hormones
• Types of Hormones
– Peptides, such as insulin, usually exert their effects at receptor
sites on the outside of a cell membrane, much like
neurotransmitters do.
– Steroids, such as estrogens and androgens, usually exert their
effects by attaching to a receptor that turns a gene on or off.
– Monoamines, such as epinephrine and dopamine, often serve a
dual role as hormone and neurotransmitter.
Where do hormones come from?
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The pituitary gland is the source of
hormones that in turn release other
hormones. But it is the brain that
controls the pituitary through
neurohormones.
The posterior pituitary is part of the
brain, and is composed of
modified neurons--neurosecretory
cells--that extend down from the
hypothalamus.
Neurosecretory cells in the
hypothalamus produce releasing
factors that cause the synthesis of
pituitary hormones.
For example, fear might cause the
hypothalamus to secrete
corticotropin-releasing factor,
which in turn releases
coriticotropin, which stimulates
the adrenal glands to release
corticol, which travel to tissues to
enable adaptation to stress.