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Nervous System Lecture Synapses and Information Processing

Synapse a specialized site of contact between two neurons or a neuron and an effector (gland or muscle) that
allows one-way flow of neural impulses (Fig 12.20); synapses are the basis for change in the nervous system
both in development and in learning and memory; synapses can excite or inhibit a postsynaptic cell
Neuromuscular junction synapse between a neuron and a muscle
Neuroglandular junction synapse between an neuron and a gland
Synaptic bulb (Fig 12.20) tips of the presynaptic neuron that contain synaptic vesicles
containing a neurotransmitter that will aid in signal transmission across the synaptic cleft (2030nm in length)
In a neuron-to-neuron synapse, the postsynaptic neuron receives the impulse (Fig 12.18, 12.19)
o ex. spinal motor neuron 10,000 synapses: 8,000 on the dendrites and 2,000 on the soma
Neurotransmitters
more than 100 different neurotransmitters have been identified since the first, acetylcholine, was
discovered in 1921
can have an excitatory or inhibitory effect on the postsynaptic cell this depends on the properties
of the receptors on the postsynaptic membrane and not the neurotransmitter itself
each neuron exposed to a variety of neurotransmitters (so we will talk about only a couple in isolation
but remember that the cells are constantly receiving signals from many presynaptic neurons with many
different neurotransmitters)
Examples include:
o acetylcholine (ACh) widespread throughout CNS and PNS; released in cholinergic synapses
and all neuromuscular junctions; excitatory or inhibitory
o norepinephrine (NE) released in adrenergic synapses; excitatory or inhibitory
o dopamine released in the brain; can be inhibitory (movement control; loss = Parkinsons
disease) or excitatory (cocaine prevents removal from synapses = high)
o serotonin CNS; low levels effects attention span and emotions, severe chronic depression
Synapse transmission excitatory cholinergic synapse
Action potential arrives at the synaptic knob; voltage-regulated Ca2+ channels in the
synaptic membrane open
Ca2+ enters synaptic knob and triggers exocytosis of ACh
ACh diffuses across the cleft and binds chemically (ligand)-regulated Na+ channels;
channels open allowing Na+ in = depolarize postsynaptic membrane 20ms
Only about half the ACh released actually binds to the postsynaptic membrane
influx of Na+ produces a local potential that carries to the axon hillock and if strong
enough will generate an action potential
Synapse transmission inhibitory GABA-ergic synapse
Steps 1 and 2 are the same except that GABA (-aminobutyric acid) is released by exocytosis
Step 3 GABA binds to chemically-regulated Cl- channels; chloride enters the postsynaptic cell
If we add negative ions to the inside of the cell what will that do to the membrane potential?
Hyperpolarize the membrane so it is harder to generate an action potential

Cessation of the synaptic signal (Fig 12-16)


While it is important to stimulate or inhibit the postsynaptic cell with a neurotransmitter, the stimulus must be
turned off otherwise the effector will continue responding to the signal when it is inappropriate and this can be
life threatening
the presynaptic cell stops releasing the neurotransmitter
the neurotransmitter is released from the membrane channel on the postsynaptic membrane and diffuses
into the extracellular fluid
o astrocytes may absorb it and return it to the neurons
o synaptic knob may reabsorb the neurotransmitter by endocytosis then break it down with an
enzyme called monoamine oxidase (MAO)
some drugs like antidepressants inhibit MAO; if you leave dopamine or serotonin in the
synaptic cleft it will maintain the good feeling
o some neurotransmitters, like ACh, are degraded in the synaptic cleft; acetylcholinesterase
(AChE) breaks ACh down into acetate and choline in the cleft; synaptic knob reabsorbs choline
and makes more ACh for later
Neuromodulators
chemicals (small peptides) released by the synaptic bulb along with neurotransmitters that modify the
effect of the neurotransmitter; bind to receptors on the pre- or postsynaptic membrane and have a longer
lasting effect than neurotransmitters
o stimulate neuron to increase/decrease number of receptors on postsynaptic membrane (this
increases the sensitivity or decreases the sensitivity to the neurotransmitter)
o alter rate of neurotransmitter synthesis, release, reabsorption or breakdown (prolong effects)
Nitric oxide used in learning and memory to enhance neurotransmitter release
Endorphins inhibit synaptic transmissions of pain signals (runners high)
Drugs and their effect on synapse activity
Drugs can mimic, enhance or inhibit neurotransmitter activity
o Prozac blocks serotonin reuptake and prolongs mood elevating effect of serotonin
o Nicotine distributed through CNS and PNS rapidly; in CNS causes dopamine release; in PNS
stimulates ACh receptors
o Caffeine competes with adenosine, an inhibitory neurotransmitter; caffeine binds to adenosine
receptors
o Cocaine and methamphetamine prevents synaptic uptake of dopamine; body cuts back on
production due to a perceived overabundance this leads to addiction
o Heroin binds endorphin receptors; addiction same as cocaine and meth
o Ecstasy binds to serotonin receptors and causes them to pump serotonin back out of
presynaptic membrane after it has been pumped in; similar effect with dopamine
So why do we have synapses? Why dont the axons take the information straight to their destination and
not slow down the signal with synapses?
Synapses are the decision-making devices of the nervous system.
The cerebral cortex-the main information-processing center of the brain is thought to have over 100 trillion (10
with 14 zeroes) synapses! The ability of your neurons to process information, store and recall it, and make
decisions is information processing or neural integration
Memory is based on the creation, modification or removal of synapses; pathways through the brain form
memory, there are not individual neurons assigned to remember things

Neural integration is based on the postsynaptic potentials produced by the neurotransmitters released.
Remember that a neuron has an RMP of -70 mV and a threshold of -55 mV. The threshold must be reached to
produce an action potential.
Postsynaptic potentials (Fig 12.24)
graded potentials that develop in the postsynaptic membrane (local potentials)
o excitatory postsynaptic potential (EPSP) graded depolarization of postsynaptic membrane:
open Na+ channels, moves membrane closer to threshold
o inhibitory postsynaptic potential (IPSP) graded hyperpolarization of postsynaptic
membrane: open Cl- channels or sometimes K+ channels; moves membrane further from
threshold
o Which will result in an action potential?
Summation (Fig 12.25, 12.26)
One neuron may receive input from thousands of other neurons. Some incoming signals may produce EPSPs
and some may produce IPSPs. The neurons response depends on the additive effects of the EPSPs and IPSPs.
So we will start with EPSPs to make it simplecombine or add EPSPs until threshold is reached and an
action potential is generated
o Temporal summation addition of stimuli in a short period of time at a single synapse
EPSP lasts 20msec; new AP can arrive every 1ms
fill a bathtub with 1 bucket by adding water quickly
o Spatial summation addition of EPSPs from multiple synapses
many friends with many buckets
We can also have temporal and spatial summation of IPSPs which would hyperpolarize the membrane
and not generate an action potential
Summation of EPSPs and IPSPs
when we combine the opposing effects of the two we have our system of information processing
o equal number and speed no change in water level (no change in membrane potential)
o more IPSPs hyperpolarization; farther from threshold
o more EPSPs closer to threshold and generation of action potential
o the results are further effected by neuromodulators and hormones, caffeine, nicotine, etc.
Facilitation
Neurons work in groups to modify each others actions. Facilitation is the process in which one neuron
enhances the effect of another.
o this can be accomplished by the arrival of EPSPs (not enough to reach but closer with each
arrival); in spatial summation (Fig 12.25) one neuron will not produce a strong enough graded
potential to produce an action potential but with all three working together an action potential is
generated
o this can also be accomplished by certain drugs and chemicals
nicotine, caffeine, theobromine (cocoa) or theophylline (tea)
lower the threshold of the initial segment and increase levels of ACh released
Presynaptic Inhibition (Fig 12.27)
the opposite of facilitation, in this case a presynaptic neuron suppresses another presynaptic neuron
alters the release of the neurotransmitter from the synaptic bulb (presynaptic neuron)
o axoaxonal synapse
inhibition lowers levels of neurotransmitter released

o GABA inactivates Ca2+ channels in presynaptic neuron preventing depolarization of the


synaptic knob; reduces/prevents neurotransmitter release
Neural coding
The nervous system must interpret and pass on qualitative (i.e. color, taste, smell) and quantitative (i.e. bright or
dim, mild or intense, loud or soft) information using only action potentials. Neural coding is the process the
nervous system uses to convert this information into meaningful patterns of action potentials.
The qualitative information is carried by specific neurons for example, sound is only carried by neurons
coming from the inner ear whereas taste is carried by neurons coming from the tongue. A sound neuron cannot
transmit taste or vice versa. Each neuron (or nerve fiber referring to the axon) is recognized as carrying a
specific type of stimulus, which normally is routed to a specific area of the brain.
The quantitative information the intensity of the stimulus is encoded two ways: neuron thresholds and
frequency of stimulation.
There is some variation in the threshold of neurons such that some neurons are stimulated by weak
stimuli while others require a much stronger stimulus to produce an action potential. Often times more
neurons are activated as the intensity of the stimulus increases (recruitment).
The frequency at which a neuron generates action potentials also signals the strength of the stimulus (Fig
12.28)
o example: 1 action potential per second = light touch (butterfly) or 100 action potentials per
second = strong pressure (someone grabs your wrist)
o the greater the degree of depolarization the higher the frequency of APs
o highest frequencies measured in human body 500-1000 per second; remember the limiting factor
is the absolute refractory period
Neural Pools and Circuits
We have talked about interactions of only a few neurons at a time in order to introduce the basic ideas of neural
activity. In fact neurons function in large pools that may consist of thousands to millions of interneurons
breathing, walking and moving arms in rhythm, interpretation of sound, etc.

Types of neural pools (Fig 12.30)


o Diverging circuit one motor neuron of the brain can stimulate thousands of muscle fibers
o Converging circuit input from eyes, inner ears and stretch receptors in the body to be directed
to the part of the brain that governs our sense of balance
o Reverberating circuit feedback loop; breathing
o Parallel after discharge no feedback loop as seen in a reverberating circuit; withdrawal
reflexes