Autonomic Nervous System
I. Introduction/Overview of the ANS
A. Comparisons with the SNS
1. ANS effectors are smooth muscle, cardiac muscle, and
glands (what does the SNS target?)
2. Autonomic motor neurons synapse in ganglia (do SNS
neurons?)
-the Pre-ganglionic neuron originates in the brain or
spinal cord
-the Ganglionic neuron has its cell body in a ganglion,
and there it synapses with the axon terminals of the Preganglionic neuron. The ganglionic neuron sends its Postganglionic fiber, or axon, to its effector (what are the
effectors of the ANS?)
3. Preganglionic axons are type-B fibers, postganglionic axons
are type-C fibers (what does this mean? Do ANS axons conduct
faster or slower than SNS fibers?)
4. SNS motor neurons all release Ach on effectors, and it's
always excitatory. ANS motor neurons, on the other hand, may
release Ach (parasympathetic) or NE (sympathetic) on their
effectors. Depending on the receptor type and effector, Ach and
NE can be either excitatory or inhibitory.
B. Overview of the divisions
1. Parasympathetic- the "resting and digesting" division. When
parasympathetic activity dominates,
-heart rate and blood pressure decline
-GI tract motility increases, and excretory activity
increases (defecation and urination)
-respiratory rate and volume decrease (breaths are
shallow and slow)
-energy in the form of glycogen and triglycerides is
stored
2. Sympathetic- the "fasting, exercise, and emergency" division.
When sympathetic activity dominates, some combination of the
following occurs (depending on the nature of the needed
response):
-heart rate, blood pressure, and muscle tone increase
-blood flow is directed so that activities that are not
immediately necessary get less blood (ex, digestive
organs), and activities that are immediately necessary get
more blood (ex, skeletal muscle)
-GI tract motility and excretory activity decrease
-respiratory rate and volume increase (breaths are deep
and fast)
-alertness increases
-energy stores are mobilized, so glycogen is broken down
to release glucose to the blood, and triglycerides are
released to the blood from adipose.
II. Parasympathetic division
A. Preganglionic fibers travel in cranial nerves and sacral spinal
nerves (trivia: 90% of all parasympathetic preganglionic fibers travel
through the vagus nerve & its branches)
B. The preganglionic neuron synapses with the ganlionic neuron/s in a
ganlion near the effector or in the effector. Preganglionic axons
release Ach onto ganglionic neuron, whose postganglionic axons
release Ach onto its effector.
C. Preganglionic fibers are long, postganglionic fibers are short.
D. Functions- see text, and above/below
III. Sympathetic division
A. The effectors innervated by the parasympathetic division are also
innervated by the sympathetic division, and the two divisions
generally have opposing effects. However, the sympathetic
division serves some effectors that ARE NOT served by the
parasympathetic. Effectors that only receive sympathetic
innervation include:
-smooth muscle lining blood vessels
-the arrector pili muscles, and
-the adrenal glands.
So, for instance, the degree of constriction of blood vessels is
dependent on the sympathetic division only.
B. Synapses and ganglia
1. Preganglionic fibers travel through the T1-L2 spinal nerves.
2. Preganglionic fibers release Ach onto ganglionic neurons in
ganglia (see below).
3. The postganglionic axons release NE (most) or Ach (some)
onto their effectors.
4. Preganglionic fibers are generally short, postganglionic fibers
are generally long.
5. Preganglionic neurons synapse with ganglionic neurons in
one of 3 places:
a. Sympathetic chain ganglia- paired, near the spinal cord
on either side
b. Collateral ganglia- unpaired, located anterior to the
vertebral column
c. Adrenal medulla- the center of the adrenal glands. The
adrenal glands are located on top of the kidneys. In the
adrenal medulla, specialized neurons produce and release
NE and Epinephrine into the blood. This is unusual
because this means that NE can serve both as a
neurotransmitter and as a hormone. Hormones are
chemicals that are released into the blood and can have
widespread effects on many different types of cells
throughout the body. NE and E have similar effects.
6. The telodendria, or axon terminal branches, of postganglionic
fibers are specialized to release Nt all along the branches, rather
than just at the synaptic terminal. Remember that the axon is a
long fiber that carries an action potential. The end of the axon
contains small branches called telodendria. Normally, the ends
of the telodendria form swollen knobs that release Nt in
response to an action potential.
In the post-ganglionic fibers of the sympathetic division of the ANS,
the swollen areas of the telodendria are not restricted to the very ends.
Instead, several areas along the telodendria swell and synapse with
effectors. These swollen areas release Nt in response to action
potentials arriving from the axon, just like synaptic knobs. They are
called varicosities. Varicosities allow one neuron to wrap its
telodendria around its effector and release Nt all over it at once.
*So, a ganglion is a swollen area of a whole nerve, which contains the axon
terminals and cell bodies of MANY neurons. A telodenrion is a type of axon
terminal which occurs on ONE neuron.
C. Functions- see text, and above/below
IV. Neurotransmitters and receptors of the ANS
A. Fiber (axon) types based on the Nt they release- right now we're
talking about what goes on at axon terminals (release of Nt from the
presynaptic neuron)
1. Cholinergic- release Ach. Include:
-All preganglionic fibers of the ANS, so the
preganglionic fibers of both divisions release Ach
-All parasympathetic postganglionic fibers, and a few
sympathetic postganglionic fibers (ex, those serving
sweat glands and those serving smooth muscle of SOME
blood vessels)
2. Adrenergic- release NE. Include:
-Most sympathetic postganglionic fibers only
*No preganglionic fibers, and no parasympathetic
neurons, release NE
3. (This will be for extra credit only) Nitroxidergic- release NO
(nitric oxide). NO is a powerful vasodilator (causes blood
vessels to dilate). Found on:
-Some sympathetic postganglionic fibers (to smooth
muscle on some blood vessels)
B. Receptor types based on what Nt they bind to and how they
respond: now we're talking about what goes on at cell bodies and
dendrites of a postsynaptic neuron or effector (where the Nt binds)
1. Receptors that bind to Ach: “cholinergic.” There are two
types of cholinergic receptors:
a. Nicotinic cholinergic- When Ach binds to nicotinic
receptors, it causes a direct EPSP*. Nicotinic receptors
are found on ganglionic neurons:
-all ganglionic neuron cell bodies and dendrites of
BOTH divisions of the ANS
-neurons of the adrenal medulla (remember, these
actually are just specialized ganglionic neurons
-(FYI: also motor end plates of skeletal muscle)
*(what does that mean about the receptor itself? Is it linked to an ion
channel? What kind of ion?)
b. Muscarinic Cholinergic- When Ach binds to
muscarinic receptors, it can cause either an EPSP or an
IPSP. The effects are indirect *. Muscarinic receptors are
found on effectors:
-All parasympathetic effectors- EPSP on most
(ex, smooth muscle lining digestive tract; activity
increases), IPSP on cardiac muscle (heart rate
decreases).
-Some sympathetic effectors- EPSP or IPSP. For
example, Ach binding muscarinic receptors on
sweat glands causes an EPSP (sweat is produced);
possibly: Ach binding muscarinic receptors on
smooth muscle of blood vessels serving skeletal
muscle/brain causes IPSP (muscle relaxes, vessel
dilates)
*(Ach binding to a muscarinic effector causes the cell to change the number
of K+ channels it contains. What do you think: on a cell that is excited by
Ach, are more or fewer K+ channels built? On a cell that is inhibited by
Ach?)
2. Receptors that bind to NE (or E, as a hormone from the
blood): “adrenergic.” NE and E cause indirect effects on target
cells. There are two broad categories of adrenergic receptors,
alpha and beta. Within each of these categories are
subcategories (alpha 1 and 2, beta 1, 2 and 3). We are not going
into the subcategories of alpha and beta receptors and their
specific effects. Know the names of them, know that they are
categories of adrenergic receptors, and know the specific
examples that I will give you. Keep in mind that only the postganglionic fibers of the sympathetic division release NE; so we
only expect to find adrenergic receptors on effectors.
a. Alpha-receptors- NE binding to alpha receptors can
cause EPSPs or IPSPs, depending on the cell type. For
example, NE binding to alpha receptors on cardiac
muscle is excitatory (heart rate increases); NE binding to
alpha receptors on smooth muscle lining the digestive
tract is inhibitory (activity decreases).
b. Beta-receptors- again, EPSPs or IPSPs. For example,
NE binding to beta receptors on cardiac muscle is
excitatory (heart rate increases); NE binding to beta
receptors on smooth muscle lining respiratory tubes is
inhibitory (muscles relax, tubes dilate)
NE binding to beta-receptors on adipose cells is
excitatory, and they release triglycerides in response.
C. Summary of Nt release and action in the ANS, and how it all
makes sense:
1. The preganglionic neurons always use Ach, which is always
excitatory and direct acting in this location. Here, ganglionic neurons
always contain nicotinic cholinergic receptors. When ganglionic
neurons are excited by Ach, they will release either Ach (if they are
parasympathetic or select sympathetic) or NE (if they are most
sympathetic) onto their effectors.
2. Parasympathetic postganglionic fibers (axons) always secrete Ach
onto effectors; the effectors possess muscarinic cholinergic receptors.
Remember, “resting, digesting, storing” are the activities the
parasympathetic division supports. Here are some examples of how
effectors respond to parasympathetic influence:
a. Smooth muscle lining digestive tract increases activity
(digestive activity increases)
b. Smooth muscle lining respiratory tubes increases activity (tubes
increase tone; constrict a little)
c. Cardiac muscle is inhibited (heart rate slows)
d. Pupils constrict
3. Most sympathetic postganglionic fibers secrete NE onto effectors; the
effectors possess either alpha (type 1 or 2) or beta (type 1, 2 or 3)
adrenergic receptors. Remember, “exercise or emergency” are the
standards to think about the sympathetic division preparing you for.
Here are some examples of how effectors respond to sympathetic
influence:
a. Smooth muscle lining most blood vessels contain mostly alpha1 receptors, binding of NE increases activity (general
vasoconstriction; increased pressure/flow/turnover; blood
shunted to necessary areas)- so now blood is being returned the
heart/lungs for O2 pickup faster, and isn’t spending too much
time feeding less necessary functions right now
b. Smooth muscle lining some blood vessels that service skeletal
muscle, brain and the heart contain beta-2 receptors, binding of
E (hormone released from the adrenal glands during
sympathetic activation) decreases activity (vasodilation of these
specific vessels, increasing flow to these specific areas; this is
also accomplished by autoregulatory mechanisms and perhaps
Ach from sympathetic fibers)- so, blood is shunted away from
major organs that are unnecessary right now, and shunted TO
necessary organs, ones that will help you escape danger and
exercise!
c. Heart rate is increased, contributing to the increase in
pressure/flow/turnover of blood
d. Sweat glands are activated- to help you keep cool while your
muscles increase tone/activity
e. Pupils dilate- to help you take in more visual information
f. Liver cells are activated to release stored glucose into the blood
to feed the extra activity of your muscles
g. Smooth muscle lining digestive tract is inhibited to slow
digestive activity and stop wasting energy on that function for
now
h. Respiratory tubes dilate, allowing more air in to recharge blood
with O2 more effectively (and breathe out all the extra CO2
you’re producing)
i. Adipose cells are activated to release stored fats into the blood
to provide extra fuel both to your muscles and the rest of the
cells of the body.
V. ANS tone
Autonomic neurons are always active to some extent. The "resting"
condition of ANS effectors is determined by the degree of influence
of each of the divisions.
For instance, heart rate is determined by the amount of NE
(excitatory) from sympathetic fibers versus the amount of Ach
(inhibitory) from parasympathetic fibers. Cardiac muscle is always
receiving some of both. When heart rate increases, the amount of NE
increases, and the amount of Ach decreases.
Another example: remember that blood vessel diameter (degree of
constriction) is determined by the sympathetic division. Smooth
muscle lining vessels is always receiving some NE, so the smooth
muscle lining vessels is always tone. To dilate or constrict a vessel,
the sympathetic division releases more or less NE onto the smooth
muscle.
VI. Visceral Reflexes- like somatic reflexes, these are simple reflex arcs
between sensory and motor neurons that bypass the brain. They can involve
an interneuron between sensory and motor neurons, or they can be direct
connections. Synapses can occur in the gray matter of the spinal cord, or can
occur in ganglia (“short reflexes”).
Examples include the constriction of pupils in response to bright light, and
The GI tract contains an extensive network of visceral neurons that
communicate via reflex arcs, and function to some extent without input from
the CNS.