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 Pre-ganglionic neuron. The ganglionic neuron sends its Post-ganglionic 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
- 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 post-ganglionic 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:
- 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.
- 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:
- Smooth muscle lining digestive tract increases activity (digestive activity increases)
- Smooth muscle lining respiratory tubes increases activity (tubes increase tone; constrict a little)
- Cardiac muscle is inhibited (heart rate slows)
- Pupils constrict
- 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:
- Smooth muscle lining most blood vessels contain mostly alpha-1 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
- 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!
- Heart rate is increased, contributing to the increase in pressure/flow/turnover of blood
- Sweat glands are activated- to help you keep cool while your muscles increase tone/activity
- Pupils dilate- to help you take in more visual information
- Liver cells are activated to release stored glucose into the blood to feed the extra activity of your muscles
- Smooth muscle lining digestive tract is inhibited to slow digestive activity and stop wasting energy on that function for now
- Respiratory tubes dilate, allowing more air in to recharge blood with O2 more effectively (and breathe out all the extra CO2 you’re producing)
- 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.