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Flashcards in Autonomic Nervous System Deck (48)
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What is Shy-Drager syndrome

1. Also called multiple system atrophy - things invlolved get smaller and disintegrate away

2. It is a progressive neurodegenerative disease

3. Initially it involves degeneration of the autonomic preganglionic neurons and in later stages can go on and affect other systems like in motor function and balance like in Parkinson disease


What is the difference in the architecture of the pathway of somatic and autonomic nervous system

The somatic nervous system directly connects from the CNS (brain and then the spinal cord) to the muscle whereas the autonomic nervous system has a CNS then a connection with a ganglion that lies outside of the CNS and then it connects to the sensory or the effector cell.

This is what defines the ANS


What are some of the other nervous system structure that have a ganglion and how is that different than the ANS

Sensory system also forms the ganglion except they do not form a synapse but at the ganglion is the cell body. (Ganglion with no interneuronal synapse)


Divisions of ANS

Sympathetic and parasympathetic nervous system: the two can be differentiated by the origin of their nerves


1. These send out information through the cranial and sacral nerves. The cranial nerves are 3,7,9 and 10. Even though the distribution is throughout the body, the origin is only through the craniosacral system.

2. The ganglia are embedded in the target organs so fairly long preganlionic axon and short post ganglionic axon

SNS: Only comes from the thoracic and lumbar regions. Most of the ganglia occur outside the CNS, running along both sides of the spinal cord is the paraverteberal chain.

Then some ganglia occur in the preverteberal ganglia that innervate the viscera (gut) and the genitalia

In SNS we have realtively short preganglionic axon and long post ganglionic axon due to this architecture


Preganglionic transmission

There are some common aspects and some differences about preganglionic transmission for SNS and PNS

Common: Acetylcholine is the neurotranasmitter and the receptors for that are the nicotinic receptors.

SNS: The axon branches and connects with more than one ganglionic cell body, hence the output is diffused

PNS: 1 to 1 relationship for axons and cell bodies, hence the output is discrete


What is convergence and divergence

The cell body is the point of convergence where mutiple axons give input to the cell body whereas the axon itself is a point if divergence where they branch and give output to different cell bodies


What are the different nicotinic receptors

Not all of the nicotinic receptors are the same, curare blocks the nicotinic receptors on skeletal muscles but the preganglionic nicotinic receptors are blocked by hexamethonium


Structure of the  postganglionic transmission

The axons travel into the effector tissue, where they come in close apposition to the cells they form dilations called varicosities, they also interact with synpathetic axons as well and form a network of nerves on the effector tissues called the ground plexus


Neuroeffector junction 

Interestingly they dont make a synapse, the axon is covered with schwann cells except at vericosities where the vessicles are released at the junction (not a synapse).

There are prejunctional receptors for the contents of the vesicles and post junctional receptors are present on the effector cells


Explain the parasympathetic transmission at the vericosisites (cholinergic)

1. Choline ingested through the diet

2. Taken up by choline transporter

3. Enzyme Acetylcholine transferase makes choline into acetylcholine

4. When a nerve impusle travels along, the acetylcholine is released into the junction

5. There are different types of receptors on post junctional point (on the effector cells) 

Muscarinic  Excitatory receptors = M1, M3, M5 (present on smooth muscles and glands)

Muscarinic Inhibitory receptors = M2 and M4 (smooth muscles and cardiac muscles (vagus nerve))

6. Acetylcholine esterase on the effector cell breaks down acetyl choline

7. Choline is taken up by the transporter

8. There are also Inhibitory Prejunctional Autoreceptors that tend to modulate how much acetylcholine is released from the axon at the junction via negative feedback loop




Define the arginine associated PNS transmission

1. Arginine taken up by diet

2. Converted into NO

3. NO released at the junction

4. NO act on Guanylate Cyclase at the effector cell (it activates GC to make cGMP which is an inhibitory molecule)

5. Function is to relax vascular and smooth muscles

6. NO isnt broken down, it simply diffuses away


Sympathetic Noradrenergic Transmission

1. Tyrosine ingested through diet

2. Tyrosine hydroxylase converts it into DOPA

3. DOPA decarboxylase converts DOPA into dopamine

4. Dopamine beta hydroxylase acts on dopamine to produce norpeinephrine which is stored in the vesicles

5. Norepinephrine acts on adrenergic receptors, alpha 1 (smooth muscles and glands excitation), beta 1 (cardiac excitation and renin release), beta 3 and beta 2 (smooth muscles and gland relaxation)

6. Norepinephrine transporter on the prejunction takes up the norepinephrine

7. Alpha 2 Inhibitory Prejunction Receptors are also present at the prejunction complex to regulate the release of norepinephrine via negative feedback loop


What is the difference in the mechanism of action of epi and norepi

Epi works on all of the mentioned receptors, it works on alpha 1, beta 1, beta 3 and beta 2 whereas norepi doesnt work as effectively on beta 2 which functions to relax the smooth muscles and the glandular secretions


How do you terminate the activity of NE in the sympathetic junctions

NE transporter reuptakes the NE, hence it is not broken down


What are some of the other receptors involved in varicosities that are not present at the junction complex

There are muscarinin inhibitory receptors present at the other side of the varicosities, away from the junction complex so if acetylcholine is released it will inhibit the vericosity from releasing NE at the junction.

One of the other receptors present is the Angiotensin II receptor and the beta 2 receptor. If epi is released and binds to beta 2 receptor, or if angiotensin II is released, the vericosity is stimulated to released NE at the junction complex


Does the previous description define all of the sympathetic transmission

No, that describes 95% of the sympathetic transmission, the other 5% is exactly like the parasympathetic transmission involving acetylcholine mechanism


What does Epi, Isoproterenol, phenylepinephrine, Clonidine, Norepi, where are they located, their action and their effects 


Where does Epi and Norepi come from

Adrenal Medulla, the cells that release are chromaffin cells, these cells have all of the same enzymes as a sympathetic nerve cell except for 1 extra enzyme that converts norepi to epi which is:

Phenylethanolamine N-methyl transferase



How is adrenal medulla stimulated

Via a preganglionic axon which has a cholinergic nicotine synapse


Denervation supersensitivity

Over the course of time, with age and/or disease there can be degeneration of the nerve fibers to certain parts or tissues of the body. This process is called denervation. The body has mechanisms to compensate for the effects of denervation in several ways

Due to denervation, less neurotransmitter is released at the junction. To make of whatever neurotransmitter is available the sensitivity and number of receptors at the post junction site is increased. This is called post junction supersensitivity. This happens in both PNS and SNS

To make maximum use of neurotransmitter availale the reuptake of neurotransmitter can be dramatically reduced, this is called pre junctional supersensitivity. This happens only in SNS and the neurotransmitter involved is norepi


How did he describe the PSN and SNS

SNS as fight or flight and PNS as feed and breed


 What are some of the rules he talked about regarding parasympathetic nervous system

1. Always acts non vascular smooth muscles except for sphincters - cholinergic muscarinic junctions

2. Always relaxes sphincters (except the one in the eye since it is not a sphincter) - cholinergic 

3. Always inhibits cardiac activity - cholinergic

4. Always activates glands - cholinergic

5. Relaxes vascular smooth muscles - nitrergic


Rules for sympathetic nervous system

1. Contracts smooth muscle via alpha 1 receptors

2. Relaxes smooth muscles via beta 2 receptors

3. Excited heart and kidney via beta 1 receptors

4. Excites adipocytes via beta 3 receptros

5. Increase glandular secretions by alpha 1, beta 3 - muscarinic


What are the effects of PNS and SNS on the gut

PNS according to the feed and breed example will promote peristalsis so will give + signals to the gut via ACh but it will give - signals to the rectal sphincter so that it can relax and promot defecation

SNS according to the fight and flight model will have - signals to the gut via Epi and NE and beta 2 receptors but it will have + signals via NE and alpha 1 receptors in the rectum.

ACh reduces the amount of NO released and NE increases the amount of epi released



Know the body of the baldder and the sphincter in the urethera


Erectile dysfunction

There is a structure in the  blood vessels which is called cavemous vessel which can fill up with blood during arousal leading to tumescence. 

Parasympathetic nerve firing makes more NO. The target of action of Viagra and other related drugs is that they inhibit phosphodiesterase type 5 so when NO acts of GC to make more cGMP, cGMP are not broken down by the phosphodiesterase type 5


Orthostatic hypotention or supine hypertension

When you stand up your blood pressure is still low, when you lay down your blood pressure is still high. This happens in shy drager syndrome


What is the name of the nerves that innervate arteriolar and venous smooth muscles and what are their types

Vasomotor nerves

Excitatoty nerves: will cause contraction of smooth muscles, the diameter will decrease

Inhibitory innervations: will cause relaxation of smooth muscles, decrease the diameter of the vessel

Arteriolar contraction increases resistance whereas the venous contraction increases venous return


3 reasons for changing vessel diameter

1. Changing local blood flow like erection, digestion etc

2. To change Total Peripheral Resistance since this should be different when we are standing or laying down

3. To change caridac output since 2/3rd of the blood is stored in the veins


What nerves cause changes in blood diameter

Sympathetic causes constriction by releasing NE that acts on alpha 1 receptors. Epi can cause vasodilation that acts on beta 2 (only released in fight or flight)

Parasympathetic = dilation by making NO