Lecture 9/10 NS - EMG and Autonomic NS

Question 1

What is the function of an EMG?

Answer 1

Record AP occurring in skeletal muscle fibres, with same electrode as in ECG

Question 2

How does EMG work?

Answer 2

The emf is recorded between 2 locations outside the cell -> so detects the difference between one part of the nerve and another part further down of the same nerve

Question 3

What happens during tetanic contractions?

Answer 3

You can’t stop contracting as it causes an increase force

Question 4

What are the 3 efferent outputs of the CNS?

Answer 4

Autonomic, Somatic (skeletal muscle) and neuroendocrine (growth, metabolism)

Question 5

What does ANS control?

Answer 5

Exocrine glands, SM, cardiac muscle, metabolism, host defence

Question 6

What are the 2 arms of the ANS?

Answer 6

Sympathetic (fight/flight) and parasympathetic (rest/digest)

Question 7

What effect does the PSNS/SNS have on the heart?

Answer 7

SNS: Increase heart rate/contractility PSNS: Decrease contractility

Question 8

What effect does the PSNS/SNS have on the small intestine?

Answer 8

SNS: Decrease gut motility PSNS: Gastrointestinal motility increased, and digestion enzymes secretion

Question 9

What effect does the PSNS/SNS have on the pupil?

Answer 9

SNS: Dilate pupil PSNS: Narrow pupil

Question 10

What are the principal targets and functions of the ANS?

Answer 10

NB: generally SNS/PSNS work in opposite functions BUT can have only one arm in some organs

Question 11

Where do the PSNS nerves emerge from?

Answer 11

Craniosacral regions

Question 12

What is the schematic of the ANS?

Answer 12

All autonomic nerves have a pre and post ganglionic neurons, just different lengths

Question 13

How are PSNS neurons structured (from craniosacral region to effector organ)?

Answer 13

Long preganglionic and short postganglionic which lies very close to the organ that they are innervating

Question 14

What is the NT of the PSNS?

Answer 14

ACh -> preganglionic nerves myelinated, post are not

Question 15

Where do SNS nerves emerge from?

Answer 15

Thoracolumbar region

Question 16

What is the schematic of ANS?

Answer 16

Short preganglionic and long postganglionic, forming sympathetic trunk-> one preganglionic influencing many postganglionic due to needing to activate many tissues at once

Question 17

What is the NT of the ANS?

Answer 17

Preganglionic releases ACh, post ganglionic tends to release NA

Question 18

What are some exceptions to the general rule of ACh (pre) and NA (post) in SNS?

Answer 18

In the adrenal gland -> only one autonomic nerve innervating (1 pre), which stimulates NA/adrenaline release into bloodstream, to affect organs. OR Sweat glands (and others) where post ganglionic releases ACh as well

Question 19

What does the ANS schematic look like?

Answer 19

NB: PSNS is localised, so 1:1 (pre:post); SNS is coordinated so up to 1:20 (pre:post)

Question 20

How is BP controlled by the ANS?

Answer 20

Arterial baroreceptor is main sensory input, sending info up afferent nerve to CNS, which mainly occurs in hypothalamus and brainstem; mainly reflex responses. Baroreceptors respond to BP in arterioles, which is sent to brain and then sends stimulatory wave, which sends signal down PS nerve, and inhibiting Symp nerve and vice versa (less inhibition of Symp nerve, so increases BP)

Question 21

How is TPR controlled by ANS?

Answer 21

SNS: increased activity, so vasoconstriction occurs, increasing TPR OR decreased activity, so vasodilatation occurs, decreasing TPR -> SO SNS stimulation of heart increases force of contraction of cardiac muscle (increasing SV and HR), so CO increases, and vasoconstriction increases TPR, hence increases BP

Question 22

What are the exceptions of the stimulation of ANS in blood vessels which cause vasodilation?

Answer 22

Increased SNS activity to some blood vessels in skeletal muscle (either cholinergic fibres or have adrenergic beta-receptors); local vasodilators (CO2, [H+], NO, histamine); increased PSNS stimulation to certain blood vessels to discrete glands/organs (penis)

Question 23

How is the GIT innervated by the ANS?

Answer 23

Enteric NS -> mini brain, modifies itself due to env and external conditions -> ANS can influence the ENS: PSNS increases gut motility, tone and secretion, causes relaxation of sphincters; SNS decreases gut motility/tone, stimulating contraction of sphincters and inhibits secretory activity

Question 24

How are the lungs innervated by the ANS?

Answer 24

PSNS is the only nerve innervating the lungs -> tends to cause bronchoconstriction; no symp nerve to the lung but there is SNS stimulation on the lung

Question 25

How does SNS increase O2 delivery to lungs?

Answer 25

Via NA/adrenaline from the adrenals binding to receptors on the lungs, which can slightly dampen down PSNS activity

Question 26

How is the eye innervated by the ANS?

Answer 26

The iris is the part of the eye that constricts/dilates -\> Circular muscle is under PSNS, which constricts pupil; radial muscle is under SNS which dilates the pupil when muscle contracts. Ciliary muscle is controlled by PSNS, to focus for near and far region, flattening or causing lens to bulge

Question 27

How is the bladder control innervated by the ANS?

Answer 27

PSN from sacral region, ganglion is in bladder, controlling Detrussor muscle to help empty bladder (MAIN influence); SNS controls the internal sphincter, to stop it emptying

Question 28

What is the bladder control reflex?

Answer 28

As pressure builds up (micturition reflex) info is sent to the spinal cord, activating PSNS nerve, causing Detrussor muscle to contract, and switches of SNS control, relaxing internal sphincter, trying to empty the bladder -\> voluntary control is needed for the external sphincter, which holds the final decision

Question 29

What are the 3 NT used by the ANS?

Answer 29

ACh, NA and adrenaline (technically not NT but used by ANS)

Question 30

What is ACh made from?

Answer 30

Acetic acid and choline

Question 31

What are NA/A made from?

Answer 31

Catecholamines -\> catechol ring and amine side group

Question 32

Where are ACh/NA/A found in the ANS?

Answer 32

PSNS -\> ACh always SNS -\> pre = ACh and post = NA; Adrenal nerve = NA and sometimes post = ACh

Question 33

If you could block ACh action in autonomic ganglia, what effect would this have on the heart?

Answer 33

It depends on what the dominant ANS was at the time -\> if PSNS dominant, then lose that stimulation, so HR would increase; if SNS then HR would decrease

Question 34

What are the 2 ACh receptors?

Answer 34

Muscarinic (tends to be within effector organ) and Nicotinic (tends to be within the ganglion)

Question 35

How does the nicotinic receptor act?

Answer 35

At all autonomic ganglia, ion-channel linked receptor (ionotropic), stimulated by nicotine/ACh and blocked by hexamethonium

Question 36

How does the muscarinic receptor act?

Answer 36

At all effector organs innervated by PSNS, stimulated by muscarine/ACh and blocked by atropine -\> G-protein coupled receptor

Question 37

What are the receptors at the end of postganglionic SNS nerves?

Answer 37

Adrenoceptors -\> alpha 1/2, beta 1/2; G-protein coupled receptors

Question 38

How is the NT generally synthesised, released and metabolised in the synapse?

Answer 38

Precursor which is enzymatically synthesised into transmitter, which is packaged in vesicles which wait at the terminal for stimulation; Ca2+ influx from AP, which causes fusion of vesicle, allowing NT into synapse, which then binds to receptor to activate the receptor -\> then breakdown and metabolisation of NT, so it can be reused/removed from synapse

Question 39

How is ACh synthesised, released and metabolised at the synapse?

Answer 39

Acetyl CoA + Choline -\> ACh + CoA [choline acetyl transferase], then packaged into vesicles, and released when AP arrives -\> in synapse binds to muscarinic/nicotinic receptors and then is broken down into choline and acetate by AChesterase, with products taken up into the synapse

Question 40

What would happen if you blocked AChesterase?

Answer 40

Prevent ACh from being broken down in the synapse, so massive receptor stimulation with ACh, as ACh builds up

Question 41

How is NA synthesised, released, taken up and metabolised?

Answer 41

Tyrosine [tyrosine hydroxylase] -\> DOPA [DOPA decarboxylase] -\> Dopamine (in vesicle) [Dopamine beta hydroxylase] -\> NA which is exocytosed, and acts on receptor, NA is uptaken by uptake 1 (into presynaptic nerve) to beak it down, or by uptake 2 in the postsynaptic nerve. In pre, either repackaged into vesicles or broken down by monoamine oxidase into metabolites. In post, broken down by COMT

Question 42

How is NA/A synthesised, released and metabolised in the adrenal gland?

Answer 42

Produced by adrenal gland which stimulates chromaffin cells to produce adrenaline. Same process as NA (tyrosine, DOPA, dopamine, NA) which is then released from vesicle and enzyme converts it into adrenaline. Release into interstitial space, and diffuses into nearest capillary -\> 80% adrenaline, 20% NA -\> Cortisol affects chromaffin cells, upregulating PNMT, so more adrenaline is produced

Question 43

What are the differences between the SNS and PNS?

Answer 43

SNS: Diffuse system which allows stimulation of multiple parts of the body at once (mass discharge) and can also have more discrete effects. PSNS: Relatively discrete system innervating individual target tissues via specific nerves

Question 44

What happens in the fight of flight response due to mass discharge?

Answer 44