Lecture 9/10 NS - EMG and Autonomic NS Flashcards
What is the function of an EMG?
Record AP occurring in skeletal muscle fibres, with same electrode as in ECG
How does EMG work?
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
What happens during tetanic contractions?
You can’t stop contracting as it causes an increase force
What are the 3 efferent outputs of the CNS?
Autonomic, Somatic (skeletal muscle) and neuroendocrine (growth, metabolism)
What does ANS control?
Exocrine glands, SM, cardiac muscle, metabolism, host defence
What are the 2 arms of the ANS?
Sympathetic (fight/flight) and parasympathetic (rest/digest)
What effect does the PSNS/SNS have on the heart?
SNS: Increase heart rate/contractility PSNS: Decrease contractility
What effect does the PSNS/SNS have on the small intestine?
SNS: Decrease gut motility PSNS: Gastrointestinal motility increased, and digestion enzymes secretion
What effect does the PSNS/SNS have on the pupil?
SNS: Dilate pupil PSNS: Narrow pupil
What are the principal targets and functions of the ANS?
NB: generally SNS/PSNS work in opposite functions BUT can have only one arm in some organs
Where do the PSNS nerves emerge from?
Craniosacral regions
What is the schematic of the ANS?
All autonomic nerves have a pre and post ganglionic neurons, just different lengths
How are PSNS neurons structured (from craniosacral region to effector organ)?
Long preganglionic and short postganglionic which lies very close to the organ that they are innervating
What is the NT of the PSNS?
ACh -> preganglionic nerves myelinated, post are not
Where do SNS nerves emerge from?
Thoracolumbar region
What is the schematic of ANS?
Short preganglionic and long postganglionic, forming sympathetic trunk-> one preganglionic influencing many postganglionic due to needing to activate many tissues at once
What is the NT of the ANS?
Preganglionic releases ACh, post ganglionic tends to release NA
What are some exceptions to the general rule of ACh (pre) and NA (post) in SNS?
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
What does the ANS schematic look like?
NB: PSNS is localised, so 1:1 (pre:post); SNS is coordinated so up to 1:20 (pre:post)
How is BP controlled by the ANS?
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)
How is TPR controlled by ANS?
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
What are the exceptions of the stimulation of ANS in blood vessels which cause vasodilation?
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)
How is the GIT innervated by the ANS?
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
How are the lungs innervated by the ANS?
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
How does SNS increase O2 delivery to lungs?
Via NA/adrenaline from the adrenals binding to receptors on the lungs, which can slightly dampen down PSNS activity
How is the eye innervated by the ANS?
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
How is the bladder control innervated by the ANS?
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
What is the bladder control reflex?
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
What are the 3 NT used by the ANS?
ACh, NA and adrenaline (technically not NT but used by ANS)
What is ACh made from?
Acetic acid and choline
What are NA/A made from?
Catecholamines -> catechol ring and amine side group
Where are ACh/NA/A found in the ANS?
PSNS -> ACh always SNS -> pre = ACh and post = NA; Adrenal nerve = NA and sometimes post = ACh
If you could block ACh action in autonomic ganglia, what effect would this have on the heart?
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
What are the 2 ACh receptors?
Muscarinic (tends to be within effector organ) and Nicotinic (tends to be within the ganglion)
How does the nicotinic receptor act?
At all autonomic ganglia, ion-channel linked receptor (ionotropic), stimulated by nicotine/ACh and blocked by hexamethonium
How does the muscarinic receptor act?
At all effector organs innervated by PSNS, stimulated by muscarine/ACh and blocked by atropine -> G-protein coupled receptor
What are the receptors at the end of postganglionic SNS nerves?
Adrenoceptors -> alpha 1/2, beta 1/2; G-protein coupled receptors
How is the NT generally synthesised, released and metabolised in the synapse?
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
How is ACh synthesised, released and metabolised at the synapse?
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
What would happen if you blocked AChesterase?
Prevent ACh from being broken down in the synapse, so massive receptor stimulation with ACh, as ACh builds up
How is NA synthesised, released, taken up and metabolised?
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
How is NA/A synthesised, released and metabolised in the adrenal gland?
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
What are the differences between the SNS and PNS?
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
What happens in the fight of flight response due to mass discharge?
