Neural Control Systems

Question 1

How is the ANS different to somatic motor nerves?

Answer 1

ANS: 2 efferent (away from) neurones arranged in series conducting electrical activity from CNS to peripheral tissue/organ
Somatic motor nerves have 1 efferent neurone connecting CNS to skeletal muscle

Question 2

What is the difference between grey and white matter?

Answer 2

The grey matter contains the cell bodies, dendrites and the axon terminals, where all synapses are.

The white matter is made up of axons, which connect different parts of grey matter to each other.

Question 3

Describe an overview of brain structure.

Answer 3

The cortex is the largest region of the brain. It’s highly folded grey matter w nerve cell bodies, synapses and dendrites.

The cortex is divided into L + R hemispheres. Each hemisphere has 4 lobes: Frontal, parietal, occipital, temporal lobe.

Below the cortex lies white matter; millions of nerve axons connecting neurons in different parts of the brain.

2 cerebral hemispheres are connected by white matter (corpus Callosum), allowing communication entre los 2.

Question 4

Label the main subdivisions of the brain

Answer 4

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Question 5

Label this brain diagram

Answer 5

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Question 6

What do the cerebral cortex and hippocampus do?

Answer 6

Cerebral cortex & hippocampus are the thinking part of the brain:
conscious perception, cognition, learning and memory, controlling voluntary movement
•different areas subserve different functions

Question 7

What is the function of the thalamus?

Answer 7

Thalamus relays signals to and from the cerebral cortex:
•sensory pathways synapse here on the way to the cortex
•these thalamic relays are switched off during sleep

Question 8

What is the diencephalon?

Answer 8

diencephalon: the caudal (posterior) part of the forebrain, containing the epithalamus, thalamus, hypothalamus, and ventral thalamus and the third ventricle.

Question 9

Describe the function of the hypothalamus.

Answer 9

Hypothalamus is the master controller for homeostasis:
•links neural and endocrine systems
•controls the systems that generate the sleep-wake cycle

Question 10

What is the brain stem?

Answer 10

The brainstem regulates involuntary cardiac and respiratory function, consciousness, and the sleep cycle. It consists of the medulla oblongata, pons, and midbrain.

Question 11

Describe the spinal cord

Answer 11

Medulla turns into spinal cord as it extends beyond the skull. The spinal cord has big white matter tracts. The core of the spinal cord is grey matter.

The spinal cord is segmented, each segment gives rise to a pair of spinal nerves. Each of the spinal nerves has an anterior and posterior root. Anterior carries efferent motor signals to the body. The posterior root carries afferent sensory signals back to the CNS.

Question 12

What is resting potential?

Answer 12

Neurons have a negative resting potential across the cell membrane. This means inside the neuron is more - than outside as hay mas + charge outside the neuron.
The resting potential is the voltage across the membrane while the neuron is at rest, about -70 mV.

Question 13

How is resting potential maintained?

Answer 13

Resting potential is maintained by keeping more + ions outside the cell. Hay more K+ inside the membrane than outside, and more Na+ outside than inside.

The neurone membrane is permeable to K+ ions due to a K+ leak channel. Buildup of K+ inside the neuron causes K+ to leave thru the channel by facilitated dif. The cell gets more negative.

However, habra buildup of + charge outside the neurone which repel each other & push K+ ions back in the neurone.

So an electrical AND conc gradient act on the K+ ions. The electrical gradient (Na-K pump) pumps K+ into the cell, but the conc gradient pulls K+ out the cell. At -70mV, the 2 gradients counteract each other, no hay K+ net movement.

Question 14

Describe depolarisation

Answer 14

Depolarisation occurs from an initial sensory stimulus. Change in voltage changes the Na+ gate shape, opening some voltage-dependent Na+ channels.
Na+ flow in, increasing depolarisation. This opens aun mas Na+ gates (positive feedback) till ALL Na+ gates open. So a. potentials are all or nothing responses.

+ charge builds up inside and reverses polarity of the membrane. Potential difference reaches +40 mV.

Question 15

Describe and explain repolarisation.

Answer 15

After 0.5 ms, voltage-dependent Na+ channels close. Voltage-dependent K+ channels open.

K+ thus diffuse down the electrical gradient, leaving the axon. Inside the cell once again becomes more negative, or repolarised.

During this repolarisation phase the cell is in its absolute refractory period- Na+ channels are inactivated & wont respond to any stimuli.

Question 16

What is hyperpolarisation?

Answer 16

The membrane is v permeable to K+ and lots more ions move out, making p.d more negative than -70 mV. This is hyperpolarisation.

Resting potential is re-established by closing voltage-dependent potassium channels. Potassium ions diffuse back into the axon to recreate resting potential.

The cell is in relative refractory period

Question 17

Draw and label an action potential graph.

Answer 17

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Question 18

What are synapses?

Answer 18

A synapse links 2 or more neurons juntos. Info travels from the presynaptic neuron, across the synaptic cleft (gap), to the postsynaptic neuron.

The synapse has synaptic vesicles w neurotransmitters which stimulate the post synaptic neuron.

Question 19

Describe pathways for para and sympathetic responses, using diagrams

Answer 19

Question 20

What is an autonomic ganglion?

Answer 20

An autonomic ganglion (plural ganglia) -Group of neuronal cell-bodies lying outside CNS

Question 21

Explain synapse transmission between autonomic nerves

Answer 21

Synthesis of neurotransmitter and storage of NT in vesicles
AP arrives at synaptic terminal, terminal depolarises
Hay activation of vgcc, hay Ca2+ influx
Hay Ca2+-dependent release of NT. NT binds to receptor and induces response
Uptake/breakdown of NT

Question 22

Describe how the sympathetic ns affects the lungs, eyes and sweat glands

Answer 22

Lungs: don’t receive sympathetic innervation. Bronchioles contain B2-adrenoceptors which are activated by circulating adrenaline to produce bronchodilation. This opens up the airways to facilitate breathing

Eye: Stimulation of A1-adrenoceptors on dilator pupillae (radial iris muscle) dilates the pupil.

Sweat Glands: Ach release acts at Mus receptors to induce sweating and ⇡ temp control

Question 23

Describe the adrenergic synapse

Answer 23

NA is synthesised and packaged into vesicles. These release NA into the synaptic cleft. NA diffuses into the post synaptic membrane and acts on diff receptor types to produce a bio response.

NA can is then taken into the presynaptic terminal by MAO uptake transporter to be broken down or recycled.

Question 24

What happens if too much adrenaline is released?

Answer 24

If mucho adrenaline is released, hay stimulation of A2-adrenoreceptors on the presynaptic terminal. This switches off neurotransmitter release from the presynaptic terminal.

This is a negative feedback mechanism.

Question 25

Adrenergic transmission can be regulated…

Answer 25

Directly: by receptor agonists called sympathomimetics bc they mimic the symp ns.

Indirectly: modulate everything but the receptors. eg synthesis, uptake transport, neg feedback mechanism etc.

Question 26

How are Noradrenaline and Adrenaline synthesised?

Answer 26

NA and adrenaline mediated at sympathetic post-ganglionic fibres, CNS, adrenal medulla.

1 (RDS): Tyrosine goes to Dopa, carried out by tyrosine hydroxylase. Dopa is produced into dopamine. In a symp post ganglionic fibre, dopamine is produced into NA, which is then packaged and released.

In the adrenal medulla NA produces adrenaline by PNMT

Question 27

How can adrenergic transmission be inhibited in terms of storage?

Answer 27

Reserpine prevents NA storage in vesicles. If NA is not in vesicles its in the cytoplasm which means its broken down by MAO.

Hay reduced NA release, so less sympathetic actions, e.g. less A1-mediated vasoconstriction.

This is early hypertension treatment and demonstrates that reducing sympathetic nerves decreases BP

Question 28

How can drugs like amphetamine or ephedrine facilitate release in adrenergic transmission?

Answer 28

Amphetamine / Ephedrine reverses uptake transporters, causing release of NA into cleft. This increases sympathetic actions e.g. Increase HR, vasoconstriction, pupil dilation

Ephedrine causes vasoconstriction of nasal blood vessels, so its used as a decongestant

Question 29

How can drugs inhibit NA release and therefore adrenergic transmission?

Answer 29

Guanethidine: Compete with NA for inclusion into vesicles. This reduces NA release

Clonidine: Stimulate pre-synaptic A2 receptors. This stimulates the negative feedback pathway and reduces NA release

These drugs used in hypertensive emergencies by reducing sympathetic activity

Question 30

What is termination inhibition in adrenergic transmission? Which drugs are involved in this?

Answer 30

Cocaine / anti-depressants inhibit uptake transporter. This ⇡ the amount of NA in the synaptic cleft, ⇡ adrenergic transmission and symp response.

MAO inhibitors mean less NA is broken down and more is recycled. This means more NA in vesicles which increase adrenergic transmission in brain.

Question 31

How does the parasympathetic nervous system affect pupil diameter?

Answer 31

The parasympathetic ns affects pupil diameter through innervation of the iris circular muscles (constrictor pupillae).

Here, ACh from parasymp nerves acts at M₃ receptors. This contracts the circular muscles, constricting the pupil

Question 32

How does the parasymp ns affect intra-ocular pressure?

Answer 32

The parasymp ns controls the volume of aqueous humour in the eye. Failure to drain excess aqueous humour causes glaucoma, reducing eyesight and damaging the eye.

ACh stimulates M₃ receptors in circular muscles at the back of the eye. This opens the Canal of Schlemm, draining aqueous humour, reducing intra-ocular pa.

So, we treat glaucoma w M₃ agonists like pilocarpine

Question 33

How does the parasymp ns control accomodation (focusing) of the eye?

Answer 33

W distance vision, ciliary muscles relax and suspensory ligaments are taught. This pulls the lens into a long, thin conformation, refracting parallel light rays to focus it onto the retina

To focus on close objects, the oculomotor parasymp nerve (CN III) releases ACh which binds to M₃ receptors in the ciliary bodies. This contracts ciliary muscles, loosening suspensory ligaments. The lens bulges, reducing focal length. The lens refracts the divergent light rays and focuses it on the retina.

Question 34

Describe the structure of the bladder and the function of the autonomic NS in the bladder

Answer 34

The bladder is smooth detrusor muscle. In the entrance of the bladder hay an internal and external sphincter which opens/closes. The bladder also has sensory nerves

The parasym ns releases Ach which acts at M3 receptors to contract smooth detrusor muscle.

The symp releases NA which stimulate B2-adrenoreceptors, relaxing the detrusor muscle. The symp also contracts the internal sphincter by acting on a-1-adrenoreceptors.

Question 35

Describe micturition (autonomic bladder control)

Answer 35

Full bladder: Pa ⇡ which stimulates stretch receptors. These send signals to the micturition centre in the brainstem.

This sends info to the symp ns in the spinal cord to switch it off. It also sends info to the sacral region of the spinal cord to switch the parasymp ns on.

Parasymp fibres release ACh acting at M₃ on the detrusor, and M₂ receptors on the internal sphincter. This contracts the detrusor and relaxes the internal sphincter.

To initiate voiding, we relax the skeletal external sphincter. Impulses to this travel via the somatic pudendal nerve.

Once the bladder empties, sensory neurones ya no son stimulated. Brainstem switches off the parasym and switches on the symp ns

Question 36

Describe The Parasympathetic Nervous System and the Lungs

Answer 36

Stimulation of M3 receptors contracts bronchi smooth muscle cells causing bronchoconstriction

Thus, Muscarinic antagonists are used as bronchodilators e.g. Ipratropium. This is used in COPD to increase airway flow

BUT: In patients with bladder outflow problems and glaucoma Mus antagonist will reduce urine outflow, increase intraocular pressure. These are potential contraindications

Question 37

Describe The Parasympathetic Nervous System and the Genitalia

Answer 37

Sacral parasympathetic vasodilator nerve innervate the corpus cavernosum of the penis

Here, they release NO which causes VSMC relaxation, increasing blood flow into the corpus cavernosum, causing an erection

Sildenafil (Viagra) is a phosphodiesterase inhibitor – it prevents the breakdown of NO, maintaining an erection

Question 38

How do M3 receptors cause contraction of smooth muscle?

Answer 38

Ach acts at protein coupled receptor M3 which is linked to Gq. This activates PLC to break down PIP2 into DAG and IP3. IP3 acts at the IP3 receptor on the SR to release Ca2+. DAG increases membreane excitability which causes depolarisation.

Hay activation of vgccs. Ca2+ comes in from outside. Ca2+ in smooth muscle activates Ca2+-camodulin which activates MLCK which initiates actin/myosin contraction.

Question 39

Describe Cholinergic Synapse transmission

Answer 39

Ach release= choligernic transmission. This mediates the effects of the parasymp ns. Remember that Ach is broken down by an Achesterase in the synaptic cleft but NA is taken up by an uptake transporter.

Question 40

How can we modulate cholinergic transmission?

Answer 40

We can modulate cholinergic transmission by:

Direct Drugs that act at cholinergic receptors

Indirect Drugs that act at altering release/ termination of transmission.

Mus receptor agonists stimulate the parasymp ns so are called parasympathomimetics

Question 41

Describe Ach synthesis

Answer 41

Ach synthesis occurs in: NMJ, ganglia, parasym post-ganglionic fibres, CNS. Its made by Choline acetyltransferase (ChAT)

Choline + Acetyl CoA → Acetylcholine + CoA

Choline is from diet (liver, fish) and is taken up by choline carrier at the pre-synaptic terminal. Acetyl CoA is produced by cellular respiration

ChaT inhibitors= v dangerous bio weapons

Changes in choline levels and acetyl CoA production will both alter Ach levels/cholinergic transmission

Question 42

Describe the effect of Clostridium botulinum on cholinergic transmission

Answer 42

Clostridium botulinum is a toxin which enters terminals and degrades Ach-containing vesicles.

ANS and motor fibres are inhibited, causing paralysis

Botox: v low levels of botulinum toxin used to produce local paralysis (cosmetic, clinical uses). Also used to prevent excess sweating (hyperhidrosis)

But adverse effects inc: tachycardia, dry mouth, blurred vision, GI tract disturbance, skeletal muscle paralysis due to decrease in cholinergic actions.

Question 43

Describe termination inhibition in cholinergic transmission

Answer 43

Anti-cholinesterases inhibit Ach breakdown at the synapse. This increases cholinergic transmission, e.g. Bradycardia, excess sweating, salivation, blurred vision, GI disturbances, excess skeletal muscle contraction – twitching, paralysis.

These drugs are classified by duration/mode of action:

Short acting: diagnostic, improves myasthenia gravis

Medium acting: reverse neuromuscular block and atonic states of GI tract after surgery

Long acting (bio weapons)– bind to and change enzyme structure, preventing its ability to work. Any new AchE synthesis will be overpowered by the drug.

Question 44

Describe cholinergic receptor pharmacology

Answer 44

Most drugs modulate cholinergic system via (ant)agonists at nic, M2 and M3 cholinergic receptors

Most clinically relevant drugs act at nicotinic receptors at the NMJ

Question 45

How can certain agonists and antagonists both produce muscle relaxation?

Answer 45

Agonists, e.g. Suxamethonium and Competitive antagonists, e.g. Vecuronium act at nicotinic receptors at the NMJ. Both cause muscle relaxant- important during surgery

Vecuronium outcompetes Ach for the same binding site on nic receptors. This ⇣ nic receptor stimulation by Ach

Suxamethonium stays at Ach site for long bc tiene poor dissociation. So, it overstimulates the nic receptor. This sustained EJP and depolarisation inactivates vgccs. This means no a.potentials or contraction

Question 46

Give Uses of Muscarinic Receptor Agonists

Answer 46

Question 47

Give Uses of Muscarinic Receptor Antagonists

Answer 47

Question 48

What is shown here?

Answer 48

Cell body: Contains all of the normal machinery of life

Dendrites: Provide a large SA for receiving info from other cells

Axon/nerve fibre: Transmits info to other nerve cells using digital signalling

Question 49

What does this image show?

Answer 49

Synaptic boutons: Location where one nerve cell passes information to another

Question 50

What building blocks of the CNS protect and support it?

Answer 50

Meninges create a tight seal between the CNS and the rest of the body, preventing unwanted chem entry

The blood brain barrier: A network of blood vessels and tissue made up of closely spaced cells. Keeps harmful substances from reaching the brain.

CSF is also for physical support and protection

Microglia: Immune cells that migrated into the brain early in development before the BBB formed

Question 51

What are astrocytes/astroglia?

Answer 51

Astrocytes (astroglia) control the environment of nerve cells to protect them

They transport substances to and from nerve cells, and process them

They instruct CNS capillaries to form the BBB

They swaddle nerve cell bodies/dendrites, adjusting the conc of substances in the fluid layer between them

Question 52

What are myelin sheaths?

Answer 52

Myelin sheaths are myelinating glial cells which ⇡ neural signal speed

Oligodendrocytes- found only in the CNS pathways. They create a myelin sheath to speed up conduction

Neurolemmocytes- AKA schwann cells

Question 53

Label and explain this diagram of grey matter

Answer 53