Neural Control Systems Flashcards
How is the ANS different to somatic motor nerves?
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
What is the difference between grey and white matter?
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.
Describe an overview of brain structure.
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.
Label the main subdivisions of the brain
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Label this brain diagram
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What do the cerebral cortex and hippocampus do?
Cerebral cortex & hippocampus are the thinking part of the brain:
conscious perception, cognition, learning and memory, controlling voluntary movement
•different areas subserve different functions
What is the function of the thalamus?
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
What is the diencephalon?
diencephalon: the caudal (posterior) part of the forebrain, containing the epithalamus, thalamus, hypothalamus, and ventral thalamus and the third ventricle.
Describe the function of the hypothalamus.
Hypothalamus is the master controller for homeostasis:
•links neural and endocrine systems
•controls the systems that generate the sleep-wake cycle
What is the brain stem?
The brainstem regulates involuntary cardiac and respiratory function, consciousness, and the sleep cycle. It consists of the medulla oblongata, pons, and midbrain.
Describe the spinal cord
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.
What is resting potential?
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.
How is resting potential maintained?
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.
Describe depolarisation
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.
Describe and explain repolarisation.
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.
What is hyperpolarisation?
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
Draw and label an action potential graph.
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What are synapses?
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.
Describe pathways for para and sympathetic responses, using diagrams
What is an autonomic ganglion?
An autonomic ganglion (plural ganglia) -Group of neuronal cell-bodies lying outside CNS
Explain synapse transmission between autonomic nerves
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
Describe how the sympathetic ns affects the lungs, eyes and sweat glands
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
Describe the adrenergic synapse
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.
What happens if too much adrenaline is released?
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.
Adrenergic transmission can be regulated…
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.
How are Noradrenaline and Adrenaline synthesised?
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
How can adrenergic transmission be inhibited in terms of storage?
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
How can drugs like amphetamine or ephedrine facilitate release in adrenergic transmission?
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
How can drugs inhibit NA release and therefore adrenergic transmission?
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
What is termination inhibition in adrenergic transmission? Which drugs are involved in this?
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.
How does the parasympathetic nervous system affect pupil diameter?
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
How does the parasymp ns affect intra-ocular pressure?
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
How does the parasymp ns control accomodation (focusing) of the eye?
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.
Describe the structure of the bladder and the function of the autonomic NS in the bladder
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.
Describe micturition (autonomic bladder control)
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
Describe The Parasympathetic Nervous System and the Lungs
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
Describe The Parasympathetic Nervous System and the Genitalia
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
How do M3 receptors cause contraction of smooth muscle?
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.
Describe Cholinergic Synapse transmission
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.
How can we modulate cholinergic transmission?
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
Describe Ach synthesis
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
Describe the effect of Clostridium botulinum on cholinergic transmission
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.
Describe termination inhibition in cholinergic transmission
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.
Describe cholinergic receptor pharmacology
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
How can certain agonists and antagonists both produce muscle relaxation?
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
Give Uses of Muscarinic Receptor Agonists
Give Uses of Muscarinic Receptor Antagonists
What is shown here?
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
What does this image show?
Synaptic boutons: Location where one nerve cell passes information to another
What building blocks of the CNS protect and support it?
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
What are astrocytes/astroglia?
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
What are myelin sheaths?
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
Label and explain this diagram of grey matter
