Biology Nervous Cordination - Helps please Watch

VBTS02
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Can anyone please read through and tell me if I got any of them wrong and what I can add to it ? Thankyou


Describe how the Pacinian corpuscle is used as an example of a receptor to illustrate that receptors respond only to specific stimuli.
Pacinian corpuscle are mechanoreceptors, they only respond to mechanical stimuli, e.g., pressure, vibration.

Describe how the Pacinian corpuscle is used as an example of a receptor to illustrate that stimulation of a receptor leads to the establishment of a generator potential.
When pressure is applied the Pacinian corpuscle deforms and stretches. This causes the stretch mediated sodium ion channels to open, there is an inflow of sodium ion into the sensory neurone. This influx of Na+ ion depolarises the membrane, this change in potential difference is the generator potential.

Recall the basic structure of a Pacinian corpuscle.
The Pacinian corpuscle is a receptor which has a sensory neurone in the middle, the sensory ending is covered in layers of lamellae. After the lamellae, the sensory neurone is myelinated.

Describe how the deformation of stretch-mediated sodium ion channels in a Pacinian corpuscle leads to the establishment of a generator potential.
Deformation of stretch mediated Na+ ion channels means Na+ ion channels are open, Na+ can diffuse into the neurone. This causes a change in potential difference this change in potential difference is the generator potential.

Describe the structure of a myelinated motor neurone.
A myelinated motor neurone has Schwann cells wrapped around the axon, there are many layers of Schwann cells wrapped around the axon in alternating pattern. There are gaps between these myelin sheath called the node of Ranvier.

Explain the establishment of a resting potential in terms of differential membrane permeability, electrochemical gradients and the movement of sodium & potassium ions.
Resting potential is established when the neurone is at rest (not being triggered), during resting potential the sodium potassium pumps 3 sodium ions out and two potassium ions in, but the voltage gated sodium ion channels are closed therefore the membrane isn’t permeable to Na+ ion. This creates a sodium ion electrochemical gradient because the membrane is more negative inside than the outside. Potassium ion channel open, some potassium ion diffuse out down the electrochemical gradient. Membrane is permeable to potassium ion but it doesn’t reach equilibrium.

Explain how changes in membrane permeability lead to depolarisation and the generation of an action potential.
When there is a stimulus the neurone becomes excited and few sodium ion channel open. Few sodium ions diffuse into the axoplasm, this results in a change of potential difference this change is generator potential. If the generator potential reaches a threshold action potential is triggered. More sodium ion channels open therefore more sodium ion diffuse in, this increases the potential difference further of the neurone as the axoplasm is more positive than outside the neurone. This is depolarisation, at depolarisation the neurone is at about +30mv to +40mv.

Describe the passage of an action potential along non-militated and myelinated axons, resulting in nerve impulses.
Action potential along non- myelinated axon -> Wave of depolarisation, When Na+ diffuses, it diffuses along the membrane. The movement Na+ along the membrane means that the neighbouring membrane becomes depolarised therefore electrical impulses propagate along the axon.
Action potential along myelinated axon -> Action potential travels by salutatory conduction. When action potential is triggered at one of the membrane it cannot along the length of the axon because the axon is insulated by the myelin sheath made up of Schwann cells. This means that the action potential jumps from one node of Ranvier to another therefore.

Describe the nature and importance of the refractory period in producing discrete impulses and in limiting the frequency of impulse transmission.
Refractory period is when there is a time delay and the action potential cannot overlap, this is because after an action potential neurone cell can’t be excited again. This limits the frequency of action potential and makes action unidirectional.



Describe factors affecting the speed of conductance: myelination and saltatory conduction; axon diameter; temperature.
Myelination = Insulates the axon, impulses travel from node to node, saltatory conduction.
Axon Diameter = Larger diameter means there is less resistance therefore a faster impulse.
Temperature = higher temperature means that the ions travel faster therefore faster action potential, temperature beyond optimum causes enzymes to lose their tertiary structure therefore increasing temperature would have no effect on the speed of impulse.

Describe the detailed structure of a synapse and of a neuromuscular junction.
Structure of a synapse -> synapse is a junction between two dendrites, synaptic ending, and between dendrites and synaptic endings.
Neuromuscular junction -> A specialised cholinergic synapse between a motor neurone and a muscle cell.

Na+

Describe the sequence of events involved in transmission across a cholinergic synapse in sufficient detail to explain unidirectionality, temporal and spatial summation & inhibition.
Action potential arrives at the presynaptic neurone. This causes voltage gates calcium ion channels to open, the calcium ions bind to the vesicles and cause them to fuse with the presynaptic membrane. The vesicles release the neurotransmitter by a process called exocytosis, in this case the vesicles release acetyl choline into the synaptic cleft. The acetyl choline diffuse across the synaptic cleft and binds to the receptor sites and Na+ ion channel open. This causes sodium ions to diffuse into the axoplasm and action potential is triggered in the postsynaptic neurone. Acetylcholinestrase breaks acetylcholine after it has been released from the receptor site and it diffuses back into the presynaptic cleft. This insures that the impulse travels unidirectionally, removing the acetylcholine will ensure that the acetylcholine won’t trigger further action potential.
If single doesn’t trigger an action potential on the post synaptic neurone multiple action potential back to back can trigger one. Some transmitters for example Cl- can inhibit action potential as it would hyperpolarise the neurone. One or more pre-synaptic neurone can release neurotransmitters at the same time on one post-synaptic neurone to ensure that post-synaptic neurone gets triggered.

Compare transmission across a cholinergic synapse and across a neuromuscular junction.




Cholinergic synapse can be formed between any types of neurone that releases Ach.

Neuromuscular junction can be formed only between motor neurone and muscle cell.

Ach isn’t always excitatory between neurones.

Ach is always excitatory between motor neurone and muscle cell.

Less receptor on the post synaptic membrane.

There are much more receptors on the post synaptic membrane.



The post-synaptic membrane has lots of folds called clefts that store Acetylcholinestrase.






Recall information provided to predict and explain the effects of specific drugs on a synapse.
Drugs that mimic neurotransmitter –Agonists – Morphine + Nicotine.
Stimulating release of neurotransmitter- Diazepam.
Inhibiting enzyme that break down neurotransmitter- clostridium, Opiods.
Blocking receptor on post synaptic neurone – Antagonists – Curare.
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Hajra Momoniat
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I feel like for the first question you could further describe why they only respond to stimuli such as pressure. You could do this by saying they have stretch-mediated sodium ion channels that are opened when pressure is applied.

For the sixth question you could mention what the resting potential is i.e. it is -70mV.

For the ninth question you could mention that the sodium ion gated channels and potassium gated channels are closed.

For the 13th question you could also add that at neuromuscular junctions there are T-tubules on the muscle.

Overall you have done really and the comments above I have made are really fussy where im literally 'splitting hairs'. You deserve my rep
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VBTS02
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(Original post by Hajra Momoniat)
I feel like for the first question you could further describe why they only respond to stimuli such as pressure. You could do this by saying they have stretch-mediated sodium ion channels that are opened when pressure is applied.

For the sixth question you could mention what the resting potential is i.e. it is -70mV.

For the ninth question you could mention that the sodium ion gated channels and potassium gated channels are closed.

For the 13th question you could also add that at neuromuscular junctions there are T-tubules on the muscle.

Overall you have done really and the comments above I have made are really fussy where im literally 'splitting hairs'. You deserve my rep
Thankyou so much x
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macpatgh-Sheldon
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Recall information provided to predict and explain the effects of specific drugs on a synapse.

Drugs that mimic neurotransmitter –Agonists – Morphine + Nicotine.
Stimulating release of neurotransmitter-
Diazepam. Inhibiting enzyme that break down neurotransmitter- clostridium, Opiods.
Blocking receptor on post synaptic neurone – Antagonists – Curare.
You could add more detail to this last Q.

A. Cholinergic synapse (neurone to neurone)
1. Muscarinic receptors (divided into 5 sub-classes: M1 to M5 (the digits are subscript)
a) Agonists: pilocarpine, carbachol (application: pilocarpine useful in reducing IOP (intra-ocular pressure) quickly in acute closed-angle glaucoma that is threatening eyesight, in combination with intra-muscular acetazolamide (carbonic anhydrase inhibitor that blocks production of acqueous humour). M1 and M3 receptors activated through action of phospholipase C on DAG [diacylglycerol), which stimulates protein kinase C.
b) Antagonists: atropine (original drug used as anti-muscarinic agent) from Atropa belladona (named as such because ladies used this plant to dilate their pupils to attract opposite sex in Victorian times - belladonna = pretty lady); homatropine - can be used as pre-op medication; tropicamide - used to block accommodation in cycloplegic refraction (determination of refractive error in order to prescribe correct spectacles).

2. Nicotinic receptors: (N receptors - divided into NG [G is subscript and stands for ganglionic as these receptors are located on sympathetic and parasympathetic ganglia] and NM [M is subscript: see B below]:
a) Agonists: (nicotine) - varenicline (partial agonist used to reduce craving of nicotine as aid in smoking cessation)
b) Antagonists: hexamethonium - no clinical application today.

B. At neuromuscular junction (NM receptors - ACh receptors at neuromuscular junction)

a) Agonists: (indirect by preventing breakdown of ACh [anticholinesterases]: neostigmine [needs to be given IM (intra-muscularly], pyridostigmine (MESTINON) used to treat myasthenia gravis [an auto-immune disease in which antibodies are produced against patient's own ACh receptors], so increasing ACh levels helps to permit striated muscle contraction.
b) Antagonists: tubocurarine (curare) used by S American Aztecs in their arrows to kill prey by causing respiratory arrest; succinylcholine used as pre-med before surgery to avoid muscle contraction interfering with operative procedure (blocks intercostal muscles and diaphragm, too, so patient will need artificial ventilation).
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VBTS02
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(Original post by macpatelgh)
Recall information provided to predict and explain the effects of specific drugs on a synapse.

Drugs that mimic neurotransmitter –Agonists – Morphine + Nicotine.
Stimulating release of neurotransmitter-
Diazepam. Inhibiting enzyme that break down neurotransmitter- clostridium, Opiods.
Blocking receptor on post synaptic neurone – Antagonists – Curare.
You could add more detail to this last Q.

A. Cholinergic synapse (neurone to neurone)
1. Muscarinic receptors (divided into 5 sub-classes: M1 to M5 (the digits are subscript)
a) Agonists: pilocarpine, carbachol (application: pilocarpine useful in reducing IOP (intra-ocular pressure) quickly in acute closed-angle glaucoma that is threatening eyesight, in combination with intra-muscular acetazolamide (carbonic anhydrase inhibitor that blocks production of acqueous humour). M1 and M3 receptors activated through action of phospholipase C on DAG [diacylglycerol), which stimulates protein kinase C.
b) Antagonists: atropine (original drug used as anti-muscarinic agent) from Atropa belladona (named as such because ladies used this plant to dilate their pupils to attract opposite sex in Victorian times - belladonna = pretty lady); homatropine - can be used as pre-op medication; tropicamide - used to block accommodation in cycloplegic refraction (determination of refractive error in order to prescribe correct spectacles).

2. Nicotinic receptors: (N receptors - divided into NG [G is subscript and stands for ganglionic as these receptors are located on sympathetic and parasympathetic ganglia] and NM [M is subscript: see B below]:
a) Agonists: (nicotine) - varenicline (partial agonist used to reduce craving of nicotine as aid in smoking cessation)
b) Antagonists: hexamethonium - no clinical application today.

B. At neuromuscular junction (NM receptors - ACh receptors at neuromuscular junction)

a) Agonists: (indirect by preventing breakdown of ACh [anticholinesterases]: neostigmine [needs to be given IM (intra-muscularly], pyridostigmine (MESTINON) used to treat myasthenia gravis [an auto-immune disease in which antibodies are produced against patient's own ACh receptors], so increasing ACh levels helps to permit striated muscle contraction.
b) Antagonists: tubocurarine (curare) used by S American Aztecs in their arrows to kill prey by causing respiratory arrest; succinylcholine used as pre-med before surgery to avoid muscle contraction interfering with operative procedure (blocks intercostal muscles and diaphragm, too, so patient will need artificial ventilation).
Omg this is so good thankyou ^-^
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Hajra Momoniat
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(Original post by VBTS02)
Thankyou so much x
Np. Which exam board do you follow.
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VBTS02
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(Original post by Hajra Momoniat)
Np. Which exam board do you follow.
AQA ^-^
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Hajra Momoniat
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(Original post by VBTS02)
AQA ^-^

O ok that's the same as me. Well what I was going to say is that you don't need to know the names of drugs that act as agonists and antagonists for AQA. But if you want to then that's fine
I make resources based on the AQA spec so if you want to check them out please click on the link and make an account (which is for free). Message me (my name on get revising is the same as the one on here) and then click on my name which will come up in blue on the right hand side in your 'sent messages'. All my resources will come up as a list

If you need any more help feel free to ask me
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