biom lt1 questions 2011

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I hav e few questions from Lecture 1 of the Bi om2011 lecture you took last week. I would really appreciate it if you could keep to layman's terms in your answers. 1 If a motor neuron activates a muscle and the signa l starts in a neuron proper i n your brain, what is the process whereby the A.P travels from brain (CNS) to muscle (PNS) See last question  3 Muscles only have excitatory respnses EPSR's. Is this because Ach is an excitatory neurotransmitter (never inhibitory). YES Is Ach the only transmitter sent across synapses to the muscles?  YES 4 What does the term 'P/Q type calcium channel' mean? I found it in the text . It is the type of voltage gated calcium cha nnel that is found at the m otor never terminal that is needed to allow calcium to come into the motor never terminal to cause ± trigger the release of acetylcholine release from the motor nerve terminal. There are other types of voltage gated calcium chann els ± for example L type voltage gated calcium channels are found in muscle. 5 I am having trouble with what connects to what in a neuromuscular synapse. If a msg comes from neurons in the brain, does it travel down nerves in the spine to reach motor neurons which are the ones that innervate muscles. Are the nerves in the spine called motor neurons or just neurons Motor neurons ± their cell bodies are in the ventral horn of the spinal cord. If a message comes from say the motor cortex ± the cell bodies for this neuron is in layer V (five) of the motor cortex (some call it an upper motor neuron) but it is formally called a cortical spinal pyramidal neuron that makes a direct connection onto alpha and gamma motor neurons within the ventral horn of the sp inal cord.  6 Would I be right to use the phrases pre and post synaptic when discussing a motor neuron and the muscle. Yes - the motor neuron nerve terminal (hence the motor neuron) is the pre -synaptic part of the n euromuscular synapses and the post - synaptic cell is the muscle. 8 When Ach binds to it's receptors (are the receptors on the muscle always ligand gated or can they be g protein coupled) it produces a response in the membrane potential of the m uscle and various r esponses on the muscle at dif ferent synapses summate and once crossing the threshold create an action potential . The acetylcholine receptors at the neuromuscular synapse are ligand gated ion channels - (the ligand being ACh) . They are the ONLY receptors that is present ± there are no G protein couple receptors at this synapse ( the neuromuscular synapse).  9 What is 'Lateral Vestibular Nucleus'  This you will learn in the next couple of lectures 10 The text mentions only temporal summation not tem poral and Spaci al. Is it only temporal summation that occurs in the muscle fibre? Yes the addition of successive

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motor neuron action potentials leading to summative increased in acetylcholinebeing released to active (open) more and more acetylcholine receptors to cause themembrane potential under the motor nerve terminal to rise and rise, which in turncauses more and more voltage gated sodium channels to open. All this is drivingmore and more Na+ to enter the muscle and hence make the membrane potentialunder the motor nerve terminal to rise (i.e. become more +ve) once the membranerises form -70/80 milli volts to -60milli volts ± this is threshold and a muscle actionpotential is generated that moves away from the neuromuscular contact zone - alongthe plasma membrane of muscle down the T tubles ± to initiate the next stage whatwill end up being a muscle contraction.

Spatial summation of action potentials ± is seen in the CNS where hundreds of synaptic endings (nerve terminals) are made onto motor neurons close to the initialaxon segment ± where motor neuron action potentials are generated or are locatedfar away on dendrites from this site.

How is this so?

11 Fast twitch muscle fibres are fast but dont have fine control. No I did not say that ± what I did say large motor units do not have fine control ± whereas small motor units can effect fine motor movements.

In your eyes we need speed (for blinking etc) AND fine control. Can a fast twitchfibre have both control and speed or do we have a mixture of fast and slow twitchfibres in our eyes. It is likely that extra ocular muscles mostly consist of fast fatigableresistant fibers ± there may be some slow but likely not to be many. The control will

come from the fact that the motor units are small.

12 A strong muscle contraction involves type 1, type 11a and type 11b musclefibres. If I am trying to evade a predator and I need an explosively fast musclecontraction is it possible to have only type IIa and IIb (fast twitch) musclesactivated? Or does a strong muscle contraction ALWAYS involve all the differenttypes of muscle fibres because type 1 are recruited first?

There are very few muscle in the body that are exclusively made up of one fiber type. Examplesbeing the soleus and extensor digitorum longus. Muscles for explosive activity will contain mostlyfast type (fatigable and fatigable resistant) .

It is not a strong muscle contraction that you need to be thinking about rather a high frequencyof action potential arriving at excitatory nerve terminal endings that connect onto motor neurons(i.e. high levels of synaptic drive) that induces high levels of excitatory neurotransmission at thesesynaptic inputs that then leads to actions potential being generated in the Motor neurons. If thisfrequency of action potentials is high enough this leads to high levels of excitatory neuronaltransmission at the synaptic contacts on motor neurons then we will see small, medium and largemotor neurons all being activated i.e. to then trigger their own action potentials these motorneuron action potentials then arrive at the motor nerve terminals to cause release of acetylcholoine

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to then cause muscle action potentials to then cause muscle contraction. Again if the high frequencyof motor neuron action potentials is passed on the muscle, ending up as high frequency of muscleaction potentials then the force of muscle (muscle fiber) contraction is greater (rate modulation). If the frequency of muscle action potentials is lower - then the contraction level is lower )

13 Just to recap the 'size principle' idea.

In your diagram the diamond shaped things are the soma of the motor neuronswhich are receiving input across the synapse from what kind of neuron? Yes. Thetypes of neurons that make connections onto moto r neurons are many. They can beinhibitory connections (glycinergic) or excitatory ± which can be glutamate or cholinergic (acetylcholine). In the size principle diagram the inputs are excitatory.These the nerve terminal endings of these inputs ±could release either glutamate or acetylcholine.

This 'input' is ACH which is released by the presynaptic neuron.

When the Ach crosses the synapse and bonds with the receptors on the musclenerve it creates a response (not an action potential) and all the responses summateand may create an action potential. Yes see my answer above

On the left side of the diagram the line with the slashes across it represents thefrequency of action potentials travelling down the presyaptic neuron. Each of theseaction potentials opens ca++ channels which causes vesicle fusion and release of

Ach. YES ± and this will control the amount of neurotransmitter being release ± fromsmall amounts to lots. If enough is released then this will raise the local membrane

potential± which will then bring the local membrane potential to threshold to trigger the generation of an action potential.

For a given synaptic input Small motor neurons with the smallest cell bodies will beactivated first- By synaptic input do you mean the amount of Ach crossing thesynapse to the post synaptic neurons (the diamonds in your diagram) .

Synaptic input, Synaptic Drive. I agree is a bit confusing. Best to think of it as thenumber of action potentials arriving at excitatory nerve terminal endings tha t aremaking connections onto small, medium and large sized motor neurons Theneurotransmitter at these synaptic connections could be glutamate or acetylcholineacting on glutamate or acetylcholine receptors respectively.

So if there are few action potentials arriving ± then we will only see action potentialscoming from small motor neurons which then make their way to their nerve terminalendings on type I (slow) muscle fibers ± which in turn can then generate a muscleaction potential to cause these slow muscle fibers to contract. If the frequency of action potentials arriving at excitatory nerve terminal endings is higher then you willnot only activate action potential in small motor neurons but now in larger motor neurons. They will in turn generate their own action potentials which then make their way to their nerve terminal endings on slow and fast type muscle fibers - which in

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turn can then generate a muscle action potentials to cause both slow and fastmuscle fibers to contract