L4- Spinal Circuitry and motor control PDF

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Spinal Circuitry and Motor Control Lecture Notes...

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The Muscle Spindle

Structure of muscle spindle  Muscle spindles lie within belly of muscle(2-4 mm long)  Extrafusal means outside muscle, what we think about when talking about muscle tissue  Ends of MS attached to outer sheaths of striated muscle fibres (extrafusal fibres). This means when muscle belly lengthens, spindle will be lengthened. When muscle belly shortened, two ends of muscle spindle will be pulled together  An average MS has 4 – 6 intrafusal fibres (3 instrafusal in second picture)  The density and structure of muscle spindles within human muscles varies in relation to the function of the muscle. In muscle groups, with dextrous function and fine control required, higher number of muscle spindles and they are larger with more intrafusal fibres. These muscles need to have detailed info about the length of muscle, speed at which it lengthens.  Large levels of afferent info required by eyes (Proprioceptive info to control eye movements), hand (dextrous and fine control) and neck (to orient ourselves) so large number and size of muscle spindles  Gamma motor neurons come in to supply extrafusal fibres Lumbar

Red line is capsule of spindle and outside of it is extrafusal muscle fibres (Pink dotted area)> Everything inside red line is inside of spindle. The capsule is connective tissue membrane,

fibroblasts tend to be flattened so thin, connective tissue capsule. It serves to insulate inside of spindle in terms of separating it from ionic concentrations outside. Remember inside of muscle spindle has free nerve endings and axons. Axons are very sensitive to ionic concentrations. We have to isolate the nerve endings from those ionic conditions. First role of capsule is to insulate, isolate the sensory endings from ionic concentrations in muscle itself. Second role of capsule is to contain viscous fluid that is inside spindle. Our spindle has gel like, thick substance. We can think of spindle like squishy cushion, bathes intrafusal fibres from mechanical perturbation of outside. We only want sensory nerve endings in spindle to respond to mechanical perturbation that arises within spindle, we don’t want them to respond to mechanical perturbations from outside. The capsule, by containing viscous fluid, creates mechanical insulation for inside of spindle. Moving on to intrafusal fibres, we see three here. Proportion of these will vary. 1. Top one in blue is abbreviated to DB (Dynamic bag), some texts called it bag Type I or D1 intrafusal fibres. Some will call it adaptive bag fibres. Called bag because centre is a bag type shape with swelling in the middle. The swelling has a viscous fluid, gel like substance. Its called dynamic and adaptive bag because it can adapt its shape in response to mechanical perturbation. This is because of the type of viscous fluid, it has a low level of viscosity, meaning it is thin and moves easily so bag fibres is easily squished. 2. In pink, is Static bag. Likewise, it has other names like type 2 bag, D2 bag, and non adaptive bag. This is non-dynamic, this bag fibre has a gel like substance in middle but it has higher viscosity and thicker, less squishy. This bag section in middle is less likely to change its shaped if you pull on it. The viscous fluid is too thick. 3. Chain fibre: we have four here and they do not have swollen central section, linear in nature and nuclei in line, not bunched together in middle. No viscous fluid, these fibres can’t change their shape. Any mechanical perturbation will not change their shape. They are often called static in nature as well or non-adaptive. Next, look away from central portion and towards end of spindle. Towards end of intrafusal fibres, is striated muscle. This portion is contractile, it can shorten and is on both ends of intrafusal fibres. If striated muscle contracts and shortens, pulls on central portion. 

Mechanoreceptors (axons are adhered to intrafusal fibres, sensory endings are called mechanoreceptors, meaning they respond to mechanical perturbation) o Mechanical deformation (tension). Both ends of spindle are pulled apart, putting intrafusal fibres under tension for their membrane, thereby tension of axon membrane. o Deformation of nerve membrane o Increase in membrane permeability. o NA+ flows in o Membrane Depolarises o > -55mv = Voltage gated channels open o Influx of NA+ o Action potential.

o Incr. Mechanical Deformation = incr. Freq Action Potentials o We call this sensory transduction, a force is transduced in to creating an AP. Stretch on spindle produced AP. The more stretch, more AP. If spindle put on a Lot of stretch, increases tension of intrafusal fibres, increases tension on axon membrane and increases permeability even more and more sodium and more depolarization, higher frequency of AP. o Sensory recfeptot generates AP at frequency directly proportional to degree of stretch and this will travel up axon and towards spinal cord to CNS, providing information of length of muscle and speed at which it lengthens. This happens to annulospiral and flower sprat endings, they are both mechanoreceptors.

Now talking about sensory receptors  Type Ia afferent and type II afferents  Afferent sensory axons can be categorized in terms of size. If prefix 1A, largest and fastest type of axon. Structure is very large, myelinated and fast conducting. This means sensory information generated, is communicated rapidly up to spinal cord and CNS at 150 m/s. Type II afferent are slightly smaller axon, slower conducting. They are also different interms of which aprt of intrafusal fibre they attach to  1A affrent; axon come sin to spindle and they are very specialized and wrap around central portion of intrasfusal fibres, we call them anullospiral endings. This is spiral ring structure wrapping around central portion of intrafusal fibre, wrap around static/dynamic bag and chain fibres. They don’t wrap around loosely, in very close contact and adhere to membrane of intrafusal fibre. If membrane of intrafusal fibre pulled and tension, membrane of axon will be pulled and tensioned, this is critical for function.  II afferent: axons come more distal, away from central portion, also adhere to membrane of intrafusal fibres but don’t wrap, instead branch out and attach, in what is called flower spray endings. These are axons that come in and also adhere to membrane

Gamma Motor Neurons: static and dynamic

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Static: Gamma motor neurons innervate intrafusal muscle fibres. Static gamma motor neurons innerve static intrafusal fibres, non-adaptive fibres (static bag and chain). Motor neurons, taking AP from motor neurons up in spinal cord, travel down, axon enters spindle, axons innervate striated muscle at end of spindles at NMJ. Dynamic: do same thing but only to dynamic bag. The specialist gamma motor neurons can contract intrafusal muscle fibres (Both ends shortening), this would tension up central component. SO gamma motor neurons are system by which we can alter level tension of central component on intrafusal fibres. This means that we have a system to alter sensitivity of muscle spindle. You already know frequency of AP being generated in axons is related to tension. The amount of tension, pertains to two things. First is if spindle is lengthening, intrafusal fibers will be tensioned and that will cause AP. Second process, gamma motor neurons by activating striated ends can also tension central component. It would take less of a stretch of spindle before AP generated. Tension of spindle through gamma motor neurons make spindle more sensitive, brings nearer to threshold. SO it takes less stretch to generate AP. Sensory receptors tell about degree of stretch and speed of stretch but we can alter its sensitivity, only sensory receptor where this happens. Level of sensitivity controlled by gamma motor neurons

Adaptive Fibres (dynamic bag) 1. A stretch tensions the Dynamic Bag Fibre causing depolarisation of the sensory endings. 2. The viscous area then stretches taking the tension out of the Dynamic Bag Fibre (adaptation). 3. The sensory endings are no longer depolarised. 4. The sensory endings are only depolarised during lengthening of the muscle. 5. The degree of depolarisation is proportional to the rate of lengthening

X axis is time, y axis is length of muscle. Blue line is length of muscle over time. Initially, muscle is held at static length, then it is lengthened and then held at this new longer length. Second part shows pattern of AP during that time. While the muscle is at static length, no AP because no tension in dynamic bag. When muscle is lengthened, there is tension in dynamic bag and AP are generated. We get a burst of AP. As soon as muscle stops lengthening, AP will stop because bag will alter its shape, de-tensioning the membrane and nothing to trigger AP. Dynamic bag fibre will only produce bursts of AP during the lengthening of muscle but will not produce AP when muscle is held at static length. Lets say muscle is lengthening rapidly, this would initially create a lot more tension and momentarily high tension before it adapts the shape. High degree of tension on membrane of bag, would cause a lot of tension on annulospiral and cause a lot of Na influx and high frequency of AP. Slow stretch would produce less tension on bag. If muscle lengthened at very slow speed, bag might be able to accommodate altered shape quickly enough to prevent any tension occurring in the first place. A very slow stretch might not put

much tension because the dynamic bag can alter shape fast enough. So very slow lengthening might not generate any AP. For dynamic bag, how long will AP be generated for. If muscle lengthened and held in longer length, will AP continued to be produced. For dynamic bag, they will stop because the bag structure will alter its shaped (due to low viscosity fluid), de-tensions membrane so permeability anullospiral membrane goes to normal, sodium stops flowing in, AP will not be generated anymore. Pattern of APs generated are time limited, there will be burst of AP at initial stretch and when stretch stops, AP will stop. If we say annulospiral endings only produce AP at high speeds at stretch and not slow, that explains what we see in patients. Some patients who have had stroke or head injury, may have spasticity. This is an impairment that affects stretch reflex, it is a hypersensitive stretch reflex, reflexes are too responsive. Size of response you get is greater than normal. When we try moving these patient, their muscles respond subconsciously. If you are lengthening their muscles, you might set off hypersensitive stretch reflexes. With patients, if we move their muscles very slowly and lengthen muscles slowly, we might be able to do this without setting off any APs and stretch reflexes. If you move their limb quickly, you will set off exaggerated stretch reflexes. Non-Adaptive Fibres- Static bag and chain fibres If we lengthen intrafusal fibers and generate AP, they continue because no c=mechanism whereby tension can be reduced. For these fibers, frequency of AP being generated will be directly proportion to length of muscle and the frequency will continue for as long the muscle is held at a given length.

1. Due to differences in viscosity and structure, static Bag fibres and chain Fibres do not stretch to reduce tension (Non-Adaptive). 2. Therefore the sensory endings on these fibres continue to be depolarised. 3. The rate of depolarisation will constantly reflect the length of these fibres. Muscle starts off at steady lengthen, then it is lengthened and held at that length, then shortened back to origin length. When muscle is at a shortened length, small tension on nonadaptive fibres so membrane of anulospiral endings under small tension, permeability slightly increased and sodium flows in but not that much, frequency of AP will be low. When muscle is lengthened, frequency of AP is increasing because tension is increased causing more depolorization and higher frequency of AP. No mechanism to reduce tension so higher frequency continues for as long as muscle is held at that length. It is not till muscle brought to shortened position, before frequency of AP goes back to lower frequency. Proprioceptive info travels up 1a afferent, providing spinal cord and CNS about length of every muscle in the body.

Adaptive and Non-Adaptive Fibres

1. Remember, the 1A afferent has receptors on static and dynamic Fibres. AP are generated from adaptive AND non adaptive travelling up axons. From dynamic bag fibre, AP travelling up afferent at frequency proportion to speed at which muscle is lengthened. There will be AP travelling from non adaptive at frequency proportional to length of muscle. T 2. Therefore the 1A afferent carries information on length and speed of lengthening. 3. This information is conveyed to several areas of the CNS

*this diagram shows adaptive fibre AP and non-adaptive superimposed on each other. When muscle at its shortened position and held steady, low frequency of AP from non-adaptive fibers. When muscle is lengthened, burst of AP from dynamic as well during lengthening, Frequency of burst directly proportional to speed of lengthening. When lengthening stopped, dynamic bag stops but we still get AP from the non adaptive fibers but slightly higher frequency, because muscle is lengthened. When muscle is shortened, nothing from dynamic bag but frequency of AP from non-adaptive goes back to original lower frequency. The tension on the dynamic bag is usually more, hence greater speed of lengthening. Dynamic bag and associated annnulospiral endings produce AP proportional to speed of stretch.

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IA afferent/ II are sensory neurons and their soma is located in DRG. Axon comes down and forms sensory receptors. Prime sources of proprioceptive information. Propriceptive info travels up dorsal columns. If quadricep muscles, afferent axons travel up femoral nerve and to spinal cord. This goes in through vacellus gracilis (for lower limbs), travels all the way to gracile nucleus and synapses on to another neuron and the next neuron takes it to thalamus where it synapses and final axon takes it up to sensory cortex of brain. Proprioceptive info also goes to cerebellum, goes up spinocerebellar tracts and helps with control of movement. Afferent info, these APs feed in to cortex sensory areas, cerebellum and to spinal reflexes to help with motor control. Gamma motor neurons located on ventral horn (anterior portion of grey matter) and this is where alpha motor neurons also are. Gamma motor neurons axons come out through ventral root, travel down femoral nerve and to quadriceps and little branches of nerve take axon down to spindle. Gamma are not as big as alpha motor neurons (largest, myelinated). Gamma are myelinated but not as much, slower conducting.

Type IA Afferent- key proprioceptive source  Spindles provide: proprioception/kinaethesia o The position of our body and limbs o Speed and amplitude of movement  Afferent drive of spinal reflexes- provides info that triggers stretch reflexes important for motor control. Don’t only think of muscles as effectors. Muscles also key source of proprioceptive info that enables motor control. Two ways to tension: lengthening of muscle, also via gamma motor neurons tightening up intrafusal fibres

Gamma Motor Neurons

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Alpha motor neurons supply extrafusal muscle fibres, gamma motor neurons supply intrafusal These neurons drive the striated muscle in the end zones of the spindle. They can therefore alter the length and tension of the intrafusal fibres. This alters the sensitivity of the spindle to stretch. Differential activation of dynamic or static gammas can alter sensitivity to length or speed of lengthening. We can tension different components separately and that’s what alters the sensitivity. If dynamic gamma cause tensioning of dynamic bag, spindle will be more sensitive to speed of stretch. If static gamma tension up static bag and chain, spindle more sensitive to length of a muscle.

Alpha Gamma Co-Activation- main purpose is to align spindle length to muscle length to maintain responsiveness of spindle  

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As a muscle contracts the MS could potentially go slack. Whenever a muscle shortens, the gamma motor neurons will ensure that intrafusal fibers will shorten accordingly so the fibers are perfectly tension for length of muscle and always remain responsible to stretch (this is called alpha-gamma co activation. If this occurs the MS cannot function as a receptor (react to stretch). Therefore the striated muscle in the end zones contracts to maintain the spindle at its optimum length If the alpha motor neurone fires to cause a contraction in the skeletal muscle, the gamma motor neurone will fire to maintain tension in the MS In red is descending upper motor neuron from corticospinal tract. Alpha gamma coactivation means that whenever input to alpha motor neuron, there will always be branches of axon supplying gamma motor neurons. When AP arrive to alpha motor neurons, also arrive to gamma motor neuron. They switch on together. Gamma motor neurons can operate separately to alter tension in spindle.

Purpose of the system is so that you get just enough tension for the task at hand. Muscle has to be able to lengthen quickly, gamma input driops and this moves spindle away from threshold and reduces responses from it. By gammas lowing their activity, dampening activity coming from spindle and stopping stretch reflex.

You might not want spindles to be sensitive, you might not want stretch reflexes to happen easily. May if you want speed of movement like running, would be inconvenient, if stretch reflex in hamstring happened every time you tried to swing leg forward. You don’t want to happen when you run. Gamma motor neuron can set sensitivity of spindles accordingly, de-tensioning it and making it less likely for stretch reflex to occur. Different motor behaviours require muscle spindles to operate at different level of sensitivity. Some situations where you want stretch reflex to happen. If you are in a club that is really busy, you need your balance responses to be fast like if someone pushes you from behind, you want a stretch reflex to pull you back. Gammas and Motor Control What may happen when someone has a stroke?  Abnormal levels of gamma activity  Spindle tensioned inappropriately  Abnormal afferent activity  Abnormal motor control What else would affect spindle activity?  Muscle contracture? Maybe Shortened muscle caused by injury, likely that extrafusal and intrafusal are both contracted and spindle become shortened and responsiveness to stretch may be altered.  Trauma? Postural changes?  Surgery  BOTOX? Blocks release of Ach, affects NMJ  Splints Golgi tendon organ

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GTO is intertwined amongst the collagen. By being closely entwined amongst connective tissues, these axons are therefore exposed to mechanical perturbation that would arise when tendon is under tension. If the muscle contracted and placed tension and force through musculotendinous junction, collagen fibers would be aligned and squished and at same, put mechanical pressure on tendons that make up GTO. The location and way they are entwined, enables these axons to respond to tension. The capsule, connective tissue sheath will have same purpose as spindle. The GTO encapsulated as well because also needs to be isolated from ionic concentrations in this area, can’t have ionic

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fluctuations affect the axons. We only want axons to respond to mechanical perturbations. Similarity between Golgi and muscle spindle is that they are both encapsulated (we need to similarities and differences between the two). Also the function of the structure for each. “the Golgi Tendon organ signals muscle tension or force it being exquisitely sensitive to the tension generated by a muscle contraction” This is a stretch receptor but its functional capacity differs from the MS due to...