Chapter 12: The Somatic Sensory System – responds to many stimuli Somatic Nervous System In the PNS How info travels from sensory nerves into CNS Introduction: ● Somatic sensation: ○ Enables body to feel, ache, sense temperature, and pressure ○ Responsible for touch, itch and pain – 3 major stimuli (each is different) ○ a group of many senses rather than one ○ Somatic sensory system is different from other systems in two ways: ■ Receptors are broadly distributed – not in one place (retina, basilar membrane, nasal epithelium, cochlea, etc) ● Throughout skin → throughout body ■ Responds to many kinds of stimuli (touch, itch, pain) → group of at least 4 senses ○ Divided into two major subsystems: ■ Mechanosensory: touch and body position (proprioception) ■ Temperature and pain ● Each has a distinct neural pathway and receptor subtype Sensory Neurons: ● cell bodies of sensory neurons in the dorsal root ganglion (DRG) – "pseudounipolar" neurons ● one axon extends to the periphery via spinal nerve entering into the sensory receptor ● another axon extends into the central nervous system (spinal cord or brain stem) via the dorsal root ● Short single process that becomes the axon → goes both into skin and elsewhere Somatosensory Receptors ● Based on function, receptors can be divided into groups: ○ 1. Mechanoreceptors – involved in touch, vibration, pressure ○ 2. Nociceptors (pain)-- detection of pain – cortically driven process ○ 3. Pruriceptors (itch) – receptors for itch ○ 4. Thermoreceptors (temperature) – diff types that have selectivity ● Based on morphology, receptors can be divided into: ○ 1. Free nerve endings (unmyelinated terminal branches (terminals that contain the sensory receptors are unmyelinated→ travels slower) – Nociceptors and thermoreceptors ○ 2. Encapsulated types: – Encapsulated: mechanoreceptors for touch – encapsulated means circles nerve endings ● Sensory Transduction: physical stimulus into a neural signal ○ All receptors function in the same manner: ■ Stimuli deform the skin ■ Receptor membrane permeability is altered ■ Depolarizing current is generated ■ Action potential is triggered in sensory receptor neuron that will ultimately be transduced into the spinal cord → from spinal cord sent through two distinct pathways into brain for further processing ○ Quality of stimulus (what it is and where it is): determined by the nature of the receptors themselves ○ Quantity: determined by rate of AP discharge>>>adaptation (sensory receptor neurons can adapt → lots of APs initially, but then decreases as get used to it) Mechanoreceptors in Skin ● “Cutaneous (skin) mechanoreceptors” – located in the skin – lots of different sensory neurons ● Nerve endings innervate the skin and then either encapsulate or don’t encapsulate the skin ● Sensitive to physical distortion: low-threshold (aka: high-sensitivity) → press on skin Receptive Fields ● Mechanoreceptors vary in their preferred stimulus properties, pressures, and RFs ○ RF of mechanoreceptor: specific area of skin where it can transduce pressure or vibration ○ Cutaneous MR: Meissner’s corpuscles and Merkel’s disks: small receptive fields ○ Cutaneous MR: Individual Pacinian corpuscles and Ruffini’s endings: large receptive fields → respond to stimulus along a large area of the hand Adaptation ● Mechanoreceptors vary in the persistence of response to long-lasting stimuli ● Meissner and Pacinian corpuscles: respond quickly but cease firing when stimulus continues—rapidly adapting ● Merkel’s disks and Ruffini’s endings: generate a sustained response to a long stimulus—slowly adapting Pacinian corpuscles: have a football-shaped capsule with layers of connective tissue arranged like an onion → respond quickly, large RF ● Nerve ending that goes into skin with layers wrapped around the nerve ending ● In-tact corpuscles: generate a large receptor potential at stimulus onset and offset ● Nerve ending becomes rapidly unsmushed → APs stop ● AP when stimulus is pulled away → capsule is stretched in opposite direction ● Rapid adaptation by rebound response ● REMOVE ONION: Bare axons generate a receptor potential that is more prolonged— slower adaptation rate → no AP when stimulus removed ● Layered capsule is required for the sensitivity to vibration ● Deformation of axon is key to the response → way that it moves if at all Mechanosensitive Ion Channels ● Mechanosensitive ion channels convert mechanical force into change of membrane potential → ionic current → generate AP ● Channels open and then cell depolarizes ● specific types of channels in most somatic sensory receptors are still unidentified Two-Point Discrimination ● A measure of spatial resolution: ability of different parts of the body to figure out two points as two and not as one ● Fingertips work best because: ○ 1. much higher density of mechanoreceptors → each transmits its own sensory information → higher spatial resultion ○ 2. Fingertips are enriched in receptor types (Merkel’s disks) that have small receptive fields ○ 3. More brain tissue is devoted to each square mm of the fingertip → somatosensory map ○ 4. special neural mechanisms devoted to high resolution discriminations in fingertips Primary Afferent Axons: axons that relay the sensory information from the periphery from cutaneous mechanoreceptors into the spinal cord ● primary afferent axons: Axons that bring info from somatic sensory receptors to spinal cord or brain stem → towards CNS ● Enter the spinal cord through the dorsal roots – cell bodies lie in DRG ● Have widely varying diameters – size correlates to the type of sensory receptor from which they receive information – key indicator of AP conduction velocity – internal resistance (less when larger diamater) ● Axon diameter: determinant of conduction velocity ● C fibers have smallest diameter and are unmyelinated–makes them the slowest ○ Mediate temp, throbbing pain, itch ● Ab axons are larger ○ conduct touch sensations (touch, vibration, pressure) via cutaneous mechanoreceptors *touch travels much faster than pain or itch* Segmental Organization of Spinal Cord ● Most peripheral nerves communicate with the CNS via spinal cord or brain stem for head mechanoreceptors ● Spinal segments (30)— paired dorsal (sensory info enters) and ventral roots (motor info leaves) ○ Correspond to the vertebrae through which they pass – most have segments of the spinal cord corresponding to them ○ spinal nerves are further divided into four divisions w/i spinal cord Dermatomes ● Segmental organization of spinal nerves and sensory innervation of the skin are related ● Dermatome: area of skin innervated by the right and left dorsal roots of a spinal segment ○ a set of (overlapping) bands on the surface of the body → if we eliminate from one section of spinal cord –. Adjacent DRG will take over and provide necessary sensory information ○ Gives segmental organization → where nerves from periphery are sensing information and where they are sending it ○ If we lesion at dermatomes → we know that all info to specific place is lost Dermatomes: Clinical Applications ● Herpes zoster virus (chickenpox) remains dormant in primary sensory neurons in one DRG ● Reactivation later in life causes Shingles ○ neurons of one DRG are infected ○ Affects only one dermatome ● Increases excitability of sensory neurons ○ Result is a constant burning sensation ○ Skin becomes inflamed and blistered (scaly) Sensory Organization of Spinal Cord ● Divisions of spinal gray matter: dorsal horn, intermediate zone, ventral horn ● Ab axons from cutaneous mechanoreceptors enter the dorsal horn → does it synapse or does axon continue → BOTH ○ One branch synapses in dorsal horn on 2nd order neurons → receiving information from primary neurons and send to motor neurons ■ Initiate or modify reflexes (info stays w/i the spinal cord) ○ Other branch ascends straight to the brain ipsilateral to stimulus → through spinal cord to thalamus ■ Responsible for perception Touch Pathways Touch ● Begins at the skin (largest sensory organ in the body) ● 2 Types of skin: ○ Hairy and glabrous (hairless—e.g., palms) ● 2 layers: ○ Epidermis (outer) and dermis (inner) ● Function of skin: ○ Protects ○ Prevents evaporation of body fluids ○ Provides direct contact with world *protect skin at all cost* Dorsal Column–Medial Lemniscal Pathway ● Mediates tactile sensation, vibration, and proprioception ○ major route for this info to cortex ● Ab axons enter spinal cord (some stay in DRG) and ascend via the ipsilateral dorsal column ○ Axons terminate in dorsal column nuclei in medulla in brain stem → neurons from dorsal column nuclei send their own axons ● Axons from dorsal column decussate and ascend via the medial lemniscus to the thalamus contralateral to the stimulus (one specific region in the thalamus → into the VPN) ○ Medial lemniscus axons synapse in the ventral posterior nucleus (VPN) of thalamus ○ VPN neurons send axons to primary somatosensory cortex (S1) for further processing *true for all except head and parts of neck* WHAT ABT FACE AND HEAD Trigeminal Touch Pathway ● Somatosensory information from face is supplied by the trigeminal nerve (CNV) → cranial nerve 5 ● Innervates the face, mouth area, outer 2/3 of tongue, and dura ● Trigeminal nerve has three branches: each innervate different parts of face ○ 1. Ophthalmic (V1) → eyes and forehead ○ 2. Maxillary (V2) → middle ○ 3. Mandibular (V3) →jawbone ● Enters brainstem at the pons (principle sensory trigeminal nucleus) ○ Decussates and sends projections to medial VPN thalamus contralaterally ● VPN sends info to S1 Somatosensory Cortex ● Somatosensory cortex (SMC): located in the parietal lobe (posterior to central sulcus (division between frontal and parietal lobes): ○ Postcentral gyrus: BA1, 2, 3A, 3B ● Laminar structure ○ Layer IV receives thalamic input ○ S1 neurons with similar inputs are stacked vertically into columns ● 3B is the primary SMC because: ○ receives input from the VPN of thalamus ○ responsive to somatosensory stimuli ○ lesions impair somatic sensation ○ stimulation evokes somatic sensory experiences Somatotopic mapping: Cortical Somatotopy—Homunculus ● Somatotopy: mapping of the body’s surface sensations onto a structure in the brain ● Relative size of cortex devoted to each body part is correlated with the density of sensory input received from that part ● High density of mechanoreceptors in hands ● Phantom Limbs – patients experience sensations (pain) in limb that doesn’t exist → amputees → usually region that is lost had lots of representation in the cortex → just because we remove that limb → representation in the cortex does not immediately go away → there is some plasticity→ adjacent areas in the cortex will overtake regions that no longer provide sensory input → but representation still persists Somatotopic Map Plasticity – ability of the brain to change → reorganization of brain tissue ● Compare somatotopy before and after ● Map regions of S1 sensitive to stimulation of the hand ● Remove one finger and re-map hand representation months later ○ Cortex devoted to removed finger now responded to stimulation of adjacent digit ○ DON'T lose that part of CORTEX → Missing digit caused reorganization → plasticity ● What if input activity to digits is increased? → stimulation of specific fingers ○ Train monkeys to use selected digits ○ Re-mapping of S1 found that representation of stimulated digits expanded ● Maps are dynamic Posterior Parietal Cortex ● BA 5 and 7 ● Involved in somatic sensation, visual stimuli, movement planning, attentiveness ● Neurons have large receptive fields with elaborate stimulus preferences → respond to lots of stimuli ● Damage to posterior parietal areas causes interesting neurological disorders ● Agnosia: inability to recognize object even though simple sensation is normal ● Astereognosia: normal sense of touch but lack the ability to identify objects by feeling them ● Neglect syndrome: a part of the body or visual field is ignored or its existence is denied (not consciously aware) ● More common following right hemisphere damage ○ “The Man Who Fell out of Bed” – didn’t recognize his limb and wanted to get rid of it Neglect Syndrome: ● Neglect symptoms often improve over time ● Sequential self-portraits made by the artist Anton Raederscheidt Pain and Itch Pain: ● Somatic system depends strongly on nociceptors ○ Free, branching, unmyelinated nerve endings that signal pain ○ Take a different path to the brain than mechanoreceptors ○ Nociception: the sensory process that provides signals that trigger pain ● Pain and nociception: not always the same thing ○ Pain is the feeling of sore, aching, throbbing sensations – conscious experience due to delivery of nociceptive information ○ There can be the sensation of pain in the absence of nociceptor activity ● Nociceptors: receptors mediating the transduction of pain ○ Ion channels opened by several mechanisms/stimuli: ■ Strong mechanical stimulation, temperature extremes, oxygen deprivation, chemicals ■ Substances released by damaged cells: ● Proteases (-> bradykinin), ATP, K+ ion channels ● Histamine ● Transduction of pain occurs in the free nerve endings of the unmyelinated C fibers and thinly myelinated A8 fibers ● Most nociceptors are polymodal (respond to many different types of pain) but show selectivity to one: ○ Mechanical: selective responses to strong pressure ○ Thermal: selective responses to extreme heat or cold ○ Chemical: showing selective response to histamine or others ■ May still respond to more than one Itch: ● Disagreeable sensation that induces desire or reflex to scratch ● Usually a brief, minor annoyance ○ can become chronic, debilitating condition ○ ~15% of people suffer relentless, long-term itch, often caused by diseases and medications ● Triggered by skin conditions or non-skin disorders (psychosomatic) ● Travels along C-fibers that are selectively responsive to histamine(itch-inducing agents) ○ released by mast cells in response to skin inflammation ○ Anti-histamine is a histamine receptor antagonist (blocks histamine from binding to C-fibers) ○ Histamine binds to receptors, causing activation of TRPV1 channels ○ Not all itch is histamine-mediated Primary Afferents and Spinal Mechanisms ● Ad and C fibers bring info to the CNS at different rates ● First pain (Ad activation): fast and sharp ● Second pain (C activation): duller, longer lasting – throbbing ○ Both are small diameter fibers that synapse within the substantia gelatinosa of the dorsal horn of spinal cord ○ 2nd order neurons decussate and ascend the contralateral side of the spinal cord at the level of the spinal cord (pain, itch temp crosses at spinal cord, mechanosensory crosses at medulla) ● Glutamate: main neurotransmitter of pain afferents → glutamatergic Pain and Itch Pathways Spinothalamic Pathway ● Pain and temperature info is conveyed from spinal cord to brain via spinothalamic pathway ● Axons of these 2nd order neurons decussate in the spinal cord and ascend via the spinalthalamic tract ● Fibers from this tract ascend to the thalamus without synapsing Trigeminal Pain Pathway ● Path to thalamus for pain and temperature info from the face and head ● Small diameter fibers from trigeminal nerve synapse onto 20 neurons in trigeminal nucleus ○ Axons decussate and ascend to thalamus via trigeminal lemniscus Trigeminal Neuralgia ● ”Suicide Disease” ● Usually caused by a blood vessel (SCA) pressing on trigeminal nerve as it exits brain stem ○ causes wearing away or damage to myelin sheath ● Anticonvulsant medicines—used to block nerve firing ○ Patients become tolerant ● Surgery to remove pressure from vessel ○ MVD: vessel (usually an SCA) that is compressing the nerve is moved away and a soft cushion is placed between nerve and vessel Pain Regulation: pain info is sent via 2nd order neurons and projects to thalamus – no interuption ● Pain perception is highly variable ● Chronic pain affects ~20% of the adult population ● Why does it feel good to rub a bruise (when we know about hyperalgesia)? ● How is pain suppressed by electrically stimulating the skin surface? ● Gate Theory of Pain: Melzack and Wall: Why do we rub an injured body part? ○ Pain projection neuron (e.g., second order neuron) is inhibited by an interneuron (the gate) ○ Interneuron is excited by the large sensory axon (Ab, via a collateral) and inhibited by the pain axon (C-fiber) ○ Activity in the pain axon alone maximally excites the pain projection neuron>>nociceptive signals go to the brain ○ If the mechanoreceptor axon signals simultaneously, the interneuron is activated and nociceptive signal is suppressed>>>gate is closed ○ Interneuron is activated by mechanosensory axon ● Referred Pain: felt at a site other than where the disease/injury occured ○ A myocardial infarct (heart attack) is often not experienced as crushing chest pain, but as pain in the jaw, arm, hand, neck or upper back ○ Referred pain: pain felt at a site different from the injured or diseased organ or body part ○ the heart tissue, jaw tissue, and arm tissues all develop from the same dermomyotome → all have same developmental origin and same innervation of neural activity→ when the heart experiences pain →other regions from same dermomyotome will experience pain Opioids and Pain: ● opioid class of drugs are narcotic analgesics ○ they reduce pain without producing unconsciousness ● create a sense of relaxation and sleep ● at high doses can lead to coma and death—due to respiratory depression ● the best painkillers but also produce a sense of euphoria ● Some opium derivatives are natural, other are “semisynthetic” (chemically modified versions of opium ingredients) ● Other narcotics are entirely synthetic Temperature Thermoreceptors: ● Neurons exquisitely sensitive to temperature ● Several TRP (transient receptor potential) channels in thermoreceptors that confer different sensitivities to temperature → each TRP channel has different sensitivities to different temperatures ● Each thermoreceptive neuron expresses a single type of channel ○ Different regions of the skin show different sensitivities to temp ● Cold receptors are coupled to Ad and C fibers, warm receptors to C fibers Hot Peppers and Pain ● Capsaicin: active ingredient ● Activates TRPV1 ion channels ○ Same channel activated by temps > 43o C ○ Permeable to both Ca2+ and Na+ ○ Mimics the effects of endogenous chemicals released by tissue damage in response to high temps Adaptations of Thermoreceptors ● Thermoreceptors show adaptation during long duration stimuli→ warm stimulus then maintained contact → less and less ● Both receptor subtypes are most responsive to sudden changes in temperature → when temp changes suddenly, AP’s fire → cold receptor subtype and warm receptor subtype mediating adaptations ● Differences between the response rates of warm and cold receptors are greatest during and shortly after a temperature change The Temperature Pathway ● Organization of temperature pathway ○ Identical to pain pathway (spinothalamic tract) – pain and itch ● Cold receptors coupled to Ad and C fibers bringing info into spinal cord ● Hot receptors coupled to C fibers ● Axons of second-order neurons decussate at level of spinal cord into thalamus without synapsing Summing it all up: The Two Ascending Pathways – comes from periphery from receptors in skin→ coming into spinal cord → going to thalamus→ go to somatosensory cortex for processing ● Touch ascends ipsilaterally until the medulla then decussate → then contralateral ● Pain ascends contralaterally from level of the spinal cord ● Leads to unique clinical features: ○ If half of the spinal cord is damaged, mechanosensitive defects occur ipisilateral to the damage—insensitivity to touch or vibration ○ Deficits in pain and temperature sensitivity will occur on the contralateral side to the damage ○ “dissociated sensory loss” → deficits on different sides ● Touch and pain pathways differ: ○ Nerve endings in the skin: ■ Touch: encapsulated structures like corpuses ■ Pain: free nerve endings ○ Diameter of axons ■ Touch: larger diameter, myelinated (Ab) ■ Pain: thin diameter, lightly myelinated and unmyelinated (C fibers, Ad) ○ Connections in spinal cord ■ Touch: ascends ipsilaterally (crosses in medial lemniscus in medulla) ■ Pain: ascends contralaterally (crosses at spinal cord level) Chapter 13: Spinal Control of Movement: voluntary and involuntary movements are produced by a pattern of muscle contractions controlled by brain and spinal cord Motor systems are organized hierarchically: spinal cord is lowest point within the motor hierarchy which receives input from many regions above it within the central nervous system → contains information from brain stem and primary motor cortex // basal ganglia modulates activity in motor cortex// cerebellum modulates activity of brain stem neurons and signals down into spinal cord to generate muscle contractions via motor neuron in ventral horn of spinal cord ○ Muscles (skeletal) and neurons that control muscles ○ Role: generation of coordinated movements (~700 muscles involved) ○ coordinated movements are produced by spatial and temporal patterns of muscle contractions orchestrated by the brain and spinal cord ○ Parts of motor control (motor programs) ■ 1) Spinal cord → contains motor programs necessary for generating coordinated movements ■ 2) Brain → controls motor programs in spinal cord *Spinal cord in “final common pathway” – motor neurons in the spinal cord* *Dorsal root – sensory (somatic and visceral afferents)* *DRG– contains somas of sensory afferents entering the cord* *Ventral root – motor (somatic and visceral efferent) – contains somas of motor neurons* Two types of muscles: 1. Smooth: digestive tract, arteries, viscera (organs) – not under conscious control a. Innervated by ANS fibers 2. Striated: a. 1. cardiac (heart) – not under conscious control (automatic) b. 2. skeletal (bulk of body muscle mass) – under conscious control (somatic nervous system) i. Within each skeletal muscle are 100s of muscle fibers Somatic Musculature: Terminology ● Muscles pull on a joint (not push) ● Flexors and extensors pull on the joint in opposite directions—antagonize each other ○ Synergistic → when flexor is activated, extensor is relaxed ● Refer to the location of the joints they act upon: ○ Axial muscles: trunk movement ■ Maintains posture ○ Proximal muscles: shoulder, elbow, pelvis, knee movement ■ Important for locomotion ○ Distal muscles: hands, feet, digits (fingers and toes) movement ■ Manipulation of objects Upper and Lower Motor Neurons Lower Motor Neurons: within ventral region of spinal cord ● Somatic muscles are innervated by somatic motor neurons in the ventral horn of the spinal cord ○ Lower motor neurons (LMNs) – send out their axons to innervate muscle fibers ● “Final common pathway” ○ directly command muscle contraction by receiving all the information from brain stem and cortical neurons ○ Diseases: ALS – neurons in ventral horn die off over time – less and less voluntary motor control – rapid course of death Upper Motor Neurons (UMNs) – primary motor cortex ● Send axons down and project on to lower motor neurons ● soma in cerebral cortex or brainstem (majority in cortex) ● Provide input to LMNs ● Only LMNs directly command muscles ● Damage to UMNs causes distinct clinical features compared with damage to LMNs ○ Hypertonia/spasticity (UMNs) vs paralysis (LMNs) Motor Neurons in the Spinal Cord ● Skeletal muscles: not evenly distributed throughout the body ○ “Limb Enlargements”: of ventral horns of spinal cod ■ LMNs are not evenly distributed evenly within the cord ■ regions of the cord where innervation of the muscles of the arms and legs occur → need more ■ Dorsal and ventral horns are “swollen” Lower Motor Neurons in Ventral Horn ● Motor neurons ● distributed in a predictable way within the ventral horn: ○ Motor neurons controlling flexors lie dorsal to extensors ○ Motor neurons controlling axial muscles (shoulder, postural control) lie medial to those controlling distal muscles (finger movement) Alpha Motor Neurons (subset of motor neuron in ventral horn of spinal cord) and Motor Units ● Two categories of LMNs in the spinal cord: ○ 1. Alpha : innervate extrafusal muscle fibers ○ 2. Gamma: innervate intrafusal muscle fibers ● Alpha motor neuron branch and innervate many fibers over a wide area ● Alpha MNs trigger the generation of force by muscles ● Motor unit: one alpha motor neuron and all the muscle fibers it innervates (many more muscle fibers than motor neurons)7 ○ “The elementary unit of motor control” ○ Muscle contraction is due to the combined action of motor units within the muscle ● Motor neuron pool: all alpha motor neurons that innervate a single muscle Types of Muscle Fibers: ● 1. Red muscle fibers ○ large number of mitochondria, rich in myoglobin, rich capillary beds (give the reddish color) ○ slow to contract>>available to sustain contraction ○ Fatigue resistant ○ Slow twitch ● 2. White (pale) muscle fibers ○ sparse mitochondria, anaerobic metabolism, contract and fatigue rapidly ○ Fast twitch Types of Motor Units: ● Slow motor units (S) ○ Small motor units - innervated by small alpha motor neurons ○ “red” muscle that contracts slowly and generates small forces ○ Resistant to fatigue ○ Important for sustained muscle contraction ● Fast fatigue-resistant motor units (FR) ○ Intermediate in size innervated by intermediate size alpha motor neurons ○ Generate twice the force of slow motor units ● Fast fatigable motor units (FF) ○ Large motor units – innervated by large alpha motor neurons ○ pale muscle fibers ○ White muscle ○ Brief exertions that require large forces, e.g., sprinting, jumping ■ All three types coexist in most muscles, but each motor unit contains muscle fibers of one type Control of Contraction by Alpha Motor Neurons (AMNs) ● Two mechanisms used to control the force of muscle contraction in a finely graded way: ○ 1. Varying the firing rate of AMNs—ACh at NMJ – amount of ACh release is dictated by amount of AP’s ■ A single AP in an AMN causes a muscle twitch ■ Sustained contraction requires continuous stimulation ● # of and frequency of APs increase ○ 2. Motor units are recruited from smallest to largest: Size Principle ■ Small motor units have small AMNs, large motor units have large AMNs ■ Small motor units have a lower threshold for activation ■ As muscle images itself, small motor units engage first and as muscle needs more finely grated control of contraction, large motor units activate ■ Increasing # of active motor units changes the amount of force produced by a muscle ■ Progressive increase in muscle tension is produced by increasing the activity of axons providing input to LMN pool ■ When synaptic input to motor pool increases, progressively larger motor units that generate more force are recruited ■ Recruitment of motor neurons in the cat gastrocnemius muscle under different behavioral conditions: ● Slow (S) motor units provide the tension required for standing ● Fast fatigue-resistant (FR) units provide the additional force needed for walking and running ● Fast fatigable (FF) units are recruited for the most strenuous activities Contractile Properties of Motor Units ● Single AP triggers contraction strengths of differing force and time-course in each of the different motor units ● When the different muscle units experience repeated APs over a longer time period, they show different rates of fatigue ○ Slow muscle show no fatigue ○ Fast-fatigue resistant: intermediate fatigue ○ Fast fatigue: high force, fast fatigue Neuromuscular Matchmaking ● Which came first: the muscle fiber or motor neuron? ○ During development, are particular axons matched with the appropriate muscle fibers or is the fate of the muscle determined by its type of innervation? ● Crossed-innervation experiment: John Eccles ○ Switched nerve input resulted in a switch in muscle phenotype ■ Protein expression was altered ■ muscle phenotype switch can occur by changing the activity in the input motor neuron (switching the innervation) → no need to steroids → can convert slow fatigue to fast fatigue Inputs to Alpha Motor Neurons ● Alpha MNs excite skeletal muscles ● Alpha MNs have three major sources of input: ○ 1. DRG neurons with axons that innervate the muscle spindle (sensory receptor within the muscle itself ○ 2. Upper motor neurons in motor cortex and brain stem ■ Important for the initiation and control of voluntary movement ○ 3. Interneurons in the spinal cord— largest input ■ Maybe excitatory or inhibitory Muscle Spindles: ● How is the activity of the motor neuron regulated? ○ muscle spindles (stretch receptors) – intrafusal fibers ■ 8-10 intrafusal fibers arranged in parallel with the extrafusal fibers ■ Located in the “belly” of the muscle ○ Group 1a sensory axons wrap around the muscle fibers ■ specialized for detecting changes in muscle length ■ Contain mechanosensitive ion channels—sensitive to stretch – when axons are stretched they produce change in receptor potential and fire AP and tell muscle spindle to adjust its length ● Situated in parallel with extrafusal muscle fibers ● la sensory afferents wrap around intrafusal muscle fibers and inform CNS about muscle length The Stretch Reflex: ● Tapping on knee transiently lengthens quads ● Quad muscles reflexively contract and leg extends ● Tests if nerves and muscles are intact in this reflex arc ● Stretch reflex (myotatic reflex): when a muscle is pulled it tends to contract ○ Monosynaptic: simple reflex ○ operates as a negative feedback loop to regulate muscle length ○ Requires sensory feedback from the muscle (via 1a axons) ○ Stretching a muscle spindle leads to increased activity in 1a afferents → increases firing rate bc its stretched its depolarized sending info back to spinal cord → ○ increase in activity of alpha motor neurons that innervate that muscle causing alpha motor neurons to increase their activity causing muscle to contract ○ When spinal nerve is cut, no reflex occurs even tho alpha motor neurons are left intact → in order for stretch reflex to occur normally, it requires sensory feedback from those 1a axons located within muscle spindle→ in absence of input from 1a axons bc spinal nerve is cut, we get no stretch reflex Gamma Motor Neurons ● LMNs that innervate intrafusal fibers inside muscle spindle ● Intrafusal fibers—skeletal muscle within the fibrous capsule ○ Extrafusal fibers form the bulk of muscle ○ Only extrafusal fibers are innervated by AMNs ● Without GMNs, muscle spindles would become very loose as the muscle contracts ● “Taut, not limp” Loading the spindle ● Stretching the muscle stretches the Ia nerve endings and activates alpha motor neuron Unloading the spindle ● Extrafusal muscle contracts and activity in Ia axon stops ● Spindle no longer sensitive to stretch Gamma motor neuron ● activity resets the length of the spindle by contracting intrafusal muscle fiber – Ia can continue to inform CNS of changes in length– Alpha and gamma co-activation normally Golgi Tendon Organs: maintain muscle force ● Muscle spindles are not the sole source of proprioceptive input from muscles ● Golgi tendon organs: strain gauges ○ Located at the intersection of muscle and the tendon ○ monitors muscle tension (contractile force) ● Innervated by Ib sensory axons ○ Branches are entwined in the collagen fibrils ○ Muscle contraction causes tension in fibrils to increase ○ Fibrils straighten and squeeze 1b axons ■ Mechanosensitive channels open ● Normal function: regulate muscle tension within optimal range ● protects muscle from being overloaded (generating too much tension) ● Important for execution of fine motor acts ○ manual object manipulation that requires a steady grip ● Group 1b axons: sensory axons with GTO ○ Activated by muscle contraction ○ enter cord and synapse on an 1b inhibitory interneurons in ventral horn ■ These synapse on AMNs innervating the same muscle ○ Decreases activation of the muscle when large forces are generated Muscle Spindles (muscle length) vs. Golgi Tendon Organs (muscle force) ● Muscle spindles: located in parallel with muscle fibers ○ 1a axons encode info about muscle length ● Golgi tendon organs: located in series with muscle fibers ○ 1b axons encodes info about muscle tension ● Passive Stretch: ○ Both afferents discharge in response ○ Golgi tendon organ discharge is less than that of the spindle ● Active Contraction (stimulation of alpha motor neurons) ○ the spindle is unloaded >>falls silent → no AP’s ○ rate of Golgi tendon organ firing increases Spinal Interneurons ● Most input to alpha motor neurons is mediated by spinal interneurons ● Inhibitory interneurons play an essential role in execution of simple reflexes ○ involved in reciprocal inhibition—contraction of one muscle set accompanied by relaxation of the antagonist muscle Flexor Withdrawal Reflex ● Not all interneurons are inhibitory ● Excitatory interneurons mediate the flexor withdrawal reflex → many synapses ○ Used to withdrawal a limb from an aversive stimulus ○ Slower than the stretch reflex ○ Process begins with pain signal from Ad nociceptive axons ○ enter the spinal cord, branch, and activate interneurons ○ Interneurons excite AMNs that control muscles in affected limb Crossed-Extensor Reflex ● Why don’t we fall over after activation of the flexor withdrawal reflex? ○ Crossed-Extensor Reflex ● Used to compensate for extra load imposed by limb withdrawal on the opposite side ● Reciprocal inhibition— activation of flexors on one side is accompanied by inhibition of flexors on opposite side→ so need to activate extensos ● Provides a building block for locomotion at the spinal level ○ Only thing left is a coordinating mechanism ● Ipsilateral : excite flexors, inhibit extensors ● Contralateral: excite extensors, inhibit flexors Spinal Programs for Walking ● Hind limbs of a cat that suffers a transection of the spinal cord are capable of generating coordinated walking movements ● Circuitry for walking resides within spinal cord → not dependent on sensory input ● Circuits that give rise to rhythmic motor activity are called Central pattern generators (CPGs) ○ Neural circuits that act as “pacemakers” ○ New strategies for spinal cord injury (SCI) in humans Presbyopia: a refractive error that makes it hard for middle-aged and older adults to see things up close. It happens because the lens (an inner part of the eye that helps the eye focus) stops focusing light correctly on the retina (a light-sensitive layer of tissue at the back of the eye) Chapter 14: Brain Control of Movement The Major Tracts: from primary cortex descending Descending Spinal Tracts: ● Brain to motor neuron communication: ○ Axons from brain descend along two major pathways: ○ 1. Lateral pathways ■ voluntary movement of distal musculature ■ Under cortical control ○ 2. Ventromedial pathways ■ control of posture and locomotion ■ Under brain stem control Corticospinal Tract: AKA: “Pyramidal Tract” ● Decussation in medullary pyramids ● Pathway carrying motor information from the primary and secondary motor cortices to the brain stem and spinal cord ● Most axons originate in primary and secondary motor cortices (BA 4 and 6) ● One of the longest and largest (106) axon tracts in the CNS ● Contralateral motor control Rubrospinal tract: ● Originates in the red nucleus of the midbrain ● Receives input from frontal regions that contribute to corticospinal tract ● Axons immediately decussate in pons (transverse pontine fibers) ● Runs parallel to corticospinal tract in lateral columns of spinal cord ● In humans, its function is largely reduced ● Important for motor control in other mammals ● Corticospinal tract takes over in humans Babinski Sign: ● Easy test for motor tract damage ○ In infants (<2), response is similar to damaged adults ■ due to immature descending motor tracts ■ Immature response → not fully developed → wouldn’t want this in adults Ventromedial Pathways: ● Four descending tracts that originate in brain stem ● terminate in spinal interneurons controlling proximal and axial muscles ○ 1. Vestibulospinal tract ○ 2. Tectospinal tract ○ 3. Pontine reticulospinal tract ○ 4. Medullary reticulospinal tract Tectospinal Tract: ● originates in the superior colliculus (optic tectum) of midbrain → which contains cell bodies ● Receives direct projections from retina: orienting response ● orienting response to project image on the fovea ● Axons decussate immediately after leaving s.c. ○ project to midline cervical regions to control muscles of neck, shoulders, and upper trunk You are performing a clinical test on a cohort of patients that have a lesion in their tectospinal tract. These patients will show a deficit in which of the following? A. When flashing a light in their peripheral vision, they fail to bring the flash of light onto their fovea B. They cannot maintain standing posture C. They show an abnormal Babinski Sign D. They cannot initiate voluntary movements Motor Cortex: ● Area 4: Primary motor cortex (M1) ○ Stimulation leads to muscle twitches on contralateral side ● Area 6: “higher” motor area (Penfield) ○ Stimulation leads to more complex movements ■ 1. Lateral region: premotor area (PMA) ■ 2. Medial region: supplementary motor area (SMA) Neuronal Correlates of Motor Planning ● BA 6 in movement planning ● Recordings from PMA neurons: ● “Ready” (a): ○ Baseline level of activity in neuron ● “Set” (b) ○ Firing of PMA neuron ● “Go”(c) ○ Shortly after movement is initiated, PMA ceases firing Mirror Neurons ● Rizzolatti, et al ● Some neurons in BA6 (PMA) respond when watching another monkey making the same movement ● May be part of extensive brain system for understanding actions, emotions, and intentions of others ○ Same motor circuits are used for planning our movements and understanding the actions of others The Basal Ganglia ● caudate nucleus • putamen • globus pallidus (internal and external) • subthalamic nucleus (STN) • Caudate + putamen = Striatum • Striatum is the target of cortical input to bg • GP is the source of output to the thalamus • Substantia nigra sends DA input to striatum Basal Ganglia: The Motor Loop
