20. Sensory Systems Flashcards

Question

What fibres types do muscle spindles and Golgi tendons send information via?

Answer 1

* Muscle spindles -\> Type Ia (Aα) and II (Aβ) * Golgi apparatus -\> Type Ib (Aα) (Remember how the I system corresponds to the Aα when in muscle. Aα fibres include both Ia and Ib fibres.) Therefore, note how Aβ fibres are also minorly involved in proprioception despite not always being mentioned.

Answer 2

* Ia (Aα) -\> Adapting, fast-responding discharge, which allows immediate reflex response to changes in length * II (Aβ) -\> Non-adapting, slower discharge, which allows constant tension depending on current stretch Ia fibres arise from dynamic and static fibres, while II fibres arise from static fibres only.

Answer 3

* Synergistic α-motorneurons * Ia inhibitory interneurons that synapse onto antagonistic α-motor neurons

Answer 4

* They synapse not only on motor neurons that innervate the muscle that needs to contract, but also on interneurons that are inhibitory to the antagonistic muscle. * Since Aα fibres are responsible for propriception, when there is stretch of the muscle, the agonist will contract slightly, while the antagonist will relax.

Answer 5

* Negative feedback during muscle contraction * This is done via inhibitory interneurons that prevent the muscle from over-contracting

Answer 6

Ib (Aα) fibres

Answer 7

Ib inhibitory interneurons in the ventral horn -\> These then inhibit synergistic α-motor neuron activity, allowing negative feedback of muscle contraction.

Answer 8

Somatosensation

Answer 9

* Meissner corpuscle * Ruffini corpuscle * Merkel cells * Pacinian corpuscle * Free nerve endings These are essentially the major mechanoreceptors.

Answer 10

* Skin that does not contain hair follicles, such as that over the palms and soles. * On the ridges of your fingerprint, there are Merkel cells and Meissner corpuscles * This means that when you run your finger along a surface, the ridges vibrate and the stimulus can be detected

Answer 11

Aβ (And also some Aδ fibres from free nerve endings)

Answer 12

* Meissner's corpuscles and Merkel cells have a small receptive field since they are quite superficial * Pacinian corpuscles and Ruffini endings have a larger receptive field since they are deeper

Answer 13

* Meissner's corpuscles -\> Rapidly-adapting * Merkel cells -\> Slow-adapting * Pacinian corpuscles -\> Fast-adapting * Ruffini endings -\> Slow-adapting

Answer 14

* There are two more superficial receptors (Meissner's and Merkel), with a smaller receptive field, and two more deep receptors (Pacinian and Ruffini), with a large receptive field * Of each category, one of the receptors is rapidly-adapting (Meissner's and Pacinian), while the other is slow-adapting (Merkel and Ruffini) * This means that a range of responses is possible

Answer 15

* 1 and 2 are opened by physical distortion * 3 is opened by an indirect process

Answer 16

* Function -\> Light touch * Location -\> Superficial epidermis, High density in fingertips * Receptive field -\> Small * Rapidly/Slow adapting -\> Rapidly adapting * Number of receptors per DRG cell -\> 10-25

Answer 17

* It has the lowest highest sensitivity to low frequency vibrations. * This is due to a low threshold and 10-25 Meissner's corpuscles per DRG cell.

Answer 18

* Function -\> Deep touch, Pressure * Location -\> Superficial epidermis, High density in fingertips * Receptive field -\> Small * Rapidly/Slow adapting -\> Slowly adapting * Number of receptors per DRG cell -\> 10-25

Answer 19

(Maricich, 2009): * Identified that a gene involved in Merkel disc development is Atoh1 * Atoh1 knockout mice allow us to see the importance of Merkel discs

Answer 20

* Function -\> Vibration * Location -\> Deep in the dermis, High density in finger tips * Receptive field -\> Large * Rapidly/Slow adapting -\> Rapidly adapting * Number of receptors per DRG cell -\> 1

Answer 21

(Lowenstein, 1959): * Experiment 1 showed that the lamellae are not required, just the nerve ending inside * Experiment 2 showed that interruption of the action potential transmission causes no response, but does not interrupt the generator voltage * Experiment 3 showed that partial degeneration of the nerve ending prevents the generator voltage Therefore, the mechanoreceptive component is the nerve ending within the Pacinian corpuscle.

Answer 22

This showed that the lamellae are important for rapid adaptation, so that the receptor can respond to a high frequency of signal.

Answer 23

* Function -\> Stretch (involved in hand position) * Location -\> Deep dermis, Fewer in fingers * Receptive field -\> Large * Rapidly/Slow adapting -\> Slow adapting * Number of receptors per DRG cell -\> 1

Answer 24

Pacinian corpuscle

Answer 25

Merkel disc

Answer 26

Ruffini ending

Answer 27

Meissner's corpuscle

Answer 28

They are arranged along tissue planes on the hand.

Answer 29

Free nerve endings

Answer 30

Transient Receptor Potential (TRP) family of proteins often located on free nerve endings (Aδ and C fibres) in mammals.

Answer 31

* Cold fibres * Warm fibres These have different firing rates at different temperatures. They both fire equally at around 37 degrees (the desired body temperature).

Answer 32

* Cold -\> 5-10mm * Warm -\> 15mm

Answer 33

* Spicy foods (and heat) open TRPV1, giving it slight permeability to cations * However, prolonged exposure to spicy foods or heat causes phosphorylation, which induces a transition to a dilated state, in which permeability to large cations is increased

Answer 34

TRPV2 -\> It responds to stimuli over 52\*C. Unlike the capsaicin receptor TRPV1, TRPV2 has no response to capsaicin or acid.

Answer 35

* Cold (TRPM8) agonists -\> Menthol, Eucalyptol * Hot (TRPV1) agonists -\> Capsaicin

Answer 36

(Bautista, 2007): * Showed that mutant TRPM8 mice have difficulty differentiating between a hot and cold space * However, below around 10\*C, they can detect a cold space, which shows that there is likely to be another thermoreceptive protein for low temperatures

Answer 37

The receptors embedded in the membrane.

Answer 38

* Thermoreceptive-\> Aδ and C fibres * Mechanoreceptive -\> Aδ fibres * Specific nociceptive -\> Aδ and C fibres * Polymodal nociceptive -\> C fibres

Answer 39

* Aδ -\> Sharper pain with reflex withdrawal, Fast-adapting (coding change) * C -\> Spreading pain, Slow-adapting

Answer 40

(More on this later, hopefully)

Answer 41

* It is pain * It is essentially the perception of extreme thermal, chemical and mechnical stimuli that could be damaging

Answer 42

* Mechanical nociceptors -\> Respond to strong stimuli and mediate sharp pain * Thermal nociceptors -\> Respond to cold and warm stimuli * Polymodal nociceptors -\> Respond to a variety of stimuli and evoke slow burning pain

Answer 43

* Receives sensory information from sensory neurons * Provides motor information to motor neurons

Answer 44

From the central axons of dorsal root ganglion neurons -\> Into the grey matter of the dorsal horn

Answer 45

* Central H-shaped grey matter -\> Neuron cell bodies * White matter -\> Myelinated axon tracts There is also the central CSF-filled canal.

Answer 46

* In the dorsal half, there are the sensory interneurons * In the ventral half, there are the: * Lateral motor column (a.k.a. pool) * Medial motor column (a.k.a. pool) * Motor interneurons

Answer 47

Horn (grey matter): * The dorsal horn receives sensory information * This can then be taken within the grey matter along a reflex arc or through segmental interneurons * Alternatively, it can be passed into the white matter White matter: * The white matter is made of axons and it is divided into tracts that carry information up the spinal cord and back down from the spinal cord

Answer 48

Ascending (sensory): * Dorsal column * Spinocerebellar tracts * Anterolateral system Descending (motor): * Corticospinal tracts (lateral + anterior) [YOU NEED TO KNOW THIS IS MUCH MORE DETAIL. MAKE SURE YOU'VE MADE MORE NOTES ON IT.]

Answer 49

Dorsal horn: * Marginal zone * Substantia gelatinosa * Nucleus proprius Lateral horn (in thoracic region?): * Thoracic nucleus (Clarke's column) * Intermediolateral nucleus Ventral horn: * Lateral motor pool * Medial motor pool

Answer 50

Large diameter axons: * Enter medially and possess ascending collaterals * Aα -\> Proprioception * Aβ -\> Mechanoceptors Fine diameter axons: * Enter laterally and project across several segments -\> Lissauer's tract (LT) * Aδ -\> Nociception, Thermal * C -\> Nociception, Thermal, Itch

Answer 51

* Originate in muscle spindles, from where they carry sensory proprioception information * Terminate at lamina 6 to 9, which includes interneurons in the dorsal horn and motor neurons in the ventral horn

Answer 52

* Originate from cutaneous receptors and static proprioceptors * Terminate in the laminae 3 to 6 of the dorsal horn (a.k.a. the nucleus proprius) * They synapse onto wide dynamic range neurons (interneurons involved in polysynaptic reflexes)

Answer 53

* Aδ -\> At the marginal zone of the dorsal horn (lamina 1) and nucleus proprius (laminae 3-5) * C -\> At the substantia gelatinosa of the dorsal horn (lamina 2) Note: Each of these fibres can synapse at multiple heights in the spinal cord.

Answer 54

* Proprioceptive/mechanoreceptive (Aα and Aβ) -\> From medial side * Nociceptive (Aδ and C) -\> From lateral side

Answer 55

* Aα -\> 6-9 * Aβ -\> 3-6 * Aδ -\> 1, 4 and 5 * C -\> 2

Answer 56

* No, they can enter and course up and down the spinal cord, innervating more than one motor/interneuron. However, all the motor neurons innervated tend to have synergistic action. * They do this via the ascending tracts

Answer 57

* On interneurons that are inhibitory to antagonistic muscles (in the dorsal horn) * On motor neurons in the ventral horn (for stretch reflex) They also send out branches without synapsing which ascend in the ascending dorsal columns to inform higher centres (conscious proprioception).

Answer 58

* These form the dorsal ascending tracts that carry proprioceptive and mechanoreceptive information up to the brain. * This allows for conscious perception of body position and touch.

Answer 59

It carries afferent proprioceptive and mechanoreceptive information: * Dorsal root ganglion axons have ascending branches that travel cranially in the dorsal column * These then synapse at the dorsal column nuclei in the medulla * The fibres then decussate (cross to the other side of the body) * They then travel up the medial lemniscus through the midbrain and to the thalamus * Relay neurons take the information from the thalamus to the somatic sensory cortex

Answer 60

* First-order neurons carry signals from the periphery to the spinal cord * Second-order neurons carry signals from the spinal cord to the thalamus * Third-order neurons carry signals from the thalamus to the primary sensory cortex

Answer 61

* Dorsal column system carries 1st order neurons, since synapsing and decussation only happens in the medulla * Anterolateral system carries 2nd order neurons, since synapsing and decussation occur within the spinal cord

Answer 62

These correspond to the cuneate and gracile nuclei in the medulla, which these join up with.

Answer 63

It carries afferent proprioceptive information from the lower limb: * Dorsal root ganglion axons at the lumbar region, which receive information from the lower limb, have branches that ascend up to the thoracic region * At the thoracic region, they terminate at Clarke's column (a.k.a. thoracic nucleus) * This sends out relay neurons to the dorsal spino-cerebellar tracts * These take the information to the cerebellum on the same side of the body -\> This is important for unconscious perception and response to the stimulus

Answer 64

* Proprioception is mediated by Aα fibres (from muscle spindles), while mechanoception is mediated by Aβ fibres (from mechanoreceptors) * These fibres then do two things: * Take the information directly to the grey matter of the spinal cord to allow reflex response * Aα fibres synapse at laminae 6 to 9, in both the dorsal and ventral horns * They synapse with motor neurons in the ventral horn and interneurons in the dorsal horn (which are inhibitory to the antagonistic muscle) -\> Allows reflex reactions so muscles to maintain position * Aβ fibres synpase in laminae 3 to 6 of the dorsal horn (a.k.a. the nucleus proprius) * These are projection neurons that decussate and enter the anterolateral system (in particular the anterior spinothalamic tract), which take the information to the thalamus (the anterolateral tracts carry CRUDE touch information) * Send out branches before they reach the grey matter, which travel up to the brain to give conscious and unconscious perception of the stimulus (and also innervate muscles at different spinal levels e.g. if the biceps needs to contract then lots of muscle bundles need to be recruited) * These form the dorsal column tracts (thes carry proprioception and FINE touch): * Fibres synapse at the dorsal column nuclei in the medulla * The fibres then decussate (cross to the other side of the body) * They then travel up the medial lemniscus (a bundle of fibres) through the midbrain and to the thalamus * Relay neurons take the information from the thalamus to the somatic sensory cortex -\> CONSCIOUS PERCEPTION * There are also the spino-cerebellar tracts, which carry afferent proprioceptive information from the lower limb: * Fibres ascend up to the thoracic region * At the thoracic region, they terminate at Clarke's column (a.k.a. thoracic nucleus) * This sends out relay neurons to the dorsal spino-cerebellar tracts * These take the information to the cerebellum on the same side of the body -\> UNCONSCIOUS PERCEPTION * Note how there is no decussation in this case Note how crude touch is carried by the anterolateral system (anterior spinothalamic tract), while fine touch is carried by the dorsal column system along with proprioception. Proprioception is also carried to the cerebellum via the spinocerebellar tracts.

Answer 65

* They are carried by Lissauer's tract up and down, before they enter the grey matter. * This allows ampification of the signal, which does not happen with proprioception/mechanoreception since these need to be localised

Answer 66

An ascending tract to the lateral side of the dorsal horn that takes the axons of nociceptive fibres up to higher spinal levels for synapsing.

Answer 67

The sensory fibres travel up the spinal cord via Lissauer's tract, then they synapse at various levels in the spinal cord. Aδ: * Some synapse at the marginal zone of the dorsal horn (lamina 1) and nucleus proprius (laminae 3-5) with projection neurons: * Projection neurons send an axon across to the contralateral side of the spinal cord * These axons then join the anterolateral system, which takes the signal to the thalamus * Relay neurons take the information from the thalamus to the somatic sensory cortex C: * Some synapse at the substantia gelatinosa of the dorsal horn (lamina 2) with interneurons: * These send axons to the nucleus proprius, which contains projection neurons * Projection neurons send an axon across to the contralateral side of the spinal cord * These axons then join the anterolateral system, which takes the signal to the thalamus * Relay neurons take the information from the thalamus to the somatic sensory cortex

Answer 68

They pass via the anterior white commissure.

Answer 69

It carries afferent nociceptive (and some mechanoreceptive) information: * Wide dynamic range neurons in the nucleus proprius send axons across the midline (via the anterior white commissure) * The fibres then travel via the anterior and lateral spinothalamic tracts to the medulla, where the spinal leminiscus * This carries the information to the thalamus * Relay neurons take the information from the thalamus to the somatic sensory cortex

Answer 70

* Nociception is mediated by Aδ and C fibres * These fibres then travel up to multiple levels in the spinal cord using Lissauer's tract (this allows for amplification) * Each each level, they enter the grey matter from the lateral side and synapse in the grey matter. * Aδ fibres: * Synapse at the marginal zone of the dorsal horn (lamina 1) and nucleus proprius (cell bodies in lamina 5 with dendrites in laminae 3-5) with projection neurons: * Projection neurons arise from laminae 1 and 5, send an axon across to the contralateral side of the spinal cord * These axons then join the anterolateral system, which takes the signal to the thalamus * Relay neurons take the information from the thalamus to the somatic sensory cortex * C: * Synapse at the substantia gelatinosa of the dorsal horn (lamina 2) with interneurons: * These send axons to the nucleus proprius, which contain projection neurons * Projection neurons send an axon across to the contralateral side of the spinal cord * These axons then join the anterolateral system, which takes the signal to the thalamus * Relay neurons take the information from the thalamus to the somatic sensory cortex

Answer 71

* In the dorsal column, the DRG afferents do not synapse, but send fibres straight up the tract, while in the anterolateral, the DRG afferents synapse and the wide dynamic range neurons send fibres up the tract (i.e. dorsal column contains 1st order axons, while the anterolateral system contains 2ns order axons) * In the dorsal column, the decussation occurs in the medulla at the dorsal column nuclei, while in the anterolateral decussation occurs at the spinal level where synapsing occurs

Answer 72

* A bundles of nerve cells in the thoracic region of the spinal cord. * It is in the LATERAL horn of the grey matter [IMPORTANT] * It receives ascending fibres from lumbar dorsal root ganglion neurons, and then passes this information on to the dorsal spino-cerebellar tracts (then to the cerebellum) * Therefore, it plays a role in UNCONSCIOUS perception of proprioceptive information

Answer 73

* Lamina 1 -\> Marginal zone (a.k.a. posteromarginal zone) * Lamina 2 -\> Substantia gelatinosa * Laminae 3-5 -\> Nucleus proprius (a.k.a main sensory nucleus)

Answer 74

* Proprioceptive/mechanoreceptive fibres -\> These synapse at just one height in the spinal cord (and although they send out collateral fibres, these synapse in the brain, unless it is in Clarke's column) * Nociceptive fibres -\> These can synapse at multiple heights in the spinal cord, with each axon terminating at more than one dorsal root

Answer 75

* The nucleus proprius (laminae 3-5) receives combined input from Aβ (mechanoreceptive) and Aδ fibres (nociceptive) * The wide dynamic range (WDR) neurons in the nucleus proprius cross the midline (via the anterior white commissure) and ascend in the anterolateral columns.

Answer 76

* It goes to the thalamus, which relays it to the primary sensory cerebral cortex (all senses except smell). * Some also goes to brainstem structures, which allows for reflex and unconscious behaviours,

Answer 77

* Dorsal column system * Anterolateral system

Answer 78

* It is the crossing of ascending and descending tracts to the contralateral side of the body. * Knowing where tracts decussate is important because it allows us to understand the consequences of various lesions.

Answer 79

* Cerebral hemispheres -\> Receive information from the contralateral side (therefore conscious perception is contralateral) * Cerebellar hemispheres -\> Receive information from the ipsilateral side (therefore unconscious perception is ipsilateral)

Answer 80

* A lesion of half of the spinal cord at a given level * It can be caused by gunshot/knife wounds, tumours or spinal disc herniation Symptoms: * Loss of proprioception/mechanoreception on the ipsilateral side -\> This is because the dorsal column system decussates in the medulla, so they have not decussated yet * Loss of nociception, thermoreception and crude touch on the contralateral side, at a lower spinal level -\> This is because the nociceptive, thermoreception and crude touch information decussates in the spinal cord and then travels up via the anterolateral system. The loss starts at a lower spinal level because Lissauer's tract carries fibres up to several levels before decussation.

Answer 81

Dorsal column: * Proprioception and fine touch * This is due to the ascending collateral fibres (first order) that are Aα and Aβ fibres. Anterolateral systems: * Nociception, temperature and crude touch * Nociception and temperature are due to Aẟ and C fibres that synapse in the nucleus proprius and supply second order fibres that arise in the. Crude touch is due to Aβ fibres that do the same.

Answer 82

The dorsal column system is faster and less susceptible to modulation, since there are fewer synapses.

Answer 83

* Aẟ, C and Aβ fibres synapse in the dorsal horn at various locations (these are covered in earlier flashcards, but don't worry too much since it is a complicated topic) * All of these either synapse directly onto projection neurons or use interneurons to converge onto projection neurons. * Projection neurons cross the midline via the anterior white commisure. * The main projection neurons arise from laminae 1 (marginal zone) and 5 (part of the nucleus proprius), but there are also some on laminae 6 and 7 * The projection neurons form three main tracts that make up the anterolateral system -\> Different tracts arise from different laminae * The spinothalamic tract is the main tract, going directly to the thalamus for conscious perception of pain, while the other two tracts synapse at lower structures and are involved in altertness and pain-control mechanisms

Answer 84

* Spino-reticular * Spino-mesencephalic * Spino-thalamic

Answer 85

* Origin: Medial laminae (6-8) of grey matter * Terminates: Reticular formation (throughout the brainstem) -\> This passes to the thalamus after this Roles: * Increases alertness in response to pain -\> ‘Reticular activating system’ -\> Projects to higher centres and alerts the cerebral cortex about stimuli. * Increases reflex activity (e.g. in muscles) -\> Via influencing the reticulospinal tracts (Note: You can try and check where these fibres from laminae 6-8 arise from, but it probably doesn't matter that much. Just assume that interneurons brought information there.)

Answer 86

* Origin: Laminae 1 and 5 * Terminates: The periaqueductal grey matter Roles: * Pain-control mechanisms -\> Via the periaqueductal grey in the midbrain, which has pathways that come back down the spinal cord * Unconscious body orientation (e.g. moving the eyes towards the painful stimulus) -\> Via the superior collicitus in the midbrain, which influences the tectospinal tracts

Answer 87

* Origin: Laminae 1 and 5 (also 6-7) * Terminates: Thalamus (in the ventral posterior lateral nucleus and central lateral nucleus) Roles: * Conscious perception of pain and its location * Also carries mechanoreceptive information (from Aβ fibres that synapse in the nucleus proprius)

Answer 88

Main sensory nucleus (a.k.a. nucleus proprius) of the dorsal horn. Also from the marginal zone.

Answer 89

Anterior white commissure

Answer 90

* Anterior spinothalamic tract -\> Crude touch and pressure * Lateral spinothalamic tract -\> Pain and temperature

Answer 91

* Central lateral (CL) nuclei -\> a.k.a. Intralaminar nuclei of the thalamus * Ventral posterior lateral (VPL) nuclei

Answer 92

These are divisions of the lateral spinothalamic tract? Old (archi) spinothalamic tracts: * Take fibres from the nucleus proprius of the dorsal horn * The nucleus proprius receives information from Aδ fibres (direct) and C (indirect via interneurons in layer 2) * The tract goes up to the central lateral nucleus of the thalamus -\> From there go to diffuse and ‘emotional’ areas of cortex (anterior insula/cingulate) New (neo) spinothalamic tracts: * Take fibres from the marginal zone (lamina 1) of the dorsal horn * The fibres that supply the marginal zone are direct Aδ fibres * The tract goes up to the ventral posterior lateral nucleus of the thalamus -\> From there go to sensory SI cortex for the location of a painful stimulus

Answer 93

* Central lateral (interlaminar) nuclei -\> Goes on to the insula cortex [IMPORTANT] as well as the diffuse and cingulate cortex. * Ventral posterior lateral (VPL) thalamus -\> Go on to the primary and secondary sensory cortex for localisation of touch

Answer 94

* The hypothalamus and amygdala supply the periaqueductal grey * The periaqueductal grey mediates nociception via: * Control of raphe 5-HT (serotonin) cells of the medulla -\> This modulates laminae 1,2 and 5 * Control of noradrenergic cells of the locus coeruleus (pons) -\> This modulates laminae 1 and 5

Answer 95

* Cuneate fasciculus -\> More lateral * Gracile fasciculus -\> More medial Remember it as "GG" in the middle.

Answer 96

In the dorsal column nuclei in the medulla -\> These are called the cuneate and gracile nuclei. (Remember, these are 1st order fibres so they have not synapsed yet).

Answer 97

* The dorsal column nuclei are the first points of synapse for mechanoreceptive (and proprioceptive) information * We want to be able to tell exactly where the information is coming from (e.g. in fine touch) * Lateral inhibition allows this: * A strongly excited second order neuron causes inhibition of neighbouring neurons * This can occur by feed-forward or feed-back inhibition * Therefore, only a single signal remains, allowing for high acuity

Answer 98

No, because it is more important for amplification to occur (via Lissaeur's tract), so acuity can be sacrificed.

Answer 99

* After they synapse at the dorsal column nuclei (in the medulla) * They cross the midline as internal arcuate fibres, then form the medial lemniscus.

Answer 100

Medial lemniscus

Answer 101

(Anterior is at the top of the image)

Answer 102

Ventral posterior lateral thalamus

Answer 103

* The point-for-point correspondence of an area of the body to a specific point on the central nervous system. * i.e. A certain part of the white matter may carry innervation from the feet.

Answer 104

Dorsal columns: * From medial to lateral, the innervation becomes more superior (i.e. medial = legs, lateral = arms) * This is because low down we start with just the gracile fascicles and then the cuneate fascicles join Medial lemniscus: * In medulla -\> Arms to legs in a dorsal to ventral direction * In pons -\> Arms to legs in medial to lateral direction * In mibrain -\> Arms to legs in ventral to dorsal direction (In the medial lemniscus it is as if the person is doing a sommersault)

Answer 105

Thalamus is a relay station, the gateway for sensory & motor information to reach the cerebral cortex (and thereby conscious perception)

Answer 106

Via the internal capsule, which is made of the white matter that goes around the lateral ventricles.

Answer 107

(Penfield, 1937): * Stimulated various parts of the brain of a patient about oto undergo surgery * Asked the patient to report what was felt every time he stimulated a part of the primary somatosensory cortex

Answer 108

Trigeminal nerve (CN V)

Answer 109

Proprioceptive input: * Αα information from the muscles of mastication passes ‘locally’ to the midbrain **mesencephalic nucleus** * Then it passes to motor nucleus V, in the pons, which is involved in reflexes, etc. Mechanoreception: * Aβ skin mechanoceptors synapse in the **principal trigeminal nucleus** * Then cross to join medial lemniscus and terminating ventral posterior **medial** nucleus Pain and temperature: * Aδ axons pass down on the ipsilateral side to **spinal nucleus** * Here they synapse and decussate to join the contralateral anterolateral system

Answer 110

Ventral posterior medial nucleus (in the thalamus)

Answer 111

* Ventral posterior lateral (VPL) thalamus -\> Main somatosensory and nociceptive nucleus receiving input from the body (via from dorsal column and spinothalamic tracts). Projects on to the primary and secondary sensory cortex for localisation of touch. * Ventral posterior medial (VPM) thalamus -\> Receives mechanoreceptive and nociceptive input from the face. Projects on to the primary and secondary sensory cortex. * Central (intralaminar) nuclei -\> Receives nociceptive inputs (from the spinothalamic tract). Projects to insular, cingulate and diffuse cortex for the affective aspects of nociception.

Answer 112

* S1 = Primary somatosensory cortex * S2 = Secondary somatosensory cortex

Answer 113

They are just behind the central sulcus (the groove that runs laterally across the superior surface of the brain) in the central gyrus (the buldge just behind the sulcus).

Answer 114

They are called Brodmann’s areas: * 1 * 2 * 3a * 3b (Note: The whole cerebral cortex is divided into Brodmann's areas - these are just the 4 in S1)

Answer 115

3b (because this is where most of the mechanoreceptive input goes)

Answer 116

Yes, there is a high fidelity, allowing precise localisation of touch.

Answer 117

Most input from the thalamus goes to areas 3a and 3b: * 3a -\> Proprioception * 3b -\> Mechanoreception Some input to areas 1 and 2: * 1 -\> Mechanoreception from receptors + Texture information from 3b * 2 -\> Muscle and joint sensory feedback from receptors (mechano and proprio?) + Size and shape information from 3b i.e. Areas 1 and 2 receive mechanoreceptive information from 3b, allowing it to be integrated, so that we have a wider understanding of the object we are touching.

Answer 118

Not really -\> Even though nociceptive information passes to the thalamus, from there it passes to the insular, cingulate and diffuse cortex.

Answer 119

* When fingertips are used to trace some letters on a rotating cylinder, the action potentials in the 3b area of S1 correspond to a precise tracing of the letters * As you progress further through the brain (areas 1 and 2), this signal is degraded, since the receptive fields are not conserved * This leads to degradation of the quality of the trace

Answer 120

Although they do not have as high fidelity (i.e. the receptive fields are larger due to convergence of fibres), they allow for integration of information from a wider areas of the body.

Answer 121

* Area 3a -\> Receives proprioceptive information, so it tells us where the hand is in space * Area 3b -\> Receives mechanoreceptive information, so it gives detailed information about touch * Area 1 -\> Receives some texture information, but mostly involved in combining mechanoreceptive information (from 3b), to get a more global picture of the shape of the object * Area 2 -\> Receives combined sensory information from muscles and joints, plus mechanoreceptve information from 3b, so it gives a 3D picture of the object The information is then passes to the posterior parietal cortex (areas 5 and 7), which is involved in memory of the object.

Answer 122

After entering mostly at areas 3a and 3b, the information has high fidelity. It then passes to areas 1 and 2, which are involved in integrating the information from various receptors into a more complete picture. All of these S1 areas then send information to: * S2 (secondary somatosensory cortex), which passes it to the temporal lobe -\> This is involved in knowing what a stimulus represents (tactile memory - "this is a book!") * Posterior parietal cortex (areas 5 and 7), which combines it with visual information it receives and also passes it to the other side of the body via the corpus callosum -\> This is involved in knowing where a stimulus ("this is where the book is!") Note: The pulvinar is a nucleus in the thalamus, involved in attention, so that you are attentive to the stimulus.

Answer 123

Inputs to the primary somatosensory cortex (from the thalamus) travel in columns from each receptor. These columns are divided into layers: * Layer 4 -\> This receives information from the thalamus, then passes it up to layers 2/3 * Layers 2/3 -\> Passes the information to S2 or back down to layers 5/6 * Layer 5 -\> Cells project down to brainstem and spinal cord * Layer 6 -\> Cells project down to thalamus It is also worth noting that layer 1 is composed of just axons that can travel to different parts of the cortex (e.g. between Brodmann areas).

Answer 124

In each column of the prrimary somatosensory cortex, cellular responses of neurons are input specific. (Check what this means and add more!)

Answer 125

Deficits in: * Sense of position * Ability to discriminate size, texture and shape * Also deficits in hand function (due to lack of descending feedback) There is also altered but not absent nociceptive sensation.

Answer 126

Problems with discrimination of texture, size and shape.

Answer 127

Problems with assessment of texture.

Answer 128

Problems with assessment of size and shape.

Answer 129

* Severe impairment * Cannot learn new tactile discrimination based on shape

Answer 130

They are frequently caused by stroke: * Anterior cerebral artery -\> Foot, leg and trunk somatosensation lost * Middle cerebral artery -\> Arm, hand and face somatosensation lost This is because of the parts of S1 that each artery supplies.

Answer 131

The somatosensory cortex uses the corticospinal (CST) tract to provide control of the ascending sensory systems (in addition to motor control).

Answer 132

(Hikosaka, 1985)

Answer 133

* In patients who have a hand amputation during development, the part of the somatosensory cortex that would usually correspond to the hand is now encoded by the face. * This means that the face covers a wider area.

Answer 134

An unpleasant sensory and emotional experience associated with actual/potential tissue damage.

Answer 135

The perception of noxious stimuli.

Answer 136

Free nerve endings of primary sensory neurons activated by chemicals, heat, or mechanical pressure, that lead to a sensation of pain.

Answer 137

The alleviation or the absence of pain.

Answer 138

Lowered threshold and excessive response to noxious stimuli (i.e. heightened pain).

Answer 139

Pressure sensitivity of bruised tissue

Answer 140

Pain resulting from stimuli that are not normally noxious.

Answer 141

Pain upon movement of joints in rheumatoid arthritis.

Answer 142

* Peripheral pain -\> Due to activation of nociceptors in the skin or soft tissue by tissue injury. * Neuropathic pain -\> Not due to nociceptor activation, but due to damage of peripheral and/or central nerves.

Answer 143

Genetic, epigenetic and environmental factors.

Answer 144

* Aẟ fibres -\> Acute sharp (‘pricking’) pain -\> Precisely localized and short duration * C fibres -\> Burning pain -\> Slower onset, diffuse, longer in duration.

Answer 145

* Aẟ -\> Lightly myelinated * C -\> Unmyelinated

Answer 146

C fibres, which are also a source of itch (aside from pain).

Answer 147

* Transient receptor potential (TRP) channels exist on nociceptive fibres (Aδ and C type) * Each type of TRP displays distinct temperature thresholds, but note that not all generate nociception * Also, some TRPs may be pain-generating mechanoreceptors

Answer 148

Ionotropic receptors: * Lead to cation entry -\> This depolarises the cell * ATP binds to P2X receptors * Protons bind to ASIC and TRPV1 receptors * Capsaicin, endovanilloids and noxious heat activate TRPV1 receptors Metabotropic receptors: * Lead to downstream cascades that affect ion channels * Bradykinin binds to B2 receptors -\> Activates PKC, which phosphorylates TRPV1 channels and increases their sensitivity * Prostaglandins bind to prostanoid receptors -\> Activates PKA, which phosphorylates voltage-gated sodium channels and increases their likelihood of causing depolarisation * Opiods, cannabinoids and noradrenaline -\> Decrease PKA, which leads to decreased activation of voltage-gated sodium channels and increased activation of potassium channels, leading to hyperpolarisation * Nerve growth factors (NGF) -\> Activates tyrosine kinase receptor, which increases the gene expression of the TRPV1 and VGSC in the membrane This allows us to see which receptors cause nociception, and which simply sensitise to it.

Answer 149

Heightened response to noxious stimuli can be caused by: * Diffusion of chemicals from site of injury * Axon reflexes causing neurogenic inflammation -\> Transmission through pain fibres causes feedback release of inflammatory factors (Histamine, 5-HT and substance P -\> See diagram) * Chemical sensitization of nociceptors (Bradykinin, prostaglandins and NGF) * ‘Wind-up’ of synaptic transmission in the spinal cord -\> Increase in pain intensity over time when a given stimulus is delivered repeatedly above a critical rate

Answer 150

* They enter into the dorsal horn * C fibres terminate mostly in lamina 2 (substantia gelatinosa), while Aδ fibres terminate both in lamina 1 (marginal zone) and laminae 3-5 (nucleus proprius) * After synapsing, the second order fibres decussate and carry the fibres up the spinal cord

Answer 151

* Enkephalins are endogenous opioid peptides * They can be released into the synapse between a sensory nociceptive fibre and a projection neuron that travels up the spinal cord * They inhibit nociception (e.g. in descending control of nociception) (ADD MORE FLASHCARDS ON THIS)

Answer 152

* Wind-up is the increase in pain intensity over time when a given stimulus is delivered repeatedly above a critical rate. * Aδ fibres do not show wind-up * C fibres do show wind-up * This is suggested to be because glutamate released from the sensory fibre acts on NK-1 receptors (Gq-coupled) on the second-order projection neurons in the spinal cord, leading to an increase in intracellular calcium * This calcium leads to increased sensitivity of the second-order neuron, possibly due to insertion of more ionotropic glutamate receptors into the membrane

Answer 153

* The pariaqueductal grey sends fibres to the locus coeruleus and nucleus raphe magnus. * The locus coeruleus releases noradrenaline onto the inhibitory enkephalin interneurons in the spinal cord. * The nucleus raphe magnus also releases 5-HT and enkephalins onto inhibitory enkephalin interneurons in the spinal cord. * The inhibitory enkephalin interneurons release enkephalins that are inhibitory to a synapse between the first and second order nociceptive neurons in the spinal cord. (Check this cos it doesn't quite agree with what Trev-dog says)

Answer 154

* The PAG is a nucleus in the midbrain that surrounds the central aqueduct * It is involved in descending control of pain perception, inhibiting synapses between first and second order nociceptive neurons

Answer 155

Those highlighted are in the spec. Others in the spec that are not mentioned here: * Tramadol (a type of opioid) * Anxiolytics (anti-anxiety drugs)

Answer 156

* Aspirin * Ibuprofen * Paracetamol (weak)

Answer 157

* NSAIDs are cyclo-oxygenase (COX) inhibitors that reduce the synthesis of prostaglandins * Prostaglandins are inflammatory mediators that sensitise the nociceptive nerves to excitation by increasing the likelihood of opening of voltage-gated sodium channels

Answer 158

* COX-1 is constitutively active (eg. produces prostaglandins to support the gastric mucosa) while COX-2 is activated by inflammation -\> Thus, COX-2 selective inhibitors (celecoxib) were developed as analgesics to avoid peptic ulcers associated with NSAID treatment * But there is current concern over cardiovascular harm associated with COX-2 inhibition (Vioxx controversy)

Answer 159

* It is a NSAID * It is a weak COX-1/COX-2 inhibitor, but the mechanism of action is uncertain

Answer 160

* Morphine * Codeine * Tramadol

Answer 161

* They stimulate opioid receptors in: * Dorsal horn (at the synapse between first order and second order nociceptive neurons) -\> Lead to * Higher pain centres (e.g. the periaqueductal gray) * Nociceptive sensory fibre endings * This leads to downregulation of nociception

Answer 162

* Adverse effects: * Sedation * Nausea * Constipation * Respiratory depression * Coma * Addiction -\> Associated with long-term use and increased mortality

Answer 163

* A headache disorder characterized by cluster of symptoms including nausea, sensory sensitivity, aura, severe headache and vertigo. * Pathophysiology likely involves changes in cerebrovasculature, inflammation and neural networks (including the hypothalamus, cerebral cortex and trigeminal nucleus) * Changes in circulating 5-HT and peptides are thought to play a role.

Answer 164

* Triptans (5-HT₁ agonists) [IMPORTANT] * NSAIDS (acute migraine) [EXTRA] * 5-HT₂ receptor antagonists (migraine prophylaxis) [EXTRA]

Answer 165

* Only triptans are mentioned in the spec: They are 5-HT₁antagonists * They: * Are vasoconstrictors of extracerebral vasculature * Reduce neuropeptide release from C fibres in the periphery * Stimulate inhibitory 5-HT₁ receptors in the trigeminal nucleus * NSAIDs block inflammation via COX inhibition * 5-HT₂antagonists also lead to vasoconstriction

Answer 166

Sumatriptan

Answer 167

They are voltage-gated sodium channel inhibitors, so they stop nociceptive fibre action potential transmission.

Answer 168

* Analgesics have different strengths (strongest opiates) to match different levels of pain severity (headache versus cancer pain) * Analgesics have different durations of action (acute versus chronic pain) * Side effects of specific analgesics can limit their use in vulnerable patient groups (eg NSAIDs contra-indicated in patients with peptic ulcers) * Certain analgesics most useful in specific pain states: * Local anaesthetics for surgical repair of wounds * Triptans for migraine * Antidepressants and anticonvulsants for neuropathic pain

Answer 169

Pain that outlives acute pain’s ‘warning’ role (3-4 months) -\> i.e. The system gone wrong

Answer 170

* 1:5 people suffer from chronic pain * On average, sufferers live with chronic pain for 7 years (20% \>20 years) * One in five reports losing a job or have been diagnosed with depression as a result of their pain * Conservative estimate annual costs $560-635b USA/€200b Europe

Answer 171

Nociception leads to pain -\> How much pain is experienced varies.

Answer 172

These can be studied using imaging techniques that allow us to see the activity of the brain upon nociceptive inputs.

Answer 173

They are free nerve endings that go all the way into the epidermis (more superficial than the mechanoreceptors).

Answer 174

* Menthol -\> TRPM8 * Capsaicin -\> TRPV1

Answer 175

1. Nociceptive afferents from periphery may synapse directly with neurons of the ascending anterolateral pathway 2. Afferents may synapse with excitatory interneurons, which relay nociceptive inputs to ascending fibres 3. Afferents may synapse with inhibitory inputs which inhibit or block completely transmission of nociceptive impulse This explains a lot clinical implications of pain, such as referred pain, and also gave rise to the gate theory of pain.

Answer 176

* The gate theory of pain states that when a nociceptive C fibre fires, if an Aβ fibres simultaneously, the Aβ fibre will stimulate an inhibitory interneuron * The inhibitory interneuron releases enkephalin [IMPORTANT] * This inhibits the second order nociceptive neuron, so that the nociception is reduced * Thus, it can be seen that pain can be reduced by providing some gentle touch stimulation to the same area (e.g. rubbing a wound after falling over)

Answer 177

* Spinothalamic -\> The big one, responsible for conscious perception of pain * Spinoreticular -\> Arousal in response to pain "wow yeah I should do something about this" * Spinomesencephalic -\> Via the brainstem, involved in descending control of nociception "this is a bit hardcore, I should modulate it"

Answer 178

* Spontaneous episodes of chronic pain in the distribution of one or more branches of the trigeminal nerve. * These episodes may be triggered by weak mechanical stimulation in same region. * Major contributing factor appears to be mechanical damage to the trigeminal ganglion by an artery that impinges on the ganglion. * Surgical displacement of the artery can resolve the condition.

Answer 179

1. Constant firing of nociceptive fibres 2. Amplification/Sensitisation of these pain signals in CNS -\> Could be due to decreased descending inhibition or increased descending stimulation 3. Maladaptive plasticity (when the brain has hindered functional recovery or the development of an unwanted symptom that can lead to pain) 4. Vulnerability towards developing chronic pain

Answer 180

These are used together: * Drugs * Cognitive behavioural therapy * Physical therapy

Answer 181

There is sensitisation of the nerves by inflammatory mediators (see Trevor's lecture).

Answer 182

(See also: Trevor's lecture)

Answer 183

* Sensitisation is the enhancement of nociceptive pathways so that a smaller or even innocuous stimulus can produce pain * Peripheral sensitisation occurs at the level of the nociceptors themselves, where release of various substances from the damaged tissue cause the nociceptor to be more primed for firing (see all the substances in Trevor's lectire) * Central sensitisation occurs within the CNS at the level of the afferent nerve terminal of the second order neuron in the dorsal horn (not dorsal column!), where various mechanisms mean that the second order neuron receives greater input

Answer 184

* Primary hyperalgesia is increased sensitivity at a wound or area of damage -\> Mostly due to peripheral sensitisation (but central sensitisation can occur too) * Secondary hyperalgesia is increased sensitivity in the area surrounded a wound or area of damage-\> Due to central sensitisation

Answer 185

There are multiple suggested mechanisms that can contribute: * Wind-up -\> High rates of C-fibre firing lead to an increase in intracellular calcium in the post-synaptic nerve terminal, which causes more ionotropic glutamate receptors to be inserted into the membrane (or their phosphorylation) -\> This leads to primary hyperalgesia. * Aβ fibres that innervate the area around the wound sprout to synapse onto the same post-synaptic neuron as Aẟ and C fibres. The same mechanism as wind-up means that mechanoreception is perceived as pain -\> This leads to secondary hyperalgesia and allodynia. * Prostaglandins in the spinal cord can bind to PGE₂ receptors on the post-synaptic membrane, causing more phosphorylation of glutamate receptors, as well as on the pre-synaptic membrane, causing more glutamate release. * Injury to the nociceptive peripheral nerve axons causes insertion of α2ẟ channels in the membrane, leading to increased glutamate release. * Synaptic disinhibition -\> Decreased GABAergic descending inhibition and increased descending stimulation (from e.g. the PAG).

Answer 186

Central sensitisation (since peripheral sensitisation doesn't really cause it)

Answer 187

* α2ẟ channels are calcium channels on the membrane of first order nociceptive fibres in the periphery * They lead to calcium influx that stimulates glutamate release and therefore downstream pain perception * They can be targeted by inhibitors such as gabapentin, which reduce pain

Answer 188

* Descending inhibition occurs via noradrenergic nerves that synapse onto enkephalin-containing nerves, which in turn inhibit the synapse between the first and second order neurons * Tricyclic antidepressants and SSRNIs (selective serotonin-norepinephrine reuptake inhibitors) can be used to increase this noradrenergic control, leading to suppression of nociception

Answer 189

* Usually, when sensory fibres are damaged, there will be loss of function (e.g. loss of vision). * However, when nociceptive fibres are damaged, they fire ectopically and therefore show increased activity. * We do not know why this happens.

Answer 190

Sensation of pain in area of body DISTANT from site of origin of the original nociceptive receptor activation.

Answer 191

* Most commonly, it is experience of cutaneous, muscle or bone pain through activation of visceral nociceptor nerve endings * Occurs through existence of common central points of convergence of nociceptive afferent inputs from viscera and somatic structures. * Same second-order neuron receives input from viscera AND the skin.

Answer 192

* We can make use of psychology by, for example, psyching ourselves up in advance of pain * This impacts the descending inhibition of nociception (from the brainstem), causing pain to be reduced * This might have potential in treatment

Answer 193

* The brainstem sends down stimulatory and inhibitory control of the nociceptive pathway * Therefore, the brainstem can control how much pain is perceived at a given time

Answer 194

(Beard, 2017): * Compared patients receiving (a) no treatment, (b) shoulder surgery known as subacromial surgery, and (c) sham surgery (i.e. the placebo) * They compared the pain scores at 6 and 12 month follow up * The two surgery group showed very similar pain outcomes, and the no treatment group showed slightly worst pain * It was suggested that it was the act of coming into hospital, going into surgery, etc. was rresponsible for the outcome * This placebo effect might be modulated by the brainstem sending increased inhibition of nociception down the spinal cord in response to the brain thinking that surgery had happened

Answer 195

* Numbness and sensory loss * Spontaneous, on-going and paroxysmal pain * Stimulus-evoked pain: * Hyperalgesia or Allodynia * Evoked by hot, cold or mechanical stimuli * Common pain descriptors: * Burning * Shooting * Electrical

Answer 196

* Pain affects are 2/3rd of patients with MS (Amatya, 2018) * Approximately 50% of the patients with MS use THC or CBD for treatment. * CBD does not bind directly to cannabinoid receptors, but instead it inhibits FAAH (fatty acid amide hydrolase), which usually breaks down anandamide (the ligand for the CB1 receptor) * Therefore, CBD increases the concentration of the ligand for the cannabinoid receptor. * Monoacylglycerol lipase (MAGL) is a key enzyme in the hydrolysis of the endocannabinoid 2- arachidonoylglycerol (CB2 ligand) -\> Potential target for treatment

Answer 197

Hargreaves test: * A mouse is placed in a chamber where it is free to move * A warm laser is placed beneath the mouse * The laser is shon onto the mouse's paw, causing it to heat up gradually * The time taken for the mouse to move away from the heat is a measure of the pain hyperalgesia in that mouse

Answer 198

* Von Frey hairs are used * These are hairs of various diameters, allowing different forces to be applied * They can be used in combination with a Hargreaves-style chamber

Answer 199

* Degenerative disorders of nociceptive pathways where nociceptor function is progressively lost. * Non-functional nociceptors such as in congenital insensitivity to pain (CIP) due to mutations in voltage-gated sodium channels resulting in nociceptors being unable to detect tissue damage. * Disorders of failed nociceptor neurodevelopment where pain-sensing neurons do not develop.

Answer 200

* Microglia are activated in pain * They produce inflammatory mediators that act on afferent neurons, stimulating nociception

Answer 201

Chemoreception (Ability to recognise and respond to environmental and internal chemicals, such as hormones and neurotransmitters)

Answer 202

* It must be taken up by ingestion, inhalation or skin contact * It must be dissolved in aqueous fluids (mucus, saliva, blood, interstitial fluid)

Answer 203

Upper posterior side of the lateral wall of the nasal cavity.

Answer 204

Ridges in the nasal cavity that direct air to the olfactory mucosa. They warm and humidify the air.

Answer 205

Around 10cm²

Answer 206

Olfactory mucosa = Olfactory epithelium + Mucus Cells in olfactory epithelium: * Olfactory receptor neurons/sensory neurons (OR/SN) * Basal cells (stem cells) * Supporting cells

Answer 207

Secreted from Bowman’s gland.

Answer 208

* Contains antibodies, enzymes, salt and odorant binding proteins * Dissolves odorants, enabled them to be sensed

Answer 209

* Each olfactory receptor neuron has a cell body and dendritic knob. * There are specialised cilia that carry odorant receptors.

Answer 210

* They are GPCR * Each neuron expresses only one type of GPCR * The receptive range of this gene can be broad or narrow, partly depending on conditions, such as concentration

Answer 211

They send unmyelinated axons that penetrate the cribiform plate of the ethmoid bone to contact the olfactory bulb.

Answer 212

* Odorant dissolves in mucus and binds to olfactory receptor * This leads to G_αolf activation, which in turn activates adenylate cyclase III * This increases cAMP, which opens cyclic nucleotide gated channels, leading to an influx of calcium and sodium * This depolarises the cell and calcium activates chloride channels that further depolarise the cell * This can trigger the firing of an action potential, which leads to release of NT onto the olfactory bulb

Answer 213

It can be terminated in several ways: * Unbinding of the odorant * Extrusion of calcium * Calcium-dependent adaptation (weakened response over time)

Answer 214

They are spherical sites in the olfactory bulb that houes synapses between olfactory receptor neurons and mitral cells.

Answer 215

* Each glomerulus receives input from one type of olfactory receptor neuron. This means that an increase in odorant concentration increases the activity at that relevant glomeruli. * However, at high concentrations of odorant there may be non-specific activation of other olfactory receptor neurons, leading to activation of other glomeruli too.

Answer 216

Mitral cells in the olfactory bulb.

Answer 217

* Olfactory receptor neurons contact mitral cells which are the projection neurons of the olfactory bulb. * These output directly to the primary olfactory cortex. * Periglomerular and granule cells provide lateral inhibition. (You do not need to know the details. Just remember the ORNs and mitral cells.)

Answer 218

The mitral cell axons form the olfactory tracts.

Answer 219

The olfactory divides into medial and lateral stria at the level of the optic chiasm: * Medial stria * Goes to the contralateral olfactory bulb via the anterior commissure. * Lateral stria * Goes to the fibres to the primary olfactory cortex (NOT via the thalamus), which outputs to the secondary olfactory cortex, limbic system and hypothalamus. * Goes to the secondary olfactory cortex (via medio-dorsal thalamus)

Answer 220

* Primary olfactory cortex -\> Temporal lobe * Secondary olfactory cortex -\> Orbitofrontal cortex

Answer 221

* Primary olfactory cortex (NOT via thalamus) -\> Then secondary olfactory cortex, hypothalamus and limbic system * Secondary olfactory cortex (via medio-dorsal thalamus) * Opposite olfactory bulb

Answer 222

Emotional, motivational, autonomic and endocrine response to the smell (partly via output to the limbic system and hypothalamus).

Answer 223

Conscious discrimination of different smells.

Answer 224

* A substance that is utilised for intra-species communications * Released by one individual and received by conspecifics * Send information about sex, strain and species to receiver * Are meaningful or informative for species

Answer 225

* Anosmia -\> Inability to detect presence of odour: * Conductive loss -\> Obstruction of nasal passage * Sensorineural causes -\> Damage to olfactory epithelium * Central dysfunction -\> In relation to CNS disease * Dysosmia -\> Difficulty with odour discrimination * Parosmia -\> Sensation of odour distinct from that present * Phantosmia -\> Perception of odour in absence of odour source Causes: * Aging (neurodegenerative diseases!) * Upper respiratory tract infections * Head trauma * Sinonasal disease * Congenital (rarely)

Answer 226

* Non-volatile * Hydrophilic * Soluble in saliva * Detection threshold high

Answer 227

* On the tongue, there are papillae which have trenches to concentrate the tastant * In the trenches of the papillae, there are taste buds * Each taste buds contains 50-150 taste receptor cells * The taste receptor cells have taste receptors on their surface.

Answer 228

* Salty -\> Enables detection of electrolytes * Sour -\> Warning of noxious chemicals * Bitter -\> Warning of noxious chemicals * Sweet -\> Enables detection of energy dense foods * Umami -\> Enables detection of amino acids

Answer 229

* Taste receptor cells * Support cells * Basal cells (stem cells) The taste buds are surrounded by epithelial cells. The taste buds themselves are essentially equivalent in structure to olfactory receptor mucosa, except the taste receptor cells release NT onto afferent nerve cells.

Answer 230

* Have apical microvilli that have receptors for tastants that enable sensory transduction * Release NT on the basal side

Answer 231

* Possibly ATP or 5-HT * Onto afferent nerve cells

Answer 232

This model has the strongest evidence in mice, but there is still some controversy.

Answer 233

* Salty * Have ENaC channels that detect sodium * Sour * Have unknown receptors for H⁺ * Sweet, Bitter and Umami (shown in diagram) * Have GPCRs that lead to increases in IP₃ * This leads to calcium release from intracellular stores * The calcium leads to influx of sodium via TrpM5 channels, which depolarises the cell and leads to NT release

Answer 234

* Sweet → T1R2 + T1R3 * Bitter → T2R * Umami →T1R1 + T1R3, mGluR4

Answer 235

* Facial nerve (VII) -\> From anterior 2/3rd of tongue * Glossopharyngeal nerve (IX) -\> From posterior 1/3rd of tongue (Remember this by their positions in this diagram)

Answer 236

To the nucleus of the solitary tract (a.k.a. nucleus solitarius or nucleus tractus solitarii).

Answer 237

* Taste receptors release neurotransmitter onto the afferent nerves (facial nerve on the anterior 2/3rd of the tongue, glossopharyngeal on the posterior 1/3rd of the tongue) * The facial nerve (VII) and glossopharyngeal nerve (IX) output to the nucleus of the solitary tract * Nucleus of the solitary tract outputs to: * Primary taste cortex (via the ventral-posterior thalamus), then to the secondary taste cortex * Hypothalamus (for endocrine responses to food)

Answer 238

Anterior insula on the insular lobe and the frontal operculum on the inferior frontal gyrus of the frontal lobe.

Answer 239

Orbitofrontal cortex (This is the same as the secondary olfactory cortex)

Answer 240

Nucleus of the solitary tract

Answer 241

Cranial nerves VII, IX and X.

Answer 242

It outputs to the lateral hypothalamus ‘feeding centre'.

Answer 243

The mechanism generally relies on ionotropic receptors: * In mechanoreceptors, this is in the form of a stretch-mediated Na⁺ channel which, when opened by stretch of the skin to which they are tethered (in a process potentially aided by ridges), will allow for a depolarising influx of sodium cations that increases the rate of signal firing along the afferent pathway. * For free nerve endings, the channels are instead gated by the specific noxious or thermal stimulus as needed – for example, heat-sensitive domains in the TRPV1 channel will only lead to a conformational change and open the pore domain of these Na⁺ channels when the temperature of the overlying skin is within a certain range.

Answer 244

* Pacinian and Meissner’s corpuscles both possess multilaminate discs which have been shown to make them responsive to on/off change in pressure only – thus adapting them for detection of vibration or changes in stimulation of the skin. * Between the laminae surrounding the nerve ending, there is lamellar fluid which is able to spread out and disperse the force so that the membranes do not stretch, and the gated channels remain closed after a constant pressure is applied. * This can be illustrated by the delamination of one of these corpuscles and measurement of the spike-train it produces; it starts to mirror that of a slow-adapting receptor instead.

Answer 245

A CSF-filled cyst that forms within the spinal cord.

Answer 246

Anxiolytics

20. Sensory Systems Flashcards

(305 cards)