Somatosensory systems Flashcards
Sensory receptors generate a receptor potential, which is…
a change in their membrane potential in response to appropriate stimulation, this process is called transduction and is different in different receptors.
How is the sensory receptor different for somatosensory systems vs other sensory systems?
For somatosensory systems the sensory receptor is the modified ending of the primary afferent neuron, and is depolarised directly by the stimulus. In other systems, the sensory receptor is a specialised cell type which forms synaptic connections with the first afferent neuron. Alterations in membrane potential alters sensory cell neurotransmitter release, with effects on the primary afferent.
In vertebrates, all sensory receptors, except which receptors, depolarise when stimulated.
Photoreceptors- hyperpolarised by light.
What are the properties of receptor potentials?
They are small amplitude, graded in size depending on stimulus strength, passively conducted over the receptor cell surface or along neurites, delay with time and distance and can be summated. A receptor potential will trigger APs for as long as it remains beyond the firing threshold, the frequency of firing will be higher the greater its amplitude. Sensory receptors demonstrate adaptation.
What are the three types of receptors in the somatosensory system?
Mechanoreceptors, found in skin, muscles, joints and viscera, thermoreceptors, confined to the skin and nociceptors, found almost every where except the brain.
How are skin mechanoreceptors classified?
As slowly or rapidly adapting and separately as being of two types, type I and type II, distinguished by their location and receptive fields.
What are the properties of the Ruffini organ?
Slowly adapting, afferent has a frequency of firing that is directly proportional to the extent to which overlying skin is indented by mechanical force. It codes skin position/ stretch.
What are the properties of Meissner’s corpuscle?
Rapidly adapting, afferent only fires when skin displacement is changing with time. It codes the velocity with which skin is displaced.
What are the properties of the pacinian corpuscle?
Adapts so rapidly that its afferents respond to skin acceleration. It is responsible for the sensation of vibration.
Where are type I mechanoreceptors located and what are examples of them?
They are superficial, lying at the boundary of the epidermis and dermis and have small RFs with well-defined boundaries. they include meissner’s corpuscles and merkels disks.
Where are type II mechanoreceptors located and what are examples?
Type II are deep in the dermis and have large RFs with poorly defined edges, and include ruffini corpuscles and pacinian corpuscles.
What is the difference between type I and II receptors in terms of sensation perceived?
Type I receptors are more concerned with form and texture perception than type II.
How do the densities of type I receptors differ across the body surface?
Highest in the fingertips, lips and tongue and lowest in the trunk. Areas with higher density have a proportionally greater representation in the somatotropic maps.
Pacinian corpuscles can respond to indentation as little as 1um, what is the process of transduction?
The force is transmitted through the corpuscle to deform the neurite within –>opening of stretch-sensitive NA channels in the membrane–> brief depolarisation–> membrane potential returns to normal very fast because the receptor adapts by individual connective tissue layers of the corpuscle sliding over each other which relieves the neurite deformation
How does innervation of hairy skin differ from that of glabrous (non-hairy) skin?
Hairy skin has a lower density of merkel’s disk and it possesses two additional types of mechanoreceptors closely associated with hairs (lanceolate and pilo-ruffini endings and hair follicle receptor)
What are the properties of skin thermoreceptors?
They are the naked terminals of small diameter afferents. They are slowly adapting and tonically active. Thermoreceptor afferents have just three to four terminals and have very small RFs, although infrared radiation is poorly localised.
There are two types of thermoreceptor, warm and cold, which fire over different temperature ranges, how do these perceive temperature?
They do not respond to noxious temperatures. Skin temperature is perceived by comparing the relative activities of warm and cold receptors. Thermoreceptors signal the direction in which temperature changes. Skin cooling briefly silences warm receptors and causes cold receptor firing rates to rise. Similarly, skin warming silences the cold receptors and boosts warm receptor firing
What are nociceptors?
The bare-endings of small diameter afferents that are receptors for noxious (tissue-damaging), pain-producing stimuli.
What are the properties of nociceptors?
They are high threshold (require intense stimulation to excite them). They have no background firing. they are classified by what excites them.
What are the four types of nociceptors?
Mechanical, thermal, polymodal, itch
What sensation does mechanical nociceptors in the skin give rise to?
Sharp, pricking pain.
What are the properties of mechanical nociceptor afferent?
Each nociceptor is one of 5-20 branches of A(delta) afferent with low conduction velocities
What do mechanoreceptors in the visceral peritoneum respond to?
Excessive distension
What are the afferents of thermal nociceptors?
A(delta) and C fibers
What do polymodal receptors respond to?
Puncture, temperatures in excess of 48 degrees, and to a wide variety of molecules liberated as a result of tissue damage (K, H, bradykinin, prostaglandins, serotonin and histamine)
Afferents of polymodal nociceptors are C fibers (conduct at less then 1 ms) what is the effect of this?
Because conduction is slow, the burning or aching pain they produce arrives last after a blow. They are responsible for visceral and muscle pain and toothache
What are the afferents of itch receptors and what do they respond to?
Belong to a separate class of C fiber that respond to histamine release from mast cells
What is a dermatome?
The region of skin innervated by a dorsal root. These are numbered for the spinal cord segment served by the dorsal root
Cutaneous low threshold mechanoreceptor primary afferents relaying skin mechanoreceptor and proprioceptor enter the dorsal roots and synapse with which neurons?
Dorsal horn cells- interneurons in Rexed laminae III-VI. They modify or mediate spinal reflexes. Each afferent sends a collateral up the dorsal columns to synapse with neurons in the dorsal column nuclei in the medulla
The dorsal column nuclei consist of the nucleus gracilis and nucleus cuneatus, what is the difference in their inputs?
The cuneate nucleus receives input from C1-8 and the gracile nucleus get its input from T7-12, lumbar and sacral spinal segments. Lateral inhibition in the DCN shapes these inputs.
Where do axons leaving the dorsal column nuclei project to?
They cross the midline to ascend on the opposite side as the medial lemniscus, terminating in the ventralposterolateral division of the ventro-basal thalamus.
What do the Ventroposterolateral neurons give rise to?
thalamo-cortical axons which project to the primary somatosensory cortex SI (brodman’s areas 1, 2, 3a and 3b) situated over the post central gyrus. SI neurons project to SII
What are the general properties of the DCML system?
-Great strength of synaptic connections
-Properties of its neuron are matched to the sensory receptors supplying them (features of stimuli transmitted with high fidelity)
-Somatotropic mapping preserves localisation at every stage.
Neurons in SI are organised into columns aligned at right angles to the brain surface, what is the significance of this?
Each column gets input from a single type of receptor, and from a specific location. Adjacent locations are represented in adjacent columns in a somatotropic manner. Extensive neural connections exist within a column, connections between columns are sparse.
What is each area in SI responsible for?
3b is important for tactile discrimination, area 1 is concerned with analysis of texture, area 2 with stereogenesis (the ability to perceive the 3D shape of an object by touch). Area 2 gets input from muscles and joints and has reciprocal connections with the motor cortex. It may inform the motor system of the sensory consequences of moving.
Where does the secondary somatosensory cortex get input from?
From the thalamus and SI. Many neurons have bilateral RFs (stimuli in corresponding regions on both side of the body will evoke a response). Inputs from the contralateral body surface arise as a consequence of the decussation of the medial lemniscus. Inputs from the ipsilateral side of the body enter SII from the contralateral side via the corpus callosum
What is the function of the SII?
By integrating information from both sides of the body, SII is the first stage in forming a whole body perceptual experience. It enables tactile discrimination learned with one hand, being easily performed with the other. It is important in controlling movement via connections with the motor cortex. It has inputs to the limbic cortex enabling tactile learning.
What makes up the descending pathway of the somatosensory cortex?
It is made by the corticospinal (pyramidal) tract either directly or via its connections with the brainstem reticular nuclei.
What is the function of the somatosensory descending connections?
They are probably the vehicle by which somatosensory input can be selectively filtered as an attention mechanism.
what is the definition of pain?
It is the unpleasant sensory and emotional experience associated with noxious stimuli, those which can cause tissue damage. Nociceptive pain is felt only in the presence of acute injury and inflammation. Pathological (clinical) pain is associated with chronic inflammatory disease or to damage or dysfunction of the nervous system and has no obvious purpose.
What sensations do the anterolateral pathways convey?
temperature and pain sensations, and poorly discriminated touch sensation
What are the primary afferents of the anterolateral pathways?
Small diameter high threshold dorsal root ganglion cells driven by nociceptors and low threshold dorsal root ganglion cells excited by thermoreceptor or mechanoreceptor input
What is the route the primary afferents of the anterolateral pathway?
They are situated laterally in the dorsal roots and enter Lissauer’s tract, where they divide into ascending and descending branches that enter the dorsal horn within within a couple of segments.
Where do the primary afferents of the anterolateral pathways synapse?
Nociceptive Alpha(delta) afferents synapse with projection neurons in laminae I and II, and with the distal dendrites of lamina V cells, although visceral and muscle nociceptors do not project to lamina II. Nociceptive C fibers synapse with other laminae I and II neurons.
Where do the primary afferents of the anterolateral pathways synapse?
Nociceptive Alpha(delta) afferents synapse with projection neurons in laminae I and II, and with the distal dendrites of lamina V cells, although visceral and muscle nociceptors do not project to lamina II. Nociceptive C fibers synapse with other laminae I and II neurons. Large diameter fibers from the mechanoreceptors enter the dorsal horn medially and synapse with neurons in deeper Rexed laminae (IV-VIII)
What are the three pain pathways?
Spinothalamic tract, Spinoreticular tract and spinoparabrachial tract
What does the spinothalamic tract consist of?
It arises from neurons in laminae I, II, IV and V, axons of which cross over and ascend on the contralateral side to the posterior (I and II) and ventroposterolateral (IV and V) nuclei of the thalamus. Thalamic neurons project to the primary somatosensory cortex.
What does the spinothalamic tract mediate?
Fast, well-localised and well-characterised pain.
The largest number of spinothalamic tract cells are found in lamina V. Where do they receive input from?
Their dendrites extend into lamina I and receive inputs from A(delta) (fast pain) afferents. They also receive connections from large diameter A(beta) mechanoreceptor afferents and are said to be wide dynamic range cells - get inputs from low and high threshold afferents.
Where do lamina IV cells get input from?
Only from large diameter A(beta) mechanoreceptor afferents and not from nociceptor afferents.
Where does the spinoreticular tract arise from?
Lamina V-VIII and makes bilateral connections with reticular nuclei in the brainstem–> second order neurons that project to reticular (intralaminar) nuclei of the thalamus–> SI, insula, anterior cingulate cortex and prefrontal cortex
What is the function of the spinoreticular tract?
Mediating emotional and cognitive responses to pain. Activation of the brainstem reticular nuclei generates autonomic responses to pain and changes in ventilation. By activating neurons in the locus coerulus the SRT increases arousal. Thalamic nuclei make connections with the basal ganglia, influencing motor activity.
What makes up the spinoparabrachial tract?
Arises from lamina I cells that get their input from C fiber afferents and synapse with cells in the parabrachial nucleus that project to the hypothalamus and amygdala
What is the functiom of the spinoparabrachial tract?
Via these connections, pain activates pituitary-adrenal axis stress responses, affects appetitive behaviour and sleep and mediates fast learning
Which system mediates visceral pain perception?
dorsal column-medial lemniscus system
What is referred pain?
Stimulation of nociceptors in internal organs is perceived as pain in muscle and skin some distance away as a result of convergence of visceral and somatic nociceptor afferents on to the same neuron. The area to which the pain is referred are known as Head’s zones.
How are the primary afferents conveying pain of the face and head projected to the ventroposteromedial and posterior thalamic nuclei?
Neurons equivalent to lamina I and V cells in the spinal cord are found in the spinal nucleus of the trigeminal nerve, which get their input from the primary afferents of the face and head.
Which laminae convey crude touch sensation?
Lamina V and IV cells when activated only by large-diameter, low-threshold afferents. These cells have small receptive fields and their projections are organised topographically to localise stimuli precisely. Convergence of inputs means they cannot discriminate well between mechanoreceptor submodalities.
Which laminae do noxious stimuli activate and why?
Both lamina I and V cells. Lamina I cells signal pain, but have large receptive fields and relay to posterior and reticular thalamic nuclei (do not have precise topographic projections to the cortex). The localisation of painful stimuli depends on the simultaneous firing of lamina V cells which project in a somatotropic fashion to the ventroposterolateral thalamus and to SI.
At the spinal cord level, whether a stimulus is perceived as painful or not is dependent on what?
Depends on the relative activity of large and small diameter fibers. High large/small diameter fiber activity reduces nociceptor input. This is gate control theory
How do large (A(beta) mechanoreceptor afferents reduce nociceptor input to lamina V cells?
They inhibit lamina V neurons via inhibitory neurons in lamina II. Nociceptor afferents excite lamina V cells via excitatory interneurons, and these can be inhibited by A(beta) driven inhibitory interneurons. Co-activation of low and high threshold afferents closes the pain gate
The gate control theory accounts for counter-stimulation analgesia, what is this?
Pain is reduced by stimulating low threshold afferents
What is the mechanism of action of transcutaneous electrical nerve stimulation?
Delivers high frequency, low intensity currents, sufficient to stimulate A(beta) fibers, and also A(delta) fibers that activate endogenous opioid-using supraspinal anti-nociception pathways
Where do supraspinal anti-nociception pathways arise from?
Brainstem nuclei that get connections from the spinoreticular tract give rise to descending supraspinal anti-nociceptor pathways.
Stimulating the per-aqueductal gray matter causes suppression of pain responses (stimulus-induced analgesia), how does it do this?
PAG activates brainstem aminergic neurons via inhibitory enkephalinergic neurons acting on GABAergic interneurons
Where does the PAG get input from?
Limbic system, hypothalamus, amygdala and insula cortex.
Neurons in the locus coerulus and nucleus raphe magnus send axons into the dorsal horn, what neurotransmitters do they use?
LC- Noradrenaline. NRM- Serotonin
How do the amines reduce transmission from nociceptors in lamina I dorsal horn cells?
-Presynaptic inhibition
-Stimulating postsynaptic receptors that open K channels –>hyperpolarization of lamina I cells
-Stimulating lamina II enkephalinergic and GABAergic inhibitory neurons –> open K channels/ close Ca channels
What is the natural counterpart of stimulus-induced analgesia?
Stress-induced analgesia
What are the properties of stress-induced analgesia?
It is rapid in onset and wears off after a few hours. Can be localised to the area or generalised. Can be endogenous opioid dependent or non-opioid dependent
What is the selective advantage of Stress-induced analgesia?
Allows an individual to continue to function to remove themselves from danger
What is the difference between non-opioid and opioid stress-induced analgesia?
Opioid analgesia occurs at a higher intensity stress. It requires enkephalinergic neurons in the PAG. Non-opioid SIA involves relief of endogenous cannabinoids that act on CB1 cannabinoid receptors in the PAG
How do the pain pathways switch on brain analgesia?
Spinoreticular tract signals to the nucleus reticularis paragigantocellularis which stimulates the serotonergic cells of the nucleus raphe magnus. The spinothalamic and spinoreticular cells activate the LC noradrenergic neurons. Both these pathways inhibit lamina I cells transmitting nociceptor signals.
How do central noradrenergic pathways shut down the spinoparabrachial tract?
Presynaptic inhibition of glutamate release from parabrachial terminals in the amygdala. NE acts at presynaptic alpha2 receptors, liberating the Beta(y) subunits of their Gprotein. The subunits block vesicle release sites at the active zone of the synapse
What is the mechanism of action of electro-acupuncture?
relies on stimulation of small diameter afferents from skeletal muscle and joints. Low frequency stimulation activates Beta-endorphin using neurons in the arcuate nucleus of the hypothalamus–> PAG–> enkephalinergic pathway. High frequency stimulation activates the parabrachial nucleus–> activates PAG pathway that uses dynorphin-secreting neurons to inhibit Dorsal horn cells
what receptors do dynorphin and enkephalin act on?
Dynorphin: k opioid receptors. Enkephalin: u and delta receptors
What are three types of altered pain states?
Hyperalgesia- Noxious stimulation becomes more painful than usual
Allodynia- Mechanical or thermal stimuli that are innocuous become painful
Spontaneous pain- Pain in the absence of a stimulus
How do altered pain states arise?
Because neurons become more excitable, their thresholds are lowered (sensitisation). Inflammation is often a major factor (inflammatory pain)
What is neuropathic pain?
Damage to pain pathways per se
Peripheral sensitisation is caused by hyperexcitability of primary nociceptor afferents, how does this occur?
At an injury site a wide variety of substances are released, including H+, adenosine, serotonin, histamine, prostaglandins and numerous peptides such as bradkinin and cytokines. C polymodal nociceptors respond to these with second-messenger mediated alterations to proteins such as ion channels, enhancing excitability
What is neurogenic inflammation?
Primary nociceptors release glutamate and peptides (Substance P). The peptides amplify and prolong the effects of glutamate. They are co-released from peripheral terminals and central endings of the nociceptor axon. Hence, stimulus evoked APs are conducted centrally and in an axon reflex (antidromically along neighbouring branches to stimulate secretion from peripheral terminals)–> classic signs of inflammation at injury site
What is the mechanism of action of aspirin and other NSAIDs?
They inhibit COX2, an enzyme involved in prostaglandin synthesis. Prostaglandins lower the threshold of nociceptors to other inflammatory mediators such as serotonin and bradykinin
What are the molecular receptors in thermal and polymodal nociceptors which sense heat stimuli called?
Capsaicin (vanilloid) receptors (TRPV1). Ligand gated calcium channels.
What does activation of TRPV1 trigger?
Transmitter release (glutamate, substance P, ATP)
What happens to TRPV1 receptors in peripheral sensitisation?
Their numbers increase and individual receptors are made more sensitive, by actions of prostaglandin and bradykinin
Where does central desensitisation arise from?
In the spinal cord, it arises from changes in behaviour of dorsal horn cells in response to prolonged nociceptor traffic. This strengthens (facilitates) the synapses onto the DHCs.
Wind-up, is a type of temporal summation, an activity dependent synaptic facilitation- what does it entail?
The release of substance P from C fiber nociceptor terminals generates slow epsps. If C fibers are stimulated a constant frequency above 0.3 Hz, these epsps summate to produce ever-larger depolarisation of the DHCs, which activates NMDA receptors –> cascade of kinase activation–> persisent increase in excitability (by eg recruiting more AMPA glutamate receptors, and the formation of new synapses)
What happens to wide dynamic range DHCs to contribute to desensitisation?
Become hyperexcitable to low threshold A(beta) input and increase their receptive field size.
How are the receptive fields of DHCs enlarged?
Under normal circumstances, stimuli applied near the edge of the receptive field of a DHC usually elicit subthreshold responses (epsps). However, if a cell is very depolarised, it is more sensitive to excitatory input. Previous subthreshold stimuli at the edge of its receptive field now become suprathreshold
How should analgesic cover in surgery be administered to prevent wind-up and central sensitization?
Given pre-emptively and topped-up frequently enough that no pain occurs
Where does central sensitization take place?
Spinal cord, rostroventral medulla, thalamus, amygdala and cingulate cortex
What is the sequence of central sensitisation following peripheral nerve injury?
Peripheral nerve injury –> activates microglia in local spinal cord –> upregulation of microglial P2X4 receptors–> stimulation of receptors by excess ATP released by damaged nerves–> microglia release cytokines –> increase sensitivity of lamina I dorsal horn cells
How do cytokines increase the sensitivity of lamina I dorsal horn cells?
The cytokines down-regulate an anion exporter in the cell bringing about a large rise in intracellular chloride concentration. These cells now respond to activation of their GABAa and Glycine receptors by a large depolarisation caused by chloride leaving the cell down the concentration gradient–> NMDA receptors can be opened by incoming excitation, triggering potentiation
How are microglia involved in central sensitization in the thalamus?
A cytokine released by thalamic neurons activates COX2 in the glia so they sythesize and secrete prostaglandin E2. This binds to prostaglandin receptors on neurons and increases their excitability by depolarisation
What is phantom pain?
After amputation of a limb or other body parts, patients experience the sensation that the limb is still present and can be painful
How is it possible for children born without limbs to have powerful, non-painful phantom limb sensations?
It implies that complete somatotropic representations can exist in the absence of peripheral inputs (also the situation in amputees)
What is the cause of phantom pain?
It is unclear. But it does involve re-wiring of the somatosensory cortex so that neurons that have lost their original inputs aquire functional connections form previously silent synapses established by neighbouring cells. With continuing cortical re-organisation phantom sensations may fade over time.
What is the placebo effect?
Refers to the therapeutic efficacy of agents or procedures that are without any physiological or pharmacological action.
What is the physiology of placebo effect?
The more the elaborate the placebo treatment the better the outcomes. there is evidence that when used to reduce postoperative pain, can be blocked by naloxone and so depends upon endogenous opioid neurotransmission. MRI shows that placebo analgesia is associated with decreased activity in brain regions associated with pain but increased activity in the dorsal lateral prefrontal cortex, an area involved in cognition. A hypothesis is therefore that expectation of pain relief activates a top-down recruitment of supraspinal opioid pathways.
Where are the receptors that detect the position and motion of the head in space located?
In organs in the vestibular part of the inner ear (labyrinth) that lies within the temporal bone.
What is vestibular input used for?
To adjust posture as forces shift the body’s center of mass by modifying the output to antigravity muscles. Conscious perception of balance is normally overshadowed by visual and proprioceptive cues to head position and motion. Also used to execute eye movements which are independant of head movement (vestibulo-ocular reflexes)
What is the membranous labyrinth?
A sensory epithelium within the bony labyrinth subserving hearing and balance.
What does the vestibular labyrinth, concerned with balance, consist of ?
Two otolith organs, the utricle and saccule, and three semicircular ducts.
How is the sensory structure detecting linear acceleration in the otolith organs (macula) different for each and what is the significance?
It is horizontal in the utricle and and verticle in the saccule for a person standing upright. The utricle is sensitive to tilting of the head while the saccule is sensitive to vertically acting forces such as gravity.
What is the sensory organ in the semicircular ducts and what does it detect?
Ampullary crest- detects angular acceleration in the plane in which the duct lies. Using signal from all 6 semicircular ducts, the brain computes the magnitude and direction of angular acceleration of the head
The vestibular labyrinth is filled with endolymph- what is made up of?
Has a potassium concentration of about 160 nM and a sodium concentration of about 2mM, and has a composition similar to intracellular fluid
What is endolymph secreted by and where does it drain to?
Stria vascularis, a specialized epithelium lining the outer wall of the cochlear duct, and drains into a venous sinus of the dura via the endolymphatic sac
The space between the bony and membranous labyrinths is filled with perilymph, what is this produced by and where does it drain to?
Secreted by arterioles of the periosteum which drains into the subarachnoid space via the perilymphatic duct
What maintains endolymph potassium concentration?
Active transport by marginal cells
What is the potential difference of endolymph with respect to perilymph and how does this favor passive diffusion of K across the hair cell?
+80 mV, the testing potential of the hair cell is about -60 mV, the effective potential across its apical border is 140 mV, hence there is a large electrochemical gradient.
What is the macula made up of?
It is an epithelial sheet of supporting cells, and sensory hair cells. Each hair cell is innervated at its base by 2 nerve fibers, a vestibular afferent and an efferent. The apical border has a single motile kinocilium, resembling a cilium and 40-100 sterocilia, microvilli which are progressively shorter the further they are from the kinocilium.
What direction id the axis of polarity of a hair cell?
From the smallest stereocilium to the kinocilium
What function do sterocilia fulfil?
they are the mechanosensory organelles of the inner ear, since their tips contain stretch-activated potassium channels that are regulated by the tip links (thin filaments connecting sterocilia lying along the same axis at their tips)
The kinocilium and sterocilia are embedded in..
A gelatinous matrix, the otolith membrane, containing tiny crystals of calcium carbonate, called otoliths
What are the properties of the hair cell at rest?
It is at rest if no force acts on the otolith membrane to cause the stereocilia to pivot. The tension in the tip links is slight so only 10 percent of the potassium channels are open, causing a small depolarisation–> tonic release of glutamate–> maintains baseline firing of the primary afferent.
What happens to the hair cell when the head tilts in the direction of the axis of polarity?
The otolith membrane pulls on the stereocilia, making them pivot, increasing the tension in the tip links.This opens stereocilia K channels, allowing potassium influx to depolarise the hair cell, increasing glutamate and raising the afferent firing rate.
What happens when the head tilts in the opposite direction of the axis of polarity?
Reduces the tip link tension so potassium channels close, the hair cells hyperpolarise, and primary afferent firing rate drops. The axes of hair cells are orientated in an orderly pattern so a given stimulus will depolarize some hair cells and hyperpolarize others
What happens when the head tilts perpendicular to the axis of polarity?
Has no effect because stereocilia are not linked in this direction.
What do head tilts in intermediate directions do the hair cell?
Cause graded receptor potentials. The responses of individual otolith afferents are proportional to tilt angle and adapt only with prolonged stimulation
Why is head rotation considered angular acceleration?
Even if the angular speed is kept constant, the direction in which the velocity vector is acting is constantly changing
What is the structure of the semicircular canals?
Both ends of each semicircular canal insert into the utricle. Within the canal is the endolymph-filled semicircular duct. At one end of each duct is a dilation (ampulla) in which sits the ampullary crest. Vestibular hair cells here have their stereocilia embedded in a gelatinous sheet (cupula)
What is the transduction mechanism in the semicircular ducts?
Rotation of the head maximally stimulates hair cells in the canals lying in the same plane as the rotation. Rotation of the endolymph lags behind head rotation so it exerts a pressure distorting the cupula, bending the stereocilia
What do the signals transmitted by the duct afferents measure?
Because the cupula is not an ideal pressure transducer, they measure angular acceleration for slow and fast rotations, but encode velocity for mid-range rotation speeds
How do semicircular ducts on each side lying in the same plane operate in pairs?
Head rotation that causes depolarization of hair cells in the horizontal duct of the left ear will hyperpolarize the cells in the horizontal duct of the right ear
What is the path of the vestibular primary afferents?
they are pseudobipolar cells with their cell bodies in the vestibular ganglion. Their axons run in the vestibulocochlear nerve to enter the vestibular nuclei which lie laterally in the medulla and pons. There are 4 nuclei
What is the pathway for conscious balance perception?
Axons of the inferior vestibular nucleus which cross to the contralateral side ascend close to the medial lemniscus to terminate in the ventral posterior thalamus–> third order neurons project to the vestibular cortex, other projections go to the superior temporal cortex
Where is the vestibular cortex?
Lies at the temporo-parietal boundary and posterior insula
Where is the superior temporal cortex?
Adjacent to the auditory area and to the frontal cortex
