Module 4 - Sensory Flashcards
L4.1 - Define the somatosensory and special sensory systems.
The somatosensory systems mediates the feeling of touch, pain, temperature and proprioception -> the somatic sense
visual, auditory, taste, smell
We also have visceral systems necessary for homeostasis and the vestibular for balance and head movement.
L4.1 - Describe the afferent pathways of somatosensory systems, ie. the anterolateral system (pain and temperature) and the dorsal-columns-medial lemniscal system (touch and proprioception).
L4.1 - Describe sensory receptors and explain their activation
Sensory receptors are generally specialized structures, that only respond to a certain modality of stimuli (adequate stimuli) with certain thresholds for activation. They can be found in accessory structures, which are specialized epithelium that are sense organs (like the nose, eyes, skin, etc.)
They are either primary (neurons), that signal through APs and have axons or they are secondary (epithelia), that signal with NTs and have no axons.
L4.1 - Define the adequate stimulus
An adequate stimulus is a stimulus that can activate a receptor based on its modality - not related to the intensity!
L4.1 - Describe receptor potential and the sensory cascade (transduction)
The receptor will receive the sensory input and create an electrical receptor potential, which refers to the amplitude and duration of the electrical signal (depends on stim intensity). The transduction is the conversion into electrical signaling, where the signal is then propagated to other cells.
Receptor Potential: Change in membrane potential produced by transduction currents.
Transduction: the conversion of stimulus energy into electro-physiological response.
Can be direct (as in hair cells) or indirect through metabotropic receptors
L4.1 - Describe regulation of repetitive firing
Response of the receptor declines under constant stimulation, proving that change is more important than steady state
L4.1 - Describe adaptation and explain adaptation mechanism
Response of the receptor declines under constant stimulation, change is more important than steady state.
Sensory receptors detect contrasts, thus changes in temporal and spatial patterns of stimulation why the constant stimulation receives less attention. E.g., you don’t feel the clothes you wear, but you might initially when you put it on.
L4.1 - Define slowly and rapidly adapting receptors
Slow adapting receptors will respond as long as a signal will be present (good to keep the the body aware of the stim being there), but rapidly adapting receptors decrease their firing and adapt to a present stimulus - they will fire again once the stim is ended or changed to signal that change.
L4.3 (touch) - To explain transmission of sensory information from receptor to the cerebral cortex
Peripheral receptor (DRG) -> Dorsal column (synapse on gracile or cuneate nucleus) -> crosses to the medial lemniscus pathway (synapse onto the VPL of the thalamus) -> project to the primary somatosensor
L4.3 (touch) - To describe distribution and classification of receptors according to adequate stimulus and adaptation
Mercel cells: in the dermis, slowly adapting - Deformation of skin, hair
bending
Meissner’s corpuscles: in the epidermis, rapidly adapting - feel surface structures
Ruffini corpuscles: Ruffini in the dermis, slowly adabting, Stretch of skin/joints
Pacanian corpuscles: in subcutanius(?), rapidly adapting - deep fast vibrations
L4.3 (touch) - To explain receptive field and lateral inhibition
Receptive field: the area of skin one receptor detects a stim from - smaller for surface receptors (the Germans)
Lateral inhibition: The primary input neurons inhibits its neighbors create contrast and thereby enable 2-point discrimination
L4.3 (touch) - To describe localization of sensory areas and processing of sensory information in the cerebral cortex
There is the primary somatosensory in the postcentral gyrus and the posterior parietal area.
the primary somatosensory cortex is divided into areas
1 (rapidly adapting receptors - surface structures - Meissner - required for 2D),
2 (deep receptors for size and shape - required for the depth - 3D),
3a (muscle receptors and nociceptors - pain & proprioception),
3b (Cutaneous receptors - touch)
the 3’s get 70% of VLP and VPM input and 1 and 2 30%
All project to the secondary somatosensory cortex and then onwards to amygdala/hippocampus
L4.4 (touch) - Describe nociceptors and nerve fibers conducting pain impulses
Nociceptors respond to noxious stimuli and sit on free nerve endings, and the fibers are c-fibers (unmyelinated, thin, glutamatergic) and a-delta (myelinated, faster). Nociceptors can be mechanoreceptors, thermal receptors or chemical receptors.
L4.4 (pain)- Describe the differences between discriminative and affective components in pain
Discriminative pain is used to act on and is mediated by a delta fibers (first pain), affective pain is mediated by c-fibers and relates to 2nd pain, which projects to affective areas ACC and the insula.
L4.4 (pain) - Define first and second pain and their central representation
First pain goes the primary somatosensory and secondary pain (more diffuse in time and location) to the ACC and the insula
L4.4 (pain) - Describe that perception of pain differs from the objective painful stimulus
Pain is the experience; nociception is the transduction through pain fibers - pain is a subjective experience that should be respected, nociception can result in pain.
L4.4 (pain) - Explain that descending tracts modulate the pain perception of a painful stimulus
The top down control (raphe nucleus and locus coeruleus) allow inhibition of the sensory cells in the dorsal horn through NE, serotonin and endogenous opioids released in the synaptic cleft and can bind to pre or post synapse to hyperpolarize the sensory neuron (can also excite an inhibitory interneuron)
L4.7 (vision) - Describe the five major excitable cell types in retina and their synaptic connections
Photoreceptors: Cones & rods - cones are for color vision (3 types: red, green and blue) and high acuity vision found primarily in the fovea. Rods are more sensitive due to convergence (many rods synapse onto one bipolar cell) to light than the cones but can’t show color, found in the periphery (discs are closed in the outer segment)
Bipolar cells can be “on” (mGlu - fires for light) or off (AMPA - fires in the dark). They get input from photoreceptors)
Horizontal cells support transmission and influence synaptic integration between the photoreceptors and the bipolar cells
Ganglion cells are known to be the first cells to fire APs, leading out the signal to the optic nerve. The “p” (petite) subtype is found in the fovea, the “m” (mega) subtype in the rest of the retina.
Amacrine cells support transmission and influence synaptic integration between the bipolar cells and ganglion cells
L4.7 (vision) - Explain phototransduction (molecular steps from photon absorption to photoreceptor hyperpolarization)
Within the discs, you have the rhodopsin (the photopigment of rods) where you will find retinal in the 11-cis form. When light hit this, it will become alt-trans. The G-protein transducence is in it’s inactive bound to GDP. However, when it becomes active, GDP is exchanged for GTP. transducence is activated by the change in retinal. The GTP takes the alpha subunit of transducence and activates a phosphodiesterase in the disc membrane. The phosphodiesterase hydrolyzes cGMP to GMP. Normally, cGMP holds the sodium channel open (why we have depolarization at rest), but when light hit the rods, these molecular processes removes cGMP and the channel closes. The many steps allow for amplification and therefore fast acting of the closure of channels.
The continued depolarization at rest of the cell allows for glutamate to be released until a bright light is present.
To return, the activated rhodopsin is phosphorylated by rhodopsin kinase, which enables protein arrestin to bind to rhodopsin (block the ability to activate transducence). We hydrolize transducence turns it off, and without it, the phosphodiesterase also turns off. Retinal is returned to its 11-cis state and in the dark more cGMP is being build up.
L4.7 (vision) - Describe the distribution of rods and cones in the retina
In the fovea you only have cones, more rods in the periphery - cones get larger receptive fields the less there is
L4.7 (vision) - Define a receptive field and describe center-surround receptive fields
The receptive field of a sensory cell is the area in which stimulation changes its signaling activity, reflected as excitation or inhibition.
The center surrounding receptive fields belong to bipolar and ganglion cells, which gets projected to the LGN
These receptive fields are the best way to create contrasts - the firing of the cells will depend on how much of the plus is being hit by light vs minus
L4.7 (vision) - To describe the trichromatic theory and the most common forms of color blindness
The idea is that the 3 color that the cones can detect can create all colors - if there is a cross over of genes during mitosis, you might end up without the gene for one of the cones, which could lead to color blindness. The gene that most often gets left out in cross over is for red and green, which is why that’s the most common. The red cone is missing for those that have the red/green color blindness. Men have higher risk of color blindness, as the mutations are recessive and many of these (including the red cone) are on the x chromosomes.
L4.7 (vision) - To explain retinal circuits for light/dark discrimination, including ON-center and OFF-center neurons
The molecular pathway for the question above shows, that when light hits retinal, it goes from 11-cit to all-trans and cGMP become GMP and the ion channels close, meaning that less glutamate is released as a result of light hitting the photoreceptor
For the on-cells, we will have inhibitory receptors (the decrease in glutamate will cause disinhibition of cells there in the dark are inhibited by glutamate) glutamate release from on-center bipolar cell to the on-ganglion cell to indicate that there is light on the center
For the off-center cells have AMPA receptors, so a decrease in glutamate will lead to a decrease in activation decrease in signaling to the off-center ganglion cell to signal that there is light in the middle
Opposite is true for less light
This also explains why there is less signaling in the resulting V1 cells when the entire receptive field is covered by light vs just the center.
Horizontal cells support the lateral/surround inhibition of the on-center photoreceptor cells if there is also light in the surrounding to give a higher contrast image in the end. Here we see that the activation of one photoreceptor can cause the horizontal cells to inhibit others to better detect edges in the environment and give sharper contrast
TLDR: the horizontal cells provide signal integration and lateral inhibition of photoreceptors to improve the contrast.
L4.7 (vision) - Describe the central pathways from retina to the primary visual cortex
L4.7 (vision) - Describe the organization of the primary visual cortex, including orientation and dominance columns
The orientation columns through all 6 layers will all preferentially respond to lines in a certain orientation. The final pattern will depend on the firing of many columns to understand how the lines in our visual fields are orientated. Ocular dominance columns are stripes of neurons in the visual cortex that respond preferentially to input from one eye or the other.
Responses in V1 are stronger when we pay attention to them. We also have evolutionary expectations to visual stimuli e.g. four-legged animals are expected to move along their body axis and not to the side.
L4.7 (vision) - Describe the concept of the ventral stream and the dorsal stream (ventral and dorsal pathways)
Ventral stream (“What”)
- leads from V1 to the inferior temporal lobe. Includes area V4
- concerned with high-resolution form vision and object recognition
- “Vision for perception”
Dorsal stream (“Where”)
- leads from V1 to the parietal lobe. Includes area MT
- concerned with spatial aspects (motion, positional relations between objects)
- important for guiding movements (“vision for action”)
L4.8 (Auditory) - To explain the role of the inner ear with inner and outer hair cells, basal membrane, endolymph and perilymph in auditory function
Inner ear: stapes kicks the oval window pushes the liquid waves in the perilymph will moves the vestibular membrane moves the basilar membrane pushes the inner hair cells up against the tectorial membrane inner hair cells will open their K+ channels, which leads to depolarization ca2+ channels open NT (glutamate) is released auditory nerve create AP to go the auditory nucleus
Outer hair cells also play a role in audition, but when they fire, they contract like muscles and move the tectorial membrane to increase firing of inner haircell
Endolymph: K+ high liquid - perilymph is NaCl (low K+) hair cells will repolarize in the body of the cell, as the body of the cell is in the perilymph area and the endolymph is in the sterocelia part.
Longer waves travel further - only long waves (low freq) are able to osscilate the basilar membrane further down the cochlea.
Width of cochlear and stiffness decides what frequencies it will respond
L4.8 (Auditory) - To describe how sound is transformed into electrical signals in the nervous system.
Top of the stereocilia gets bend (they’re connected by adhesion molecules) the inner hair cells have to be moved towards the kinocilia, the tips are stretched and the hair mechano-electoral transduction channels are opened and k+ flows in from the endolymph. The graded potential’s size relies on the level of the bend. The k+ influx triggers ca2+ channels, which triggers glutamate release to the afferent nerve (auditory nerve), which holds the spiral ganglion, and makes an AP that propagates down the nerve
L4.8 (Auditory) - Describe active amplification and attenuation in the auditory system
Amplification: outer ear catches sound and funnels it in the inner ear is smaller, so the pressure per cm2 is larger - the 3 bones in the middle ear also amplifies the signal
The outer hair cells also help by moving the tectoral membrane more, so the inner hair cells get more active (the outer hair cells can also get efferent input that can modulate sensitivity selective hearing)
Amplification is 36 db
Attenuation: the jump from air to liquid decreases the signal (30 db). We also have muscles that can stop the ossicles from beating super hard on the oval window to stop damaged in case of surprising loud noises
L4.8 (Auditory) - Describe auditory pathways and central processing, including localization of source and frequency
Auditory nerve –> cochlear nuclei in the medulla –> bilaterally superior olive –> nucleus of the lateral lemniscus –> inferior colliculus –> MGN of thalamus –> A1
A1 is tonotopically organized (low frequencies anterior) - Wernickes area is nearby
Encoding is based on firing frequency of inner hair cells and the number of inner hair cells firing
Localization happens in the superior olive, based on delay of the sound (medial! only works on lower frequencies, as the frequency of firing can’t be quicker than the speed of the AP - interoral phase delay) or intensity of the sound (lateral), which will be louder for the closer ear (you can also have a sound shadow created by your head). Lateral SO has contralateral inhibition thorough MNTB
L4.8 (Vestibular) - Describe the role of the otolith organs and semicircular canals in vestibular function
Helps the body understand movement and rotations and can help us adapt through the VOR, VCR and VSR reflexes
The Otolith organs: Sacculus and utriculus sense linear acceleration / force
The saccule is for back and forth and a little up and down
The utricle is more the lateral but a little up and down
The tonic firing is modulated if the hair cells bend towards the kinocilium (for all vestibular system) - crystals will sense the movement and tilt to move the hair cells
Semicircular canals will sense rotations (3 for each of the planes)
Cupula has the hair cells inside (is a membrane) - endolymph is surrounding the hair cells the combination of the 3 canals will help us understand the direction
L4.8 (Vestibular) - Describe the central vestibular pathways to explain the vestibulo-ocular reflex
Vestibular information is used for:
1) Postural control together with proprioception and vision
2) Control of the position of eye in orbitae and head for visual
stabilization / compensation of head and body movements
Nystagmus: Rapid and uncontrollable eye movements
VOR:
important function of semicircular canals at the bottom, there is an illustration of each canal - here there is one for the horizontal plane. When the head moves, the eyes make a countermovement to keep your eyes stuck
L4.10 (Chemical) - Describe the sensory receptors and layout of the olfactory system
Receptors are odorant receptors (400 types), which is g-protein coupled - will respond to odorants, but only one receptor type is found per neuron (otherwise we couldn’t determine which input meant what). Combinatorial coding allows us to detect over 100K smells with only 400 receptors, showing that they’re broadly tuned.
Transduction cascade
Odorant binds to the receptor Golf detaches and will activate ACIII ACIII transform ATP to cAMP –> activates the cAMP channel –> entry of ca2+ –> ca2+ activates the cl- channel –> cl- goes out of the cell. Normally there is more cl- outside, but these cells store cl- to have a gradient.
adaptation is important - you stop smelling things over time - this is mediated by calmodulin, which combines with ca2+ and will lower the affinity of the cAMP gated channel, so less ca2+ can enter the cell
Odorants hit the olfactory receptors at the olfactory epithelium. These cells project to the Glomerulus in the olfactory bulb (olfactory nerve), which is a spherical neuropil, where these neurons will project to the mitral cells in the olfactory bulb. These axons project to the cortex through the lateral olfactory tract.
NB: each olfactory receptor cell project to 2 Glomerulus
Projections from the olfactory bulb can go to the pyriform cortex and from there to the orbitofrontal cortex goes around the thalamus and might therefore not be consciously processed
L4.10 (Chemical) - Describe the sensory receptors and layout of the taste system
Sweet, umami, bitter, salty, sour
On the tounge we have papilla. In these round structures there are clefts, where you taste taste buds, that contain taste cells. Here the receptors are in the microvilli, and the afferent gustatory axons gather in the papilla and move down. The basal cells are the stem cells to replace the tastebuds. Each taste cell is specific for one type of taste, but different taste cells can be present in one tastebud.
the receptor is different in the beginning, the process is the same –> g portin activate phospholipase C –> breakdown Pip2 to DAG, H+ and IP3 –> Ip3 opens the iP3R3 trigger ca2+ to enter cytoplasm from the stores in the cell –> ca2+ triggers na+ channel to open and allow na+ into the cell –> trigger voltage depended ion channel that lets ATP out
ATP and seretonine is the NT (not still clear)
When considering the cation channels (sour and salty), the na+ (salty) or H+ (sour) influx will activate voltage-gated Na+ and Ca2+ channels leading to the release of neurotransmitter (ATP) at the basal synapse with afferent nerve
Taste cell facial (7), glossophoringial (9), vagus (10) nerves (with cells) NTS VPM of the thalamus insula/frontal
L4.11 (Plasticity) - Describe sensory plasticity and critical periods in sensory system development
Sensory plasticity is the sensory systems ability to change its responses and connections internally or externally (one system can change within). It can rely on the Hebbian principle, which is what fires together wires together. Generally, we the number of synapses increasing until the age of 11. After this, there is a sharp decrease due to synaptic pruning. The synapses are formed to enable us to adapt to any space. After this, what is not used gets lost (use it or lose it).
You can also have non-Hebbian plasticity, e.g., by the axonal initial segment moving based on frequent stimulation.
Critical periods are the periods where the sensory system forms. For vision, we known that there is ocular dominance, which creates a competition for CNS targets. This is seen when shutting the eye of a cat, the other eye will take over the cortical space.
Later in development, we see plasticity e.g. for the somatosensory areas when a finger is lost (cortical space is taken over my other fingers) or when a limb is used more (gains more cortical space). It seems that myelination also increases with activity, which is another plastic mechanism.
L4.1 - Describe the afferent pathways of vison
L4.1 - Describe the afferent pathways of hearing
L4.1 - Describe the afferent pathways of olfaction
L4.1 - Describe the afferent pathways of the VOR
L4.1 - Describe the afferent pathways of taste
