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 Perception: Conscious interpretation of the environment around you

 Prior experiences
 Senses
 Psychological being
 Sensory receptors detect information in the periphery to the CNS
 Visceral receptors
 Detect and relay information from the internal environment
 Not conscious
 Examples: baroreceptors, chemoreceptors, mechanoreceptors
 Visceral receptors transmit info the CNS by visceral affarents
 External sensory receptors
 Detect and relay information from the external environment
 Information reaches consciousness and is perceived
 Ex: nociceptors, thermoreceptors
 Law of specific nerve energies: a given sensory receptor is specific for a particular
modality (the energy form of a stimulus). The modality to which a receptor responds
best to is an adequate stimulus

 Sensory Transduction
 The conversion of stimulus energy into electric energy
 Receptor or generator potentials
 Graded potentials
 I/o being due to neurotransmitters causing post synaptic potentials, it's
caused by opening or closing of ion channels
 Triggered by sensory stimuli
 If the receptor potential exceeds threshold, it can generate an action potential
 Sensory receptors: two types
 Specialized structure at peripheral end of afferent neurons
 Opening/ closing ion channels
 Sensory receptor as a separate cell communicating with afferent neuron
through chemical synapses
 Stimulus opening a calcium channel, causing neurotransmitter to be
released in cleft, action potential
 Changes in the receptor cell's membrane potential cause release of a
chem messenger or a transmitter, the greater the excitatory stimulus,
the more transmitter is released. The transmitter then binds to
receptors on the afferent neuron & causes change sin the membrane
potential of that cell. If the afferent neuron is depolarized to threshold,
an action potential is generated and transmitted by that cell to the CNS
 Receptor adaptation
 Receptors become adapted to the stimulus if you were to continuously stimulate
that receptor
 Slowly adapting receptors (tonic receptors) : Receptor potential that is initially
created decreases even though the stimulus remains the same
 Ex: stretch receptors in the muscles & merkel's disks which detect pressure on
skin
 Rapidly adapting receptors: very rapidly adapts and becomes insensitive to
continuous stimulus
 Off response occurs when you remove the stimulus, brief hyperpolarization
 Ex: olfactory receptors & pacinian corpuscles which detect vibration
 Sensory pathways
 Labeled lines: specific neural pathways transmitting information of a specific
modality
 Activation of a specific pathway causes perception of the associated modality
regardless of which stimulus actually activated the pathway
 Sensory unit
 Single afferent neuron plus all receptors associated with it
 All receptors are of same type
 Receptive field: if you have stimulus anywhere in this area you will stimulate this
sensory unit
 Helps to localize where the stimulus is coming form
 Generalized pathway: receptive fields apply to first, second, and third order neurons
 1st order neuron in PNS, the rest are in CNS
 2nd order neurons transmit to thalamus
 3rd order neurons transmit to cerebral cortex
 Sensory areas: visual cortex, somatosensory cortex, gustatory cortex, visual cortex,
olfactory cortex, auditory cortex (don't really need to memorize but have overlap
with certain lobes)
 Sensory Coding
 Coding for stimulus type
 Receptor activated by stimulus and brain often integrates information from
different sensory systems
 Ex: wetness
 Ex: latex glove and stick it in a bucket of water, mechanoreceptors
perceiving the touch and temperature receptors in the hot or cold water
and you may think that your hand is wet
 Coding for stimulus intensity
 Frequency of action potentials (frequency coding)
 Stronger stimulus, larger receptor potential
 As long as the graded potential/receptor potential exceeds threshold for
an action potential, stronger depolarizations can overcome the relative
refractory period of an action potential and produce a higher frequency
of action potentials
 Stronger stimulus, increase in action potentials
 What is the significance of the downward slope?
 Number of receptors activated (population coding)
 Stronger stimulus activates more receptors (recruitment)
 Can be from same afferent neuron or can be from other afferent neurons
 More receptors activated, the receptor potentials generated can sum, greater
frequency of action potentials
 Coding of stimulus location
 Based on receptive fields (tactile, proprioceptive, & visual)
 Acuity depends on size of receptive field, degree of overlap, and lateral
inhibition
 Afferent neurons: first order neurons
 Second order neurons
 Y1 is stimulated and as it's stimulated it's synapting with inhibitory
interneurons which are inhibiting X2 and Z2 (inhibiting action potentials
in the second order neurons). Neurons X and Z aren't as close. Helps us
figure out where the stimulus is originally from.
 The synapse is occuring at two axons (axoaxonic)
 Acuity is improved by the overlapping of the receptive fields of
different afferent neurons bc overlapping improves the localization via
the fact that nay stimulus that occurs within the region of overlap b/w
the receptive fields of two afferent neurons activates both neurons and
lateral inhibition
 Two point discrimination test
 Ability to perceive two points on the skin
 Smaller receptive fields have more neurons & have greater overlap
 Areas with larger receptive neurons with larger receptive fields won't be
able to distinguish, will interpret it as one pin prick
 Two separate neurons, two separate fields, perceived as two points
 Humonculi
 Two point discrimination threshold: small receptive field, neurons closer
together, take up greater space in brain
 In some sensory systems, localization is unrelated to coding by receptive fields
 These sensory systems code for quality and intensity
 Ex: sound, smell
 Localization is accomplished by time of arrival to receptor
 The systems also rely on behavioral actions
 Ex: smell a firecracker, turn her head towards it to figure out where it's
coming from
 Auditory is more acute than olfactory
The Somatosensory system
Somatosensory receptors
 Proprioceptors, mechanoreceptors, thermoreceptors, nociceptors
 Most are specialized structures at nerve endings
 Free nerve endings lack specialized structures
 Mechanoreceptors: rapidly adapting (vibration) & slowly adapting (pressure)
 Rapidly adapting: hair follicle receptor, meissner's corpuscle, pacinian corpuscle (ex:
vibration)
 Slowly adapting: pressure
 Receptive fields vary greatly
 Thermoreceptors
 Warm receptors: respond to temperature in the range of 30-45 C
 Cold receptors: respond to 5-35C with peak around 20, and after 45C
 Several different types and the channels are also associated with nociceptors as well
and chemical sensitivity
 Free nerve endings
 Transient receptor potential ion channels (TRP)
 Temperature sensitive ion channels
 Can respond to chemical stimuli, and can transduce pain
 Involved in taste, olfaction, vision, visceral responses
 Both warm and cold receptors are rapidly adapting. When temp decreases, freq of
action potentials in axons associated with cold receptors increases sharply then
decliens gradually.
 Axons associated with warm receptors show freqency of action potentials
decreasing sharply when the temp is dropping and increasing rapidly when the temp
returns to its relative resting state
 Nociceptors
 Free nerve endings
 Three types: mechanical, thermal and polymodal (histamine, prostaglandings)
Somatosensory Cortex
 Perception of somatic sensations begin in the primary somatosensory cortex
 Columnar organization: one column-one modality (pressure, vibration, cold etc)
Somatosensory Pathways
 Spinothalamic tract: pain & temp
 Receptors going into the dorsal horn into the CNS and synapsing with the 2nd order
neuron which then travels up to the thalamus to synapse with the third order
neuron
 Dorsal column-medial lemniscal pathway: proprioceptors & mechanoceptors
 First order neuron travels to the dorsal horn, there's a reflex and a collateral that
synapses with the second order neuron in the medulla (crosses to the other side)
and a third order neuron in the thalamus
 Main difference is where the 2nd order neurons are.
Pain
 Produced by tissue damaging or potentially tissue damaging stimulus
 What type of responses does the pain response elicit? Reflexes
 Autonomic responses- inc in bp, hr, blood epiephrine, glucose, dilation of pupils
 Fast pain: A fibers, sharp, pricking sensation, easily localized
 More myelinated
 Slow pain: C fibers, dull aching, poorly localized
 Less myelinated
 Supstance P, CGRP, glutamate
 Glutamate is released from primary afferent neurons, binds to receptors on 2nd order
neurons that ascend to the thalamus via spinothalamic tract.
 Pathways ascend to the reticular formation of the brain stem, hypothalamus, and the
limbic system
Visceral pain
 Pain originating in internal organs
 Sensation referred to body surface
 Ex: arm pain may indicate heart attack
 Occurs because second-order neurons also receive input form somatic afferents (neurons
that are either directly have the somatic receptors on them or coupled with the sensory
receptor)
 Ex: as we have information coming from the heart, we are interpreting that as pain in the
skin
Modulation of Pain
 Gate-control theory: somatic signals of non-painful sources can inhibit signals of pain
 Ex: bee is stinging you and it hurts but when you put pressure and activate
mechanoreceptors that alleviates pain
 Modulation of pain: mechanoreceptors activate inhibitory interneurons that
decrease the signal sent to the thaalmus from the second order neuron
 TENS: transcutenaeous electrical nerve stimulation to treat pain, small current is
applied through the skin overlying a nerve activates large diameter afferents
 Endogenous analgesia system: produced by brain, endogenous opioids (enkephalin)
 Internal mechanism that will reduce pain
 Descending pathways
 Under stress, this system can block pain transmission at the level of the synapse b/w
the nociceptive afferent neuron & the 2nd order neuron.
 Periaqueductal gray matter in midbrain communicates to the lateral reticular
formation and to the nucleus raphe magnus of the medulla. These regions have
neurons that descend to the dorsal horn of the spinal cord and activate inhibitory
interneurons that release enkephalin which blocks the communication by
presynaptic inhibition of substance P release from the nociceptive afferent and
production of IPSPs on the 2nd order neuron.
Vision
 3 layers:
 Outermost: sclera and cornea
 Sclera: white of the eye
 Cornea: outermost transparent structure, allows light to come in
 Middle:
 Chorioid: there's a vascular layer that nourishes the inner layer of the eye,
located beneath the sclera
 ciliary body (focus images by changing the shape of the lens)
 Iris: controls how much light is coming in
 zonular fibers: attached to the ciliary body, and attach the ciliary body to the
lens
 lens
 Pupil: hole in the center of the iris that allows light to enter the posterior part
of the eye, not a structure
 Inner: retina
 Fovea: concentration of the photoreceptors, where light is focused in the
retina
 optic disk: where blood vessels travel through, blindspot
 Retinal pigmented epithelium: located just outside the retina and attached to
the choriod contains a high conc of black pigment melanin which absorbs the
light that strikes the back of the eye
 Fluid filled
 The lens and the ciliary body separate the eye into 2 fluid filled chambers
 Anterior segment: anterior chamber, nourish the lens and the parts of the eye
 Anterior chamber: b/w cornea & iris
 Posterior chamber: b/w iris & lens
 Filled with aqueous humor
 Posterior segment (jelly like)
 Behind the lens & the ciliary body
 Gives the eye structure and firmness
 Vitreous chamber
 Avian eye
 More oval shaped
 Light waves
 Reflection: we perceive light waves reflected off objects
 White is all colors, black is no colors
 Refraction: the bending of light waves as they pass from one medium to another
 Important concept for focusing
 Degree of refraction depends on three factors
 Differences in densities
 Angle of light waves
 Curve of the transparent surface through which light passes (lens)
 Concave spreading, convex focal point
 Cornea vs lens
 Cornea: has greater refractive power than lens, corneal refraction is constant, lens
can adjust to focus
 Lens is less flexible with age
 Lasik: reshape cornea
 Accommodation: increasing lens curvature enables the eye to focus on near objects
 Viewing a near object: lens is convex and it can diverge light rays so it focuses
back on the fovea
 Distant objects: weak refraction focusing the light at the fovea
 Under parasympathetic control
 For far distant objects, lens is flatter, no parasympathetic stimulation, ciliary
muscles relaxes so zonular fibers pulling tight for the lens to be flat
 Focusing: parasympathetic signals, ciliary muscles contract, zonular fibers slap
(relax) so lens becomes more convex shape
 Vision
 Distant object: lens is focused on the retina, no accommodation, the lens is not
adjusting
 Near object: the lens needs to change the refraction of the light to focus on the back
of the eye, accommodation
Clinical defects
 Myopia: nearsighted
 lens of the eye is too strong for length of eyeball so it bends lightwaves too much
 Can see near objects without accommodation
 Light from distant objects is focused in front of the retina --> blurred
 Myopia is corrected with concave lens (scatters lightwaves), which decreases the
overall refractive power so the light is focused on the retina. Corrective lenses are
compensating for what the biological lens aren't able to do.
 With this correction, distant objects will be in focus w/o accommodation and
near objects need accommodation
 Hyperopia: farsighted, lens of eye too weak for length of eyeball
 The eye can focus on distant objects with accomodation but the lens can't increase
accomodation enough to adjust for near vision so the light from near objects comes
to focus behind the retina
 Convex lens correct it by increasing overall refractive power, causes light to
converge before reaching the eye. The eye can see distant objects w/o
accomodation to enable seeing it w/ accomodation.
 Hyperopia and myopia possibly bc the muscles aren't working properly?
 Eye strain: causes muscles to be contracted for too long
 Maybe football shape of the eye (retina)
 Ciliary muscles not working so well?
 Myopia: too spherical, muscles in the eye are too tense
 Presbyopia: hardening of the lens
 Makes accomodation for near vision much more difficult
 Cataract: discoloration of lens
 Glaucoma: increased volume of aqueous humor
 Damage to retina and an put pressure against the optic nerve --> could lead to
blindness
 Can distort the shape of the cornea & shift the position of the lens --> compress
optic nerve, reduce blood supply
 Astigmatism: irregularities of lens or cornea, erratic bending of light waves

Regulating the light entry into the eye (iris)


 Pupil size determines how much light reaches retina. The size of the pupil is controlled by
the iris.
 Iris consists of two layers of smooth muscle
 Outer radial muscle: dilator
 Sympathetic stimulation of radial muscle
 Open the pupil, let more light in
 Inner circular muscle: constrictor
 Parasympathetic stimulation: makes the muscles contract
 Makes pupils smaller
Retina
 Neural tissue
 Contains photoreceptors
 Three layers
 Light comes in and hits the back of the retinal wall, there are cones and rods attached to
the retinal wall and bipolar cells and ganglion cells
 Amacrine & horizontal cells: lateral inhibition, moderate the singals as they go through
 Optic nerve: blind spot
 Macula lutea: small indentation around the fovea, an area where there is an absence of
blood vasculature because it allows the light to come through a little bit better so the
photoreceptors are getting as much light as possible. Bipolar & ganglion cells are laterally
displaced creating a depression in the center of the retina.
 Macular degeneration: degeneration of this area
 Dry: macula just degenerates (photoreceptors degenerate)
 Wet: angiogenesis, inappropriate growth of blood vessels --> loss of vision
 Diabetes
 A person with this loses high acuity central vision but maintains peripheral vision
 Retinitis pigmentosa: degeneration of photoreceptors in the peripheral retina, tunnel
vision, no peripheral vision/night vision
 rods & cones
 Rods: vision in dim light
 Many more rods than cones
 Cones: high acuity color
 But we see better in day light bc high acuity and concentrated in the fovea
 Depending on where you are in the eye, different concentrations of rods and cones
 No rods at the fovea, and highest concentrations of cones at the fovea
 See color, fovea is less useful in the dark
 If you want to focus on an object in the dark, look to the side or above etc not
directly
 Optic disk: no receptors, blind spot
Phototransduction
 Conversion of light energy to electrical energy
 Accomplished by rods and cones
 Light is absorbed by photopigments
 Each has retinal and opsin
 Opsins for rods: black & white
 Rhodopsin
 Opsins for cones: color
 L opsin: red
 M opsin: green
 S opsin: blue
 Each absorb at different wavelengths
 Components of rods
 Composed of disks which have photo absorbing pigment in it
 State of photoreceptor in the dark
 cGMP levels high in the cytosol
 Sodium channels are open
 Sodium enters the cell, causing a depolarization (not an action potential) that
spreads from the outer segment to the terminal
 Calcium channels open in response to depolarization
 Calcium enters the cell, triggering exocytosis of transmitter
 Transmitter causes graded potentials in bipolar cell
 Responses of photoreceptor to light
 Light is absorbed by photopigment
 Retinal and opsin dissociate (leaving bleached opsin, photoreceptors become less
sensitive to light)
 Transducin is activated so alpha subunit breaks off
 Phosphodiesterase is activated
 cGMP levels in cytosol decrease
 Sodium channels close
 This is where the potassium channels are important. Potassium channels are
hyperpolarizing the cell, the channels are open the potassium is flowing out.
 With less sodium entering the cell, the cell hyperpolarizes
 Calcium channels close
 Transmitter release is decreased
 Graded potential in bipolar cell gets smaller
 *** Light is inhibiting the release of neurotransmitter release
 Not an action potential, it's graded. Even when hyperpolarized still releasing
neurotransmitter.
Rod and Cone Sensitivity
 Rods
 Scotopic (monochromatic) and mesopic vision
 Sensitive in dim light
 In bright light rods become saturated, completely bleached, hyperpolarized as
possible & can't code for any additional brightness
 Cones
 Mesopic (both rods and cones) and photopic vision
 Require bright light
 Many more rods but cones have higher acuity and concentrated in the fovea so we see
better in day light
 Seeing colors
 Each type responds best to its color
 More than one type of cone is necessary to distinguish colors
 The brain discerns colors by comparing responses of different cone types
 Opponent process theory: stimulation of one color inhibits the other (can't see
reddish green)
 Red/green
 Blue/ yellow
 Black/white
 Color blind glasses: they help to filter the areas of overlap so the brain can differentiate
better
Circadian rhythms
 Photoreceptors are intrinsically photosensitive retinal ganglion cells (ipRGCs)
 Use melanospin as photoreceptor
 Optimum wavelength is blue light
 Link to rhythm-generating center of the brain
 Communicating in the pineal gland
 Horses are seasonal breeders, shut off reproductive systems in the winter time, gestation
is 11 months , wouldn't want offspring being born in the winter
Bleaching of photoreceptors in light
 Going from light to dark
 Exposure to light "bleaches" the rods
 Most of the rhodopsin has absorbed light and the opsin is in its active form
 Opsin separated from retinal
 No more light can be absorbed
 Move to dark
 Sensitivity of rods is low due to previous bleaching
 Retinal and opsin reassociate (can again detect light) (unbleaching)
 Going from dark to light
 Exposure to dark maintains rods in most sensitive state
 Opsin and retinal are associated
 Readily absorb light
 Move to bright light
 Sensitive rods are overwhelmed
 Rods begin to be bleached
Neural processing in the retina
 Convergence
 More than one photoreceptor to bipolar neuron
 More than one bipolar cell to ganglion cell
 Rods converge more
 Lower visual acuity
 Greater sensitivity (greater convergence, greater sensitivity to light bc of spatial
summation of inputs from several photoreceptors onto one bipolar cell)
 In fovea (predominantly cones)
 Less convergence
 One cone communicates with one bipolar cell
 Greater acuity
 Lower sensitivity
 Bipolar cell receptive fields
 Glutamate
 The action of the ligand is dependent on the receptor
 Stimulatory at inotropic receptors (cation channels)
 Inhibitory at metabotropic receptors (g proteins)
 Release is high in the dark
 Center receptive fields: direct input from photoreceptor to bipolar cells
 Bipolars inhibited by glutamate are excited by light
 ON bipolar cells because they turn on to light
 Bipolars excited by glutamate are inhibited by light
 OFF bipolar cells bc they turn off to light
 Surround receptive fields: indirect input form photoreceptor to bipolar cells
Bipolar cells are capable of transmitting graded potentials but not action potentials.
Ganglion cells can transmit action potentials and their axons make up the optic nerve and
serve as the output neurons of the visual pathway.
 Neural pathways for vision
 Optic chiasm: half of axons from each eye to contralateral cortex
 all input form one visual side is processed on contralateral cortex
 Parallel processing in the visual system
 Parallel pathways transfer different types of visual information
 Color, shape, movement
 Depth perception
 Binocular visual field
 Brain constructs 3-D image
 Predators: eyes on front, allows for greater overalp b/w left and right visual fields
 Preys: eyes on sides, determine if something is chasing them
Vision
 Compare the amount of cortical real estate between the fovea/macula and the peripheral
visual field?
 Fovea takes up more space

Hearing
 Sound waves: air molecules put into motion
 Compressed or rarefied
 Rarified waves is how you determine frequency
 Pitch: frequency
 Hertz: waves per second
 Can hear from 20-20,000 HZ, greatest sensitivity b/w 1000 & 4000 Hz
 Ears have the ability to hear in certain frequency ranges
 Loudness: proportional to the density of molecules during compression or rarefication
 How densely are the molecules being compressed?
 Greater the difference in densities, louder the sound
 Middle ear: ossicles
 Middle ear is air filled
 Eustachian tube: regulates pressure, allows for change in air pressure to not affect the
 When you're sick it's clogged
 Sound is amplified in the middle ear
 Stapes terminates at the oval window at the cochlea
Signal Transduction for Sound
 Conversion of sound energy into action potentials
 Occurs in the cochlea of the inner ear
 Cochlea is fluid filled
 3 compartments along the cochlea separated by membranes
 3 sections of fluid
 Basilar membrane, tectorial membrane, vestibular membrane
 Soundwaves traveling in fluid, they bump against the membrane in cochlea, and bending
the hairs on the cilia
 The cilia are immersed in high potassium concentrated fluid
 Stereocilia have mechanically gated K+ channels
 Potassium channels on tips of the cells and connected by bridges
 As they bend, the force causes potassium channels to open
 Influx of potassium
 Open voltage gated calcium channels
 Depolarization triggers exocytosis
 When it bends the other way we have a decrease in exocytosis
 Hair cells bend in opposite direction and the direction of the bend helps determine
frequency
 Intensity coding: loudness (amplitude)
 Based on degree of deflection and opening of ion channels in stereocilia
 The direction of the bend determine frequency but the intensity of the bent which
causes the increase in potassium channels opening determines the loudness
 Frequency coding: pitch
 Based on the location on the basilar membrane where deflection occurs
 Hair cells closer to the oval window, higher pitch
Neural pathways for sound
 Cochlear branch 8th nerve
 Cochlear nuclei in medulla oblongata then hops into other nuclei and the cortex
the Ear and Equilibrium
 Vestibular apparatus
 Located in the bony labyrinth
 Detects acceleration of the body
 Similar fluid as in cochlea
 Detection of movement
 Anterior: yes
 Posterior: head to movement
 Lateral canal: no
 Utricle and saccule: acceleration
 Semicircular canals: detecting rotation
 Has hair cells like cochlea , endolymph, has cupula- geleatin like structure and
the cilia are embedded into that, don't have protein bridges
 As the cupula moves it's bending all of the cilia
 Detecting changes in the rate of rotation
 Turn our head, acceleration to the right or left and cause an increase or
decrease in action potentials
 Has to do with the direction of bending
 Linear acceleartion
 One flat genlatinous layer and otoliths (mineral deposits) that add weight to
the structure
 Utricle: detects forward and backward motion
 Saccule: detects up and down motion
Neural pathways for equilibrium
 Input from sensory systems that help with our perception
 Vestibular nuclei provide feedback control of movement for balance and eye movements
 Multiple sensory inputs contribute to balance

Gustation
 Tate buds, more than 10,000
 Tongue, roof of mouth, pharynx
 50-150 taste receptors per bud
 It's important that the pore be exposed to saliva to conduct
 4 primary tastes with different transduction mechanisms
 Sour & salty: action through ion channels
 Sweet & bitter: ligands, G protein coupled receptors
 Umami: amino acids, action through GPCRs
 Different mechanisms involved for depolarization
 Each taste receptor cell can respond to all four primary taste
 But they respond to one taste more than others
 Different types of receptor cells located within a taste bud
 Some differential distribution
 Coding of taste is complex, impacted by sense of smell
 Neural pathways for taste (not too important)
 3 major nervous pathways going into the solitary nucleus in medulla oblongata
 Travels ipsilateral to thalamic nuclei and the gustatory cortex

Olfaction
 Receptors communicating through the cribriform plate
 Receptor cells are neurons themselves, not communicating neurons.
 These are affarent neurons, specialized nerve endings
 Basal cells: will eventually become receptor cells
 The nose recycles its receptor cells
 Bowman's gland: makes mucus
 In order to have odors bind to the cilia we need the mucus layer
 Neurons synapse in the olfactory bulb
 Synapse with the glomeruli with the mitral cells which can synapse with multiple receptor
neurons at multiple different sites --> variety of cells
 Cilia project into mucus, have chemoreceptors
 Hydrophilic molecules diffuse through mucus
 Hydrophobic molecules bind to olfactory binding proteins
Signal transduction:
 chemical binds to the receptor and activates Golf, adenylate cyclase catalyzes cAMP which
directly binds cation channels, depolarization occurs (Na+ and Ca2+ channels)
 Calcium is also opening chloride channels, which is further depolarizing the cells
 One of the important implications of the calcium channels
 Specificity of binding
 Specific olfactory receptor cells exist for each type of odorant binding protein
 1000+ genes have been identified that code for olfactory receptors
 Neural pathway for olfaction
 Multiple olfactory neurons communicate with each mitral cell
 8000 glomeruli per olfactory bulb
 Smell perception depends on the pattern of receptor neuron activation
 Neural pathway
 Olfactory tract leads to the olfactory tubercle which terminates in olfactory cortex
and limbic system
 Axons of the olfactory neurons: olfactory nerve
 Olfactory tract is the signals that are coming from the bulb up to the olfactory cortex
 Dogs have a highly bony structure, multiple folds, increases surface area so allows for a lot
more receptors and a lot more information to be detected
 Pattern for air flow in the nose

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