Unit 3b - Special Senses

Olfaction

the only sensory modality that does NOT go to thalamus first and does NOT cross the midline

the only special sense where the sensory cell is the neuron itself that carries information to the CNS

way more important as a sense in other species since it’s closely linked with taste, emotion, memory

Olfactory Receptor Neurons

bipolar neurons that are replaced about 60 days (neurons are never replaced nor divide except for these)

• dendrites end in non-motile cilia expressing odorant receptor proteins

• axons go through gaps in cribiform plate; synapse on 2nd order neurons

odorant receptor proteins are GPCRs, one of the largest gene families in vertebrates

Olfactory Quality

each olfactory receptor neuron expresses only one type of odorant receptor protein (GPCR) but each receptor can recognize more than one odorant AND each odorant can stimulate more than one receptor

subsequent processing en route to olfactory cortex in combination with 100s of other olfactory neurons is then interpreted as a particular odour

Receptor Codes and Perception

octanol smells fruity and floral but octanoic acid is rancid → changing a functional group changes a lot about how we perceive the smell

Linda Buck nobel for the receptor perception chart

Gustation (Taste)

combination of 5 basic tastes: sweet, sour, salty, bitter, umami

taste receptor cells are non-neural epithelial cells that release signal onto primary afferent neuron and frequently come into contact with noxious chemicals

the map of regions of tongue for different tastes is a myth

Taste Buds

number per papillae depends on type

each taste bud has 50-150 taste receptor cells

supporting epithelial cells secrete fluid into lumen of taste pore

How many receptor cell types are there for each taste?

1; 4/5 tastes only express one but bitter receptors are generic with lots of GPCRs to detect the range of bitter flavours

Taste Transduction

sweet, umami, and bitter ligands bind to GPCRs and ultimately release ATP as the signalling molecule

1. ligands activate taste receptor cell

2. various intracellular pathways activated

3. Ca2+ signal triggers exocytosis or ATP formation

4. neurotransmitter or ATP released

5. primary sensory neuron fires to send APs to brain

Transduction of these two tastes is poorly understood.

sour and salty

Taste Pathway to Brain

travels via various cranial nerves to medulla → thalamus → gustatory cortex → integrated with smell

Anatomy of the Ear

• external ear canal

• tympanic membrane aka eardrum vibrates

• sound is transduced by malleus, incus, and stapes

• oval window

• vestibular apparatus does equilibrium

• cochlea is the sensory structure

A longer wavelength of a sound wave means what?

lower frequency and therefore lower pitch since less wavelength/time

Sound Transmission Through the Ear

1. sound wave reaches tympanic membrane from air-filled external canal

2. vibrates bony ossicles

3. transduced through oval window

4. fluid-filled compartment (vestibular duct filled with perilymph) vibrates to make fluid wave

5. cochlear nerve

Cochlea

perilymph found in vestibular duct and tympanic duct is similar to plasms (high sodium low potassium)

endolymph in cochlear duct is similar to intracellular fluid (low sodium high potassium)

• cochlear duct contains Organ of Corti with sensory hair cells and support cells

The tips of hair cells are stuck in the ____ _____ to increase the chance of being bent.

tectorial membrane so that pressure wave of fluid is felt

Do hair cells for equilibrium have directionality?

yes; when fluid pushes in one direction, more channels open and cation entry depolarizes cell to increase AP frequency

when hairs bend in the opposite direction, channels are closed and less cation entry hyperpolarizes the cell for no APs

Place Code Hypothesis

sound waves trigger activity at different places along the cochlea’s basilar membrane and are perceived as different pitches - tonotopic map

• wave travels along cochlea, hair cells in the area that bend the most at a given frequency encode that pitch

• basically the labelled line based on which hair cells are stimulated

based on anatomy of ear

Temporal Coding Hypothesis

frequency of sound wave determines frequency of APs travelling along auditory nerve, perceived as pitch

e.g. low frequency sound → slow waves along basilar membrane → low firing rate of primary afferent neurons → perceived as low pitch sound

problem with this idea is we can hear sounds up to 20k Hz but no neuron can transmit this fast

Current Hypothesis of Coding for Pitch

multiple neurons with staggered firing rates carry the temporal code - pooled neural response interpreted as pitch (convergence)

place coding (hair cells along basilar membrane are stimulated) also plays a role

relative importance of place and temporal coding depends on pitch

Neural Pathways for Auditory Information

sound waves reach both cochleas

• travel to cochlear nuclei via cochlear branch of vestibulocochlear nerve

• cerebellum

• right and left thalamus

• right and left auditory cortices

Conductive Hearing Loss

no transmission through either external or middle ear due to issues with earwax or fluid in middle ear

can usually be repaired

Central Hearing Loss

damage to neural pathway between ear and cerebral cortex or damage to the cortex itself

uncommon but occurs in stroke

Sensorineural Hearing Loss

damage to structures of inner ear like death of hair cells due to loud noises

common in both young and elderly; hair cells can be replaced in other vertebrate groups but not mammals

Equilibrium - Vestibular Apparatus

dynamic component - movement of body through space

static component - position of head

integrated with information from other sensory systems like muscle and joint proprioceptors and visual information

detected by hair cells lining fluid-filled chambers (otolith organs - utricle and saccule for linear acceleration and head position; semicircular canals for rotational acceleration)

Cristae

hair cells grouped here, within ampulla of canals, detect spin (rotational acceleration) for equilibrium

Maculae

in utricles/saccules

otoliths are crystals that move in response to gravitational forces (sit on top of mass to increase the chance of it bending)

utricle detects forward/backward acceleration, saccule for vertical acceleration

Neural Pathways for Equilibrium

goes from vestibular branch of vestibulocochlear nerve to cerebellum, NOT thalamus

cerebellum is the primary center for equilibrium

Gross Anatomy of the Eye

canal of Schlemm is similar to CSF and catches fluid in aqueous humour

optic disk is the blind spot where the optic nerve and blood vessels leave the eye

optic nerve is where afferent info goes

lens bends light to focus on the retina

Neural Pathways for Vision - Dorsal

optic tract: bundle of axons in CNS

optic chiasm: crossing over point

optic nerve: bundle of axons in PNS

Pupillary Light Reflex

control of pupil diameter according to intensity of light

non-visual, autonomic reflex where:

• detector = photoreceptors in retina

• afferent = afferent neurons travelling in optic nerve

• integrating center = thalamus/brainstem (midbrain)

• efferent = motor neurons travelling in occulomotor nerve

• effectors = smooth muscles regulating pupil diameter (sphincter constriction or radial dilation)

light in eyes → optic nerve → optic chiasm → optic tract → thalamic relay → midbrain

Phototransduction

conversion of light into changes in membrane potential by photoreceptor cells in retina (rods or cones)

• special population of ganglion cells that mediate pupillary light reflex, circadian/seasonal rhythms

Cellular Organization of Retina

all vertebrates have inverted retina

light goes through ganglion cells, then bipolar cells (both are neurons where signals from rods and cones are integrated) and then rods and cones

photoreceptors (rods and cones) don’t make APs even though they’re neurons; only ganglion cells do

Fovea

is a dent in the retina for better access to photoreceptors

made of almost all cones

very low convergence; super sensitive spot where pigment epithelium absorbs excess light

outside of fovea there is convergence with a high chance of AP but low resolution

Peripheral Retina vs. Fovea

peripheral retina has mostly rods, monochrome, high convergence, high sensitivity, low resolution

fovea: all cones, low convergence, small receptive fields, low sensitivity, high resolution

Pendred Syndrome

autosomal recessive mutation in gene that codes for pendrin protein which is a transmembrane anion exchanger in ear, thyroid, kidney

loss of this in rodents causes abnormal composition of endolymph, deterioration of stria vascularis, abnormalities in inner ear structure, hearing loss

Retinal

rhodopsin is GPCR where retinal absorbs a photon to change its shape, dissociate, and activate GPCR

• in resonse to light 11-cis retinal goes to all trans retinal

in the dark: cGMP is high, CNG channels are opened by cGMP, there is tonic release of glutamate

in light: retinal absorbs and dissociates, GPCR is active, cGMP is low so CNG channels close, K+ leaves still so cell hyperpolarizes and less glutamate is released

Voluntary vs. Reflexive Movement

voluntary movement is planned and intentional, initiated by decision making in brain, integrated in motor cortex, integrated lots in cerebral cortex, activates somatic MNs, activates proprioceptors, definitely informs cerebellum

reflexive movement is hard wired, initiated by external stimulus, integrated in the spinal cord, not usually integrated in cerebral cortex, activates somatic MNs, doesn’t activate proprioceptors