Vertebrate Sensory Systems Midterm

Tympanic membrane (ear drum)

Flat cone pointing inward that separates outer and middle ear and vibrates with sound; the malleus attaches to it at the manubrium (tense portion).

Middle ear

Air-filled cavity connected to the pharynx by the Eustachian tube; contains the three ossicles.

Ossicles (in order)

Malleus (hammer) -> incus (anvil) -> stapes (stirrup). Smallest bones in the body; malleus attaches to the ear drum, stapes foot attaches to the oval window.

Purpose of the ear drum and ossicles

To AMPLIFY sound: sound energy is greatly attenuated at an air/fluid interface (air in outer/middle ear to fluid in inner ear), so the tympanic membrane and ossicles work together as an amplifier.

Stapedius

Muscle that inserts on the neck of the stapes; contraction also attenuates sound.

Eustachian tube

Connects the middle ear to the pharynx (equalizes pressure).

Cochlea

Snail-shaped, fluid-filled inner ear structure containing the hair cells that transduce sound.

Vestibular system

Three semicircular canals, the saccule and the utricle; senses balance/head position using hair cells.

Oval window

Membrane where the stapes passes vibrations into the cochlear fluid; start of the scala vestibuli.

Round window

Membrane at the end of the scala tympani where the fluid wave through the cochlea terminates.

Scala vestibuli

Cochlear fluid compartment that starts at the oval window.

Scala tympani

Cochlear fluid compartment that terminates at the round window.

Scala media

Cochlear compartment between the other two (separates them except at the helicotrema); contains endolymph and the organ of Corti.

Basilar membrane

Site of auditory transduction. Its mechanical properties vary along its length so different points vibrate to different frequencies.

Tonotopic map

Orderly mapping of frequency to position: high frequencies at the base of the cochlea, low frequencies at the apex (log relationship between frequency and position). Preserved all the way up the auditory pathway to cortex.

Organ of Corti

Epithelial strip along the basilar membrane containing the hair cells (one row inner, three rows outer), supported by phalangeal and pillar cells; hair bundles project into endolymph.

Tectorial membrane

Gel-like membrane overlying the hair cells; outer hair cell stereocilia are attached to it.

Endolymph

Unique extracellular fluid bathing the apical surface of hair cells: very high K+ (~140-154 mM), very low Na+ and very low Ca2+; isolated from other fluids by tight junctions.

Hair bundle

The receptor organ ("biological strain gauge"): cluster of 20-300 stereocilia in a stepped (graded height) array, plus one kinocilium (lost in mature cochlear hair cells).

Stereocilia

Rigid projections made of cross-linked actin, arranged in rows of graded height; their deflection gates mechanically sensitive ion channels.

TOWARD

Deflection [TERM] the tallest stereocilia opens channels -> depolarization.

Kinocilium

A single true cilium per hair cell; orients the cell (opposite side to neural output) and sets directionality but does not directly mediate mechanical-to-electrical transduction.

Kinocilia: cochlea vs. semicircular canals

Cochlear hair cells LOSE kinocilia after maturation (directionality is already set by the tallest stereocilia). Semicircular canal hair cells KEEP them because directional mapping is needed for 3D head orientation.

How semicircular canal hair cells detect head rotation

Head rotates -> fluid inertia causes relative motion in the opposite direction -> stereocilia move relative to the kinocilium. Hair cells are oriented in many directions, so a tilt/rotation in any direction activates some afferents.

Outer hair cells (OHCs)

Lateral (non-neural) side; ~12,000; V-shaped stereocilia arrays. AMPLIFY vibrations by contracting/elongating the cell body (prestin), pushing and pulling on the basilar and tectorial membranes; sharpen tuning. Sparse afferent input, dense efferent input.

Prestin

Voltage-sensitive motor protein in outer hair cells that drives cell-body contraction/elongation (electromotility) = cochlear amplification.

Inner hair cells (IHCs)

Medial (neural) side; ~3,500; linear stereocilia arrays. Integrate and TRANSMIT sound signals to spiral ganglion neurons. Dense afferent input, sparse efferent input.

Spiral ganglion (cochlear ganglion)

Cell bodies of the auditory afferent neurons that receive input from hair cells; their axons form the cochlear nerve.

Ribbon synapse

Hair cell synapse that converts the Ca2+ signal into glutamate release. Synapse position on the hair cell sets sensitivity (also used by photoreceptors).

Cochlear nerve

Auditory branch of CN VIII. Axons of spiral ganglion neurons exit via the modiolus, are tonotopic (outer fibers = base/high freq, core fibers = apex/low freq), and project to the cochlear nucleus. Each fiber has a preferred frequency but responds outside it at higher intensity.

Cochlear nuclei

First CNS relay: EVERY auditory nerve fiber synapses in the ipsilateral cochlear nuclei (medulla/pons). Three parts: DCN, AVCN, PVCN; each tonotopic. Each fiber branches to all three: parallel processing, with different cell types extracting different features.

Stellate cells

(PVCN) Fire regularly ("chopper") despite noise; encode stimulus INTENSITY and spectral features; can population-code frequency.

Bushy cells

(AVCN) Fire at stimulus onset; preserve/enhance TIMING information; essential for sound LOCALIZATION (interaural time/intensity differences, horizontal axis).

Fusiform cells

(DCN) Multisensory integrators; use pinna-generated cues to determine sound ELEVATION (vertical localization) and to distinguish self-generated from external sounds.

Octopus cells

(PVCN) Coincidence detectors specialized for temporal precision; detect sound ONSET and transients (e.g., clicks).

Olfaction

chemoreception, Smell = distance (airborne chemicals)

Cochlear nucleus: cell type to location to feature

DCN: fusiform = multisensory integration. AVCN: bushy = localization/timing. PVCN: stellate = intensity; octopus = rapid onset (clicks).

Superior olivary nucleus (olivary body)

First site where signals from both ears converge (binaural). Most VCN fibers decussate via the trapezoid body to the contralateral superior olive; some stay ipsilateral. Used to localize sound.

Trapezoid body

Region where fibers from the ventral cochlear nucleus cross (decussate) to the contralateral superior olivary nuclei.

Medial superior olive (MSO)

Codes INTERAURAL TIME DIFFERENCES (ITD); works best for low-frequency sounds.

Lateral superior olive (LSO)

Uses INTERAURAL INTENSITY differences (head attenuates sound, so it is louder at one ear); works best for high-frequency sounds.

Lateral lemniscus ("ribbon")

Brainstem tract carrying ascending auditory fibers from the cochlear nuclei (DCN, VCN) and superior olive up to the inferior colliculus. Carries information from BOTH ears bilaterally.

Inferior colliculus

Midbrain structure ("little hill"). Outer cortex/shell = multisensory (auditory + somatosensory); central nucleus = tonotopic main pathway. Converges frequency, timing, intensity and binaural cues; projects to the ipsilateral medial geniculate nucleus.

Medial geniculate nucleus (MGN)

Thalamic relay for hearing. Ventral MGN = main tonotopic pathway; dorsal/medial MGN get somatosensory and visual input (diffuse functions, e.g., attention). Has reciprocal connections with auditory cortex (not a simple relay). Projects to A1.

Primary auditory cortex (A1)

Brodmann areas 41 and 42 on the dorsal surface of the temporal lobe; tonotopic (frequency map) and organized in binaural columns.

A1 summation columns (EE)

Excitatory/excitatory: neurons excited by sound at either ear, with enhanced response when both ears are stimulated.

A1 suppression columns (EI)

Excitatory/inhibitory: neurons excited by one ear (usually contralateral) and inhibited by the other (usually ipsilateral); suited to interaural level differences. EE and EI columns alternate, running at right angles to the tonotopic map.

Auditory pathway: hair cell to cortex

Hair cell -> spiral ganglion -> cochlear nerve (CN VIII) -> cochlear nuclei (DCN, AVCN, PVCN) -> superior olivary nucleus (partial decussation via trapezoid body) -> lateral lemniscus -> inferior colliculus -> medial geniculate nucleus (thalamus) -> primary auditory cortex (A1).

Why central hearing loss is rare

Above the cochlear nucleus, information from both ears travels bilaterally in each lateral lemniscus, so supranuclear (central) lesions rarely cause serious hearing impairment. Most hearing problems are conductive or sensorineural.

Conductive hearing loss

Sound fails to reach the cochlea (e.g., earwax blockage, perforated eardrum, ossicle damage, fluid in middle ear). Cochlea and nerve are fine; the problem is purely mechanical. Combat by removing blockage, repairing the drum/ossicles, grommets to drain fluid, or amplification (hearing aid).

Sensorineural hearing loss

Hair cells are damaged or dead (e.g., noise exposure, aging); sound reaches the cochlea but cannot be converted to an electrical signal. Treated with a cochlear implant (needs an intact spiral ganglion/nerve).

Auditory neuropathy

Hair cells may be intact but spiral ganglion cells/auditory nerve fail to transmit the signal (e.g., poor synaptic transmission, demyelination). Sound is detected but poorly relayed.

Central deafness

Ear, nerve and brainstem are functional but damage higher up (auditory cortex or the pathway from brainstem to cortex) prevents the brain from interpreting the signal. A cochlear implant cannot fix this.

Hair cells

shared mechanoreceptor for both hearing (cochlea) and balance (vestibular system).

Gustation

Chemoreception, Taste = contact.

Five basic taste qualities

Sweet, bitter, sour, salty, umami. Function: identify foods as safe/unsafe and choose between food items (nutritional quality).

Taste bud

Cluster of 50-100 taste receptor cells, located on papillae.

Types of papillae

Filiform (no taste buds; rough/abrasive), fungiform (front), foliate (parallel folds at back edge), circumvallate (back center).

Labelled line model of taste

Receptor cells respond to a single taste quality and are innervated by individually tuned nerve fibers (one bud, one neuron, one quality).

Across-fiber patterning model of taste

Individual cells/neurons respond to multiple taste qualities, and taste is encoded by the pattern of activity across fibers.

Taste receptor cell signaling

Receptor cells do NOT fire action potentials: they show graded depolarization (proportional to the amount of "taste") and release neurotransmitter (serotonin) onto cranial nerve afferents.

Umami (receptor)

T1R1 + T1R3 heteromeric GPCR; responds to amino acids, especially glutamate in humans. Signals via G protein (gustducin) -> PLC -> IP3 -> Ca2+ and TRPM5 -> depolarization.

Sweet receptor

T1R2 + T1R3 heteromeric GPCR; "promiscuous" (recognizes many shapes: sucrose, fructose, amino acids, saccharin). Same PLC/IP3/TRPM5 pathway.

Bitter receptors

T2Rs (TAS2R family, ~30 genes in humans): GPCRs, each highly specific; several can be in one taste cell. Signal via gustducin -> PLC -> IP3 -> Ca2+ and TRPM5. Broad tuning across the family = toxin avoidance.

Sour receptor/mechanism

Proton donors (acids). H+ blocks K+ channels in microvilli, or enters via a proton channel (PKD2L1 is the candidate sour receptor) -> depolarization. Ion channel mechanism, not a GPCR.

Salty receptor/mechanism

Na+ enters through an amiloride-sensitive Na+ channel (ENaC) at the microvilli -> depolarization. Direct ion channel mechanism, not a GPCR.

Why sour and salty use ion channels

Their stimuli are simple ions (H+, Na+) that can pass through or block channels directly, so no GPCR is needed; this is also faster/simpler.

Genetic variation in taste

Salty and sour taste are relatively uniform; bitter, sweet and umami are genetically determined (T2R diversity). Different mouse strains prefer different sweet compounds.

Gustatory pathway: cranial nerves

Facial nerve (CN VII, chorda tympani): anterior 2/3 of tongue. Glossopharyngeal (CN IX): posterior 1/3. Vagus (CN X): epiglottis and pharynx. All target the solitary nucleus.

Nucleus of the solitary tract (NTS; gustatory nucleus)

Medulla; all three taste nerves synapse first in the rostral NTS (also receives respiratory/gut interoceptive input).

Gustatory pathway: NTS to cortex

NTS (medulla) -> ventral posteromedial nucleus of thalamus (VPMpc) -> primary gustatory cortex = insula (interoception hub) and frontal operculum (basic taste qualities).

Secondary/associative taste areas

Orbitofrontal cortex (integrates taste with smell, texture, vision into flavor and hedonic value), amygdala (emotional/hedonic valence), hypothalamus (links taste to feeding and satiety).

Full gustatory pathway

Taste bud receptor cell -> CN VII / IX / X -> NTS (medulla) -> VPMpc (thalamus) -> insula/frontal operculum (primary gustatory cortex) -> OFC, amygdala, hypothalamus.

Innate craving for salt

When NaCl balance is impaired (humans: Addison's disease/adrenal insufficiency; rodents: adrenalectomy).

Conditioned taste aversion

Learned avoidance of a flavor paired with nausea (internal cue with internal consequence). Rats given flavored water + light/click: nausea group avoided the water; shock group avoided the light/sound. Cues are selected according to the nature of the reinforcement.

Learned positive taste preference

Associating a taste with high dietary reward (e.g., gut infusion of fat/sugar = post-ingestive gut-brain reinforcement), pairing a new taste with a preferred one (bacon/butter), or familiarity/exposure.

Learned satiety

Associating a taste with satiety signals so food intake can be regulated before the satiety signals kick in.

Central chemoreceptors

Ventral surface of the medulla; sense H+ (pH) in CSF as an indirect readout of blood CO2 (CO2 crosses the blood-brain barrier and acidifies CSF). Slower than peripheral but ~70-80% of CO2 drive.

Chemesthesis

Chemical sensation by free nerve endings of the trigeminal nerve (CN V) in oral/nasal mucosa and skin: burning, cooling, tingling, stinging (e.g., capsaicin, menthol).

TRP channels

Transient receptor potential channels: nonselective cation channels, several gated by temperature. They link chemical and thermal sensing at the same receptor.

Thermosensitive TRP channels

TRPV1 (>43 C, noxious heat); TRPV3/4 (warm); TRPM8 (<25-28 C, cool/cold); TRPA1 (<17 C, noxious cold).

Capsaicin

Chili pepper compound; binds TRPV1, opening the channel (same conformational change as heat) -> cation influx -> depolarization -> afferent fires = "burning" with no actual heat. Sustained activation desensitizes nociceptors (topical analgesic patches).

Menthol

Binds TRPM8 and lowers its activation threshold so it opens at warmer ambient temperatures -> cation influx -> afferent fires = "cooling" with no actual temperature change. Not a cold mimic: receptor properties are changed.

TRPM8

Cold- and menthol-activated cation channel (cool/cold, <25-28 C).

TRPV1

Heat- (>43 C) and capsaicin-activated cation channel; noxious heat.

Enteroendocrine cells

Specialized gut epithelial cells that directly sample luminal contents ("taste without taste"): T1R2/T1R3 detect sugars -> GLP-1 release; GPR40/GPR120 detect long-chain fatty acids; GPCRs detect amino acids/peptides.

Slow + small RF

Merkel disk

GLP-1

Glucagon-like peptide-1, made by enteroendocrine cells and neurons in the caudal NTS; triggered by luminal glucose and fat. Stimulates glucose-dependent insulin secretion, suppresses glucagon, slows gastric emptying, suppresses appetite centrally.

GLP-1 agonist drugs

Engineered long-acting GLP-1s (half-life days vs.

Interoception pathway in the gut-brain axis

Vagal and humoral gut signals converge on the NTS (with respiratory and cardiovascular afferents) -> arcuate nucleus (integrates with hormones) and insula/amygdala (conscious representation of internal state, mood, anxiety).

Somatosensation

The body's system for sensing touch, temperature, pain and body position (proprioception).

Purpose of somatosensation

Provides sensory data to guide skilled, active action (object manipulation, tool use, grooming). Patient GO (large-fiber sensory loss, motor intact) could not feel light touch, vibration or joint position and had severe deficits in skilled motor action.

Proprioception

Sensing body position and movement, an active process that lets us adjust our actions (e.g., hold a mug steady while it fills).

Mechanosensitive channels

Convert force into voltage by directly opening ion channels via membrane tension; much faster than second-messenger (GPCR) transduction. Piezo2 loss of function in humans causes deficits in touch and proprioception.

Muscle spindle

Proprioceptor in muscle signaling muscle LENGTH and velocity (stretch); signals CNS to initiate contraction; firing rate increases with load. Detects the tap in the knee-jerk stretch reflex.

Golgi tendon organ

Proprioceptor in series with muscle fibers at the tendon that signals contractile FORCE/tension; inhibits a contraction that becomes too forceful, protecting the muscle from tearing.

Joint receptors

Add position information: signal range of motion (stretch/pressure) and pain; increase firing at the ends of range to prevent overextension.

Stretch reflex (knee jerk)

Tendon tap stretches muscle -> muscle spindle afferent -> spinal cord (local circuit) -> motor neuron -> muscle contracts. Bypasses the brain (no conscious processing) while also sending information up for perception. Lost in patient GO because sensory afferents were missing.

Glabrous vs. hairy skin

Glabrous = hairless, thick, many touch receptors (e.g., palm). Hairy = hair follicles, sebaceous glands, fewer touch receptors (e.g., arm).

Receptive field

The area of skin where stimulation alters the firing rate of a given sensory fiber/neuron (exciting or inhibiting it).