Exam 2 Flashcards
(233 cards)
1
Q
• What are the three parts of the ear?
A
o External, middle, and inner ear
2
Q
What is the function of the external ear?
A
o Air waves generate vibrations in tympanic membrane
3
Q
• What is the function of the middle ear?
A
o Ossicles (malleus, incus, stapes) transmit sound to inner ear
4
Q
• What is the function of the inner ear?
A
o Vibration conducted through fluid into cochlea
5
Q
• What are the regions of the external ear?
A
o Auricle, helix and antihelix, tragus and antitragus, concha and lobule
6
Q
• What structures are found in the auricle?
A
o Elastic cartilage covered with skin; sebaceous glands associated with hairs
7
Q
• What are ceruminous glands?
A
o Modified apocrine glands that secrete cerumen; protects ear canal against physical damage and microbial invasion
8
Q
• What is ear wax?
A
o Mixture of cerumen, sebaceous gland secretion and desquamated meatal cells; found in outer 1/3 of ear canal
9
Q
• What part of the outer ear is easily traumatized?
A
o Inner 2/3, due to thin skin over osseous canal
10
Q
• What is the sensory innervation of the external ear and external acoustic meatus? Middle ear?
A
o Greater auricular; lesser occipital; auriculotemporal, V3; facial; vagus o Glossopharyngeal (IX)
11
Q
• What does the tympanic cavity contain?
A
o The ossciles and their muscles
12
Q
• What does the auditory (Eustachian) tube do?
A
o Connects tympanic cavity to nasopharynx
o Tubal cartilage: opened by levator/tensor palate. Salpingopharyngeus
13
Q
• What do the ossicles do?
A
o Amplify vibration from wide tympanic membrane through narrow base of stapes
14
Q
• What are the ossicles and their roles?
A
o Malleus: vibrated by tympanic membrane
o Incus: transmits from malleus to stapes
o Stapes: transmits vibrations through oval window to cochlea
15
Q
• What are the muscles that dampen ossicle mov’t? Innervation?
A
o Tensor tympani: dampens extreme low frequency vibrations; innervated by V3
o Stapedius: dampens extreme vibrations of stapes; innervated by VII
16
Q
• What is the physical route of the chorda tympani?
A
o Passes b/w tympanic membrane and malleus (possibly impacted by otitis media)
o Branches from facial nerve in tympanic cavity, exits and joins V3 as it approaches the oral cavity
17
Q
• What type of neurons in the chorda tympani?
A
o Contains both sensory and autonomic neuronal axons
o Sensory neurons mediate taste from anterior 2/3 of tongue
o Parasympathetics to submandibular and sublingual salivary glands
18
Q
• Where do the post-and preganglionic axons of chorda tympani come from?
A
o Pre: from superior salivary nucleus
o Post: from submandibular ganglion
19
Q
• What is the central feature of the tympanic membrane?
A
o Umbo: central depression created by tension of the malleus
20
Q
• What are the visible landmarks in an auriscopic view?
A
o Malleus (lateral process, handle, umbo); incus; stapes; cone of light; flaccid and tense parts of TM
21
Q
• What is otitis media?
A
o Infection/inflammation of the middle ear; fluid buildup blocks middle ear, air is absorbed, negative pressure pulls TM inward (or viral/bacterial-laden fluid upward from pharynx into tympanic cavity)
22
Q
• How can otitis media be treated? What can happen if untreated?
A
o Fluid drained by tube inserted in TM
o Infection can get through TM or spread through tegmen tympani; meningitis or brain abscess
23
Q
• What is cholesteatoma?
A
o Skin cyst; skin from ear canal fills with cysts and migrates through a hole in TM; grows out of control, damages middle ear and mastoid
24
Q
• What is the cochlea?
A
o Part of inner ear; fluid-filled spirally formed bony canal; contains the membranous cochlear duct that contains the hearing receptors
25
• What does the term cochlea technically refer to?
o The helical bony canal (as distinguished from cochlear duct)
26
• What are the parts of the cochlea?
o Cochlear duct (scala media); separated from other spaces by the vestibular and basilar membranes; contains endolymph (secreted by stria vascularis)
o Scala vestibule
o Scala tympani (both scala are continuous, meet at the apex (helicotrema) and contain perilymph)
27
• What are the parts of the cochlear duct?
o Membranous tube that encloses organ of corti; contains endolymph, surrounded by perilymph; oval window; round window
28
• What are the electrolyte concentrations in perilymph and endolymph?
o Perilymph: high Na+
| o Endolymph: high K+
29
• What happens at the oval window?
o Base of stapes triggers fluid vibrations in perilymph
30
• What happens at the round window?
o Absorbs outward displacements of fluid vibrations
31
• What are the sound transductions of the external, middle, and inner ears?
o External: air waves
o Middle: ossicle vibrations
o Inner: fluid vibrations in cochlea
32
• What is the organ of corti?
o covered in hair cells (I and O) with many nerve receptors; covered by the tectorial membrane
33
• What type of cells are in the organ of corti?
o Inner and outer layers of non-neural receptor cells (“hair cells”) embedded among support cells on the basilar membrane
o Cells have stereocilia (actually, microvilli) that contact the overlying tectorial membrane
34
• What do hair cells do?
o Activate sensory neurons of the cochlear (auditory) nerve
35
• What do sound waves do as they travel through the cochlea?
o Produce vertical oscillations in the basilar membrane against the tectorial membrane, whose shear forces bend the receptor stereocilia
36
• What happens when stereocilia are bent?
o Distortions trigger depolarization (K+ influx) followed by release of transmitter onto sensory neurons
37
• What happens in the cochlear nerve when hair cells are bent?
o Sensory neurons respond and form the cochlear portion of CN VIII; spiral ganglion contains cells bodies of sensory neurons
38
• What is tonotopic representation of sound?
o Frequency (pitch) of incoming sound is initially coded by difference in basilar membrane stiffness and width from base to apex
39
• Even though the sound wave travels along the full length of the basilar membrane, what happens?
o There are only certain locations where a complex sound wave has a maximal amplitude; where the membrane has the physical properties to resonate with the vibration of the certain pitch
40
• What is resonance frequency?
o A specific frequency of sound produces an envelope of pressure waves in the basilar membrane, with a maximum amplitude at a unique point
41
• What cells does the organ of corti use to transduce vibrations into neural auditory information?
o Inner and outer hair cells
42
• What are inner hair cells?
o Primary sensory cells transmitting sound info to the brain; respond to basilar membrane mov’ts at specific frequencies
43
• What innervated the inner hair cells?
o 95% of sensory neuron axons in cochlear nerve (other 5% for outer hair cells)
o Cochlear nerve projects inner cell activity to cochlear nuclei in the medulla
44
• What is the main purpose of outer hair cells?
o Mostly don’t activate sensory neurons; act as mechanical amplifiers that enhance weak auditory signals transduced by the IHCs
45
• What happens in OHCs when cilia are bent?
o Produces electromotile response in which the cell contracts and then elongates to its original length with each deflection of the basilar membrane
46
• What happens as OHCs elongate against the tectorial membrane?
o The recoil force pushes in the basilar membrane amplifying its oscillation; outer cells responses are frequency specific
47
• How does OHC response produce a positive feedback?
o Enhances the amplitude of basilar membrane oscillation and IHC responses (like pushing someone on a swing at the right frequency)
48
• What can happen with overstimulation of the OHCs?
o Produce a vibration that returns through the oval window and ossicles and projects out through the tympanic membrane as sound (oto-acoustic emissions, OAEs, like a loudspeaker)
49
• What is the result of too much loud noise?
o Destroys mostly outer hair cells leading to hearing loss (dead zones in the cochlea)
50
• What is the form of the sound wave without the action of OHCs?
o Dull and rounded peak, passively stimulating many adjacent frequencies simultaneously
51
• What is accomplished in the form of the sound only with OHCs?
o Sharpening of the peak; increases the ability to distinguish b/w frequencies that are close together
52
• What 2 auditory pathways arise from the medullary cochlear nuclei?
o dorsal and ventral (goes to superior olive)cochlear nuclei; both project up lateral lemniscus -> IC -> medial geniculate -> primary auditory cortex in temporal lobe
53
• What is the dorsal cochlear nucleus?
o Quality of sound: analyzes tiny frequency differences among “bet,” “bat,” and “debt”
54
• What is the ventral cochlear nucleus?
o Localization: disparity in time and intensity b/w R and L sounds localizes object in space
55
• What happens when sound approaches from an angle?
o Reaches each ear at different time and intensite/amplitude/loudenss;
56
• How are high and low frequencies localized when sound comes at an angle?
o Time difference localizes low frequencies; intensity differences localize high frequencies
57
• How does the IC get auditory and somatosensory input?
o Auditory: from cochlear nuclei and superior olive
| o Somatosensory: orient:ation of head and other body regions for sound localization
58
• What does the medial geniculate body of thalamus do?
o Projects sound to cortex tonotopically
59
• Where is the primary auditory cortex and what does it do?
o Superior temporal lobe; tonotopic organization of frequencies is synthesized into sound forms
60
• What is the ventral stream of the auditory association cortex?
o For speech comprehension (voice, language, or any symbolic system), flows to temporal lobe; largely bilateral
o Includes Wernicke’s area, angular gyrus and other association cortices
61
• What is Wernicke’s area?
o Integrates auditory, visual and somatosensory aspects of language; for understanding speech, writing, or any symbolic system
62
• What is Wernicke’s are connected to?
o Speech motor area in premotor cortex of frontal lobe (Broca’s area) via the arcuate fasciculus (Ex: can still read jumbled words if first are last letter are correct)
63
• What is the dorsal stream of the auditory association cortex?
o Sensory-motor integration of vocal articulation that projects to the parietal-temporal junction of frontal lobe, esp Broca’s area; left dominant
o Localization of sound in body schema
64
• What is the old view how music is processed?
o Lateralization of auditory functions on the right and left sides of cortex; rhythm on left, melody on right
65
• What is new view of how music is processed?
o Temporal, parietal and motor cortices all involved bilaterally in higher levels of auditory activity
66
• What sides of brain associated with speech, rhythm and melody?
o Uses both sides, but asymmetrically
67
• What sides of brain for speaking and singing?
o Both sides, but singing is more pronounced in right auditory region of temporal lobe; motor areas related to vocal production
68
• How does music affect emotions?
o Music activity in auditory cortex can modulate activity in limbic regions of emotions, like amygdala, cingulate cortex, orbitofrontal cortex; other areas affected include hippocampus and insula
69
• What is auditory selective attention?
o Efferent olivocochlear neurons from the superior olive terminate on IHC/OHCs to regulate their sensitivity and electromotility responses to sounds
70
• How do olivocochlear efferents indirectly inhibit inner cell responses?
o Inhibit outer cell responses to basilar membrane waves; especially to low level sounds
71
• What happens in a quiet situation?
o Efferent activity inhibits outer cell responses to low level sound detection
72
• What happens when there is background noise?
o Efferent activity improves signal detection and discrimination by suppressing the low level background noise responses -> inhibition “unmasks” the louder, primary sound to be heard (convo in noisy restaurant)
73
• What is efferent control stimulated by?
o Sensory input from cochlear nuclei; auditory cortex; reticular formation (locus ceruleus- NE), to focus attention on specific stimuli
74
• What are the 2 types of deafness?
o Conductive: due to damage of tympanic membrane, ossicles, etc (eg otitis media)
o Sensorineural: damage of cochlea or cochlear portion of CN VIII (eg Meniere’s dx, toxins, acoustic neuroma, diabetic neuropathy)
75
• What are the 2 types of tinnitus?
o Subjective and somatic
76
• What is subjective tinnitus?
o Sensation of sound w/o external stimulation- a phantom auditory perception, eg cicadas, winds, grinding steel, escaping steam
77
• What is the mechanism of subjective tinnitus?
o Abnormal neural activity in brain stem auditory pathways; DCN is a possible site of conditioning and plasticity that can produce long term increases in spontaneous activity and changes in sensitivity to sound
78
• How can subjective tinnitus be treated?
o Deconditioning via methods such as white noise
79
• How is the phantom sound created in subjective tinnitus?
o Changes in primary auditory cortex
80
• What are possible causes of subjective tinnitus?
o Disease processes (TMJ, noise-induced OHC damage)
o Neurological: whiplash, VIII tumors, MS
o Infections: otitis media, meningitis
o Side effects of drugs (aspirin)
81
• What is somatic tinnitus?
o A form of subjective tinnitus, usually triggered by synergistic effects of 2 or more causes, including somatosensory stressors
82
• What is the mechanism of somatic tinnitus?
o Trigeminal and dorsal root ganglia relay afferent somatosensory info from periphery to secondary sensory neurons in brainstem, specifically spinal trigeminal nucleus and dorsal column nuclei, respectively. Each structure sends excitatory projections to cochlear nucleus and can thus enhance tinnitus (hence cnxn of tinnitus w/ whiplash and TMJ)
83
• Where does cochlear nucleus project to and bias sensation?
o Somatic efferent systems (hearing a high pitched sound alters sense of texture)
84
• Where is the vestibular system located?
o Within the petrous portion of the temporal bone
85
• What is the vestibular system?
o Bony labyrinth, complex system of canals, subdivided into vestibule and semicircular canals
86
• What is the membranous labyrinth?
o membranous tube with receptors for head mov’t/position; divided into semicircular ducts (in semicircular canals) and Saccule & Utricle (in vestibule)
87
• What is endolymph?
o Secreted by cochlear duct; drains into dural sinuses via endolymphatic duct
88
• What is perilymph?
o Secreted by periosteum; drains into CSF via perilymphatic duct
89
• What is Meniere’s disease?
o Transient vertigo and dizziness, nausea, vomiting and abnormal saccadic eye mov’ts (nystagmus)
o Excess endolymph secretion and fluid pressure affect receptor function
90
• What are the semicircular ducts/canals?
o Anterior (superior), horizontal and posterior ducts; mutually perpendicular; rotation of ducts with head mov’t causes flow of endolymph
91
• What is the crista (ampullaris)
o Receptor in the ampulla of each semicircular canal; covered in hair cells, supporting cells, gelatinous mass (cupola), sense angular acceleration
92
• What are the features of the hair cells of the crista?
o Have a single kinocilium and several stereocilia which project into the gelatinous mass (cupola)
93
• What distorts the hair cells of the crista?
o Relative motion of endolymph during head rotation; most sensitive to angular acceleration (0.1 degree/sec)
94
• What happens as the skull turns?
o Endolymph maintains position due to inertia and creates a relative motion b/w bone and fluid; differential fluid flows in all three ducts, generates patterns of neural activity in the vestibular nerve
95
• What does vestibular nerve do?
o Hair cells trigger Aps in vestibular nerve; Activity conveys the net direction of head mov’ts
96
• What is the macula?
o in both utricle and saccule, detect linear acceleration; covered in hair cells and gelatinous layer (the otolithic membrane)
97
• What are otoliths?
o Calcium carbonate stones embedded in gelatinous layer
98
• What are the 2 types of cilia on macular hair cells? What do they do?
o A single kinocilium (tallest) and several stereocilia; cilia penetrate up into gel layer; sensory neurons innervate the hair cells
99
• What is the orientation of maculae?
o Maculae of saccule and utricle are oriented at right angles; saccule is a vertical plane, utricle is mostly vertical
100
• How do hair cells respond optimally?
o To acceleration in the direction of its alignment, increasing firing rate when the stereocilia are deflected toward the kinocilium, decreasing away from the kinocilium
101
• How are otoliths moved and what does this cause?
o Due to gravity or head mov’t; embedded within the gel, bend the cilia of the hair cells generating receptor potential
102
• What does linear acceleration do?
o Distorts receptors directly w/o endolymphatic mov’t; direction of move’t determines which receptor cells are affected
103
• How are hair cell cilia distorted?
o Inertia of otoliths during mov’t; gravitational pull on otoliths during head tilt
104
• What is the vestibular nerve?
o Sensory neurons from semicircular canals, saccule and utricle converge to form the vestibular nerve; part of CN VIII
105
• What is vertigo?
o Disorientation and a sense of spinning leading to a loss of equilibrium; can be due to an acoustic neuroma or to Meniere’s disease
106
• What is acoustic neuroma?
o A benign tumor of the myelin-forming cells of the inferior vestibular nerve (part of CN VIII); causes ipsilateral sensorineural deafness or tinnitus
107
• What does the vestibular disturbance of acoustic neuroma cause?
o Unstable gait, vertigo, nausea and vomiting (vestibular nuclei project to NTS, site of stomach afference and likely site of initiating nausea)
108
• What happens due to acoustic neuroma compressing facial nerve?
o Any symptoms are rare
109
• What are symptoms of benign paroxysmal positional vertigo?
o Dizziness, vertigo, imbalance, nausea
110
• What is mechanism of benign paroxysmal positional vertigo?
o Otoliths from utricle fall into semicircular canals and trigger apparent motion from the crista
111
• What can cause otolith dislodgement?
o Head injury, infection, or degeneration with age
112
• What produces the apparent shift in position and body motion of benign paroxysmal positional vertigo?
o Conflict of sensory input b/w the dysfunctional vestibular and normal somatosensory, visual and proprioception senses
113
• What does the maneuver of benign paroxysmal positional vertigo do?
o Relies on inertia, so transition must be done very quickly (sitting, lie to right side, the quickly transition to left side)
114
• Where does the vestibular nerve conduct its activity to?
o Vestibular nuclei in brain stem and vestibule-cerebellum (flocculonodular lobe)
115
• Where does vestibular nuclei in brain stem project to?
o Thalamus and cortex, spinal cord for postural control, brain stem nuclei for eye mov’ts, autonomic centers for vascular control
116
• Where does vestibulo-cerebellum (flocculonodular lobe) project to?
o Sends processed info back to vestibular nuclei; facilitates vestibular reflexes
117
• What governs posture control?
o Vestibulospinal tracts regulate motor output to muscles for posture and balance
118
• What is the vestibulo-ocuar reflex (VOR)?
o Adjusts eye mov’ts to rotation of head to fix gaze on a visual object; rotation ofhead causes oppsite mov’t of eyes for tracking; requires vestibule-cerebellum for precision
119
• What is the mechanism of VOR?
o Ex: rightward mov;t of head stimulates horizontal semicircular ducts; vestibular nerve stimulates the pathway to the abducens and oculomotor nuclei (via the reticular formation) to divert eyes to the left
120
• What is nystagmus?
o Involuntary saccadic mov’ts when the eyeball is moving (physiological) or at rest (pathological). Many types
121
• What is physiological nystagmus?
o Normal part of the VOR, which consists of smooth eye mov’t away from the direction of travel (VOR trying to keep the eye fixated on one spot) followed by a fast mov’t in the direction of travel (to keep up with the head)
122
• What is pathological nystagmus?
o Spontaneous and independent of head mov’ts; resultof damage to one or more components of the vestivular system, eg semicircular canals, utricle, saccule and vestibule-cerebellum
123
• What is the vestibulo-sympathetic rflex (VSR)
o Vestibular activitry also modulates autonomic and limbic activity in response to locomotion and changes in posture; increases skin vasoconstriction (pallor) and sweating during nausea, eg sea sickness
124
• What is the mechanism of the VSR?
o Vestibular nuclei project to RVLM, which innervates preganglionic sympathetic neurons in the intermediolateral cell column of spinal cord
125
• What is purpose of VSR?
o Enhances vasoconstriction to protect against syncope during postural changes or emotional stress
126
• How does VSR work to increase MAP following postural change (standing)?
o Increased otolithic activity enhances sympathetic activity to blood vessels in skeletal muscle and kidney, but not in GI system
127
• What is the vestibular cortex?
o Vestibular input ascends from the vestibular nuclei to the thalamus (VPL)
o Thalamus projects to several cortical area including TPJ (temporal parietal junction) and parietal areas 3aV, 2V, and 7 and the insula
128
• What is the vestibular cortex comnpletely integrated within?
o Parietal association and insular regions (TPJ, or PIVC, parietal-insular-vestibular cortex)
129
• What does TPJ activity do?
o Reflects visuo-vestibular effects on self-location and first-person perspective; particularly involved in embodiment (sense of being localized within one’s physical body)
130
• How is the vestibular cortex mapped?
1) vestibular illusions in epilepsy
| 2) neuro-imaging of vestibular responses to caloric and galvanic vestibular stimulation
131
• How do you maintain integrity and sense of self-location and first-person perspective?
In terms of body, personal space and extra-personal space: by convergence and congruence of visual, auditory, tactile, proprioceptive and vestibular input
132
• What happens with erroneous or inappropriate input of one sensory system?
o Create a conflict among sensory inputs; the cortex reconciles mismatching info when it can, but can cause illusions or delusions
133
• What is autoscopy?
o See one’s own body separately in extrapersonal space; due to lack of congruence among the sensory outputs
134
• What is a doppelganger?
o A double of a living person and sometimes portrayed as a harbinger of bad luck; seeing someone else means illness or danger; seeing one’s own is omen of death
135
• What are the 3 types of autoscopy?
o Autoscopic hallucination: see a double of self in extrapersonal space, but with no disembodiment
o Heautoscopy: intermediate form; see double of self, but uncertain if disembodies or self localized in the physical or autoscopic body
o Out-of-body experience: feel self-center of awareness is located outside of physical body (disembodiemtn); see own body (autoscopy) and environement from an elevated perspective
136
• What causes heautoscopy?
o Disintegration in personal space (body ownership) due to conflicting tactile, proprioceptive and visual info; some from extrapersonal space; some vestibular dysfunction
137
• What causes sutoscopic hallucination?
o Disintegration of personal from extrapersonal space (disembodiment) due to conflicting vestibular and visual info; minimal vestibular dysfunction
138
• What cause out-of body experience?
o Strong vestibular dysfunction in TPJ, strong disintegration of both personal space, and b/w personal and extrapersonal space
139
• What regulates cerebral blood flow?
o Vestibular system; when standing up, blood descends and blood pressure drops
140
• How is adequate cerebral blood flow maintained?
o By increasing MAP via baroreceptor and vestibular mediated vasoconstriction
o Increasing cerebral blood flow by vasodilating cerebral vessels
141
• What are the 2 pathways vestibular system dilates cerebral vessels to enhance cerebral blood flow?
o Sympathetic inhibition- vestibular nuclei projects to cerebellum and then to RVLM (pacemaker of sympathetic NS), to inhibit vasoconstriction of cerebral vessels
o Vestibular nuclei project to NTS, then pterygopalatine (parasympathetic) ganglion whose neurons vasodilate cerebral arteries
142
• Where are taste receptors found?
o On the surface of the tongue, along the soft palate, and in the pharynx and epiglottis
143
• What are the 4 types of tongue papillae?
o Filiform: no taste buds; for touch, pain, and temperature
o Fungiform: anterior part of the tongue (pink dots) and contain one or more taste buds
o Circumvallate (12): distributed in the shape of an inverted V near back of tongue
o Foliate: in small trenches on the sides of the posterior tongue
144
• What are taste buds?
o Onion-shaped structures consisting of 50-100 taste receptor cells; each cell has microvilli that project through the “taste pore” and respond to specific chemicals or chemical combinations
145
• What was the original concept of 4 tastes? More current?
o Sweet, sour, salty, bitter perceived in different parts of the tongue
o The list is always increasing, now including astringency, pungency, fat, starchy, metallic and umami (MSG)
146
• How do receptor cells respond to the tastes?
o Have receptors for most taste sensations, but are tuned primarily to one
147
• What is the new model of taste regions?
o Instead of taste-specific regions (old model), one region will have groups of taste buds each tuned to a specific taste
148
• What are supertasters?
o People with heightened response to taste; women more likely, and Asians, Africans, South Americans. Only 25% of European descent; cause may be increased fungiform papillae (more and smaller, others have fewer and larger)
149
• What are tastants?
o Taste stimuli; molecules that interact with either ion channels or membrane receptors that trigger 2nd messengers
150
• How are taste receptors expressed?
o Selectively, in subsets of cells, so different taste cells respond to different categories of tastes
151
• So how can we perceive 4 or 5 taste modalities at a time?
o Activation of 4 or 5 different cell types on the tongue that transmit activation along labeled lines to the brain
152
• What do taste neurons respond to?
o Have several receptor types, so respond to multiple taste stimuli (sweet, salty, sour, bitter, etc); but usually respond most strongly to one type
153
• What can modulate taste reception?
o Local peptides; GLP-1 and its receptor are released from taste cells in response to food; alters cell responsivity to taste (ex: enhances sensitivity to sweet, decreases umami, etc); GLP-1 usually associated with intestinal activity
154
• What cranial nerves are responsible for taste in different areas of the tongue?
o Facial- anterior 2/3; glossopharyngeal- posterior 1/3; vagus- palate and epiglottis
155
• Where do taste neurons project to?
o NTS in medulla -> ipsilaterally to ventral posterior medial nucleus (VPL) of thalamus -> limbic cortex
156
• What is the involvement of the insula in taste?
o Primary gustatory cortex; taste identification and intensity (discriminative aspects of taste); damage (like stroke) leads to inability to ID tastes
157
• What is the orbitofrontal cortex (OFC) involvement in taste?
o Secondary gustatory cortex; receives input from insula (primary); appreciation of flavor, food reward, feeding control; site of integration for taste, olfactory and visual cues for eating; decision to ingest or reject a food
158
• What is the olfactory nerve?
o CN I; receptor bipolar cells from nerve that projects to olfactory bulb; axons project through cribriform plate to reach olfactory bulb
159
• Where are odorant receptors found?
o On cilia, that project from mucus layer; only mucus soluble materials can activate receptors; olfactory epithelium located in upper regions of nasal cavity
160
• What is the life span of olfactory receptors?
o 1-2 months and are replaced by basal stem cells; generally numbers decrease with age, including area of epithelium
161
• What do odorants activate? What does this cause?
o Na/Ca and Cl ion channels on receptors microvilli; opening Na/Ca channels opens more Cl channels (out) leading to depolarization and an AP
162
• What is sensory adaptation?
o Decreased activity with prolonged stimulation
163
• What ion is involved in sensory adaptation?
o Involves several Ca-dependent/independent pathways that inhibit receptors, close ion channels and enhance outward pumping of ions
164
• How many odorant receptors do humans have?
o Each receptor cell has one odorant receptor (cells spread throughout olfactory epithelium); humans have 300 types, some mammals more than 1000
165
• Where do odorant receptors converge to?
o Axons of cells with common receptors converge/ project through cribriform plate in bundles of 10-100 and innervate olfactory bulb mitral cells
166
• Where does the olfactory bulb project to?
o Piriform cortex on medial surface of temporal lobe -> amygdala, hippocampus, and prefrontal cortex
167
• What is the piriform cortex?
o Primitive cortex with only three layers, but still has high level characteristics like consciousness of odors, singularity and habituation
168
• What is singularity of odor perception?
o Neurons in piriform respond to a mixture, not the components; olfactory conscious experience is usually singular with one odor perceived at a time; expert perfumists can detect up to 3 components and can recall mental images of odors
169
• What is habitation in piriform cortex?
o Rapid reduction in cortical response to continued chemical stimulation (in addition to receptor adaptation in olfactory epithelium)
170
• What is the purpose of habituation?
o Helps olfactory system detect new odorants against the background, so that persistence of one will not block perception of another
171
• How do olfactory memories (amygdala) compare to visual or auditory cues?
o More emotionally laden; words are more affect laden, with more unpleasant than pleasant
172
• Where does amygdala project to?
o Hypothalamus to generate olfactory related alterations in autonomic and endocrine systems
173
• What are some emotionally arousing odors that may influence cognition and emotion?
o Citrus: improves psychological states and immune function of ppl with depression
o Rose: inhibits stress-induced skin-barrier disruption and elevation of salivary cortisol in humans
o Orange and lavender: reduce anxiety at dentist’s office
174
• How are odors involved in conditioning?
o Can be conditioned to aversive or pleasant events
175
• What is the hippocampus/entorhinal cortex?
o Piriform projects here as well; episodic long term memory; can you recall a smell?
176
• Where do piriform cortex and amygdala project to?
o Orbitofrontal cortex (OFC, part of PFC); acts with amygdala in emotion and associative learning; subjective pleasantness or unpleasantness of odors
177
• What does OFC do?
o Associates olfactory with taste, oral texture, visual inputs, to produce multimodal representation of reward value (like food)
178
• How does taste interact with smell?
o Via retronasal olfaction
179
• What is the significance of the valuation of the OFC?
o Important in emotion and autonomic responses, like heart rate and skin conductance response, mediated by amygdala
180
• How can olfactory system easily spread pathogens to CNS?
o Receptors make direct contact with the external environment and brain (olfactory bulb)
181
• How are infective viral particles (like measles) transported to brain?
o Along axons to olfactory bulb, and transynaptically to the limbic system; infections can induce behavioral disturbances
182
• How can bacteria (like pneumococci) and amoebae Naegleria fowleri get to brain?
o May potentially penetrate olfactory mucosa and be transported into the subarachnoid space and cause meningitis
183
• How can insulin be delivered to CNS via intranasal infusion?
o Enters nasal mucosa and transported extracellularly along axon bundles of olfactory receptor cells to the olfactory bulb, hippocampus and other regions of brain and upper spinal cord
184
• What is another pathway from nasal mucosa to CNS?
o Trigeminal neural pathway
185
• Where are taste receptors found?
o On the surface of the tongue, along the soft palate, and in the pharynx and epiglottis
186
• What are the 4 types of tongue papillae?
o Filiform: no taste buds; for touch, pain, and temperature
o Fungiform: anterior part of the tongue (pink dots) and contain one or more taste buds
o Circumvallate (12): distributed in the shape of an inverted V near back of tongue
o Foliate: in small trenches on the sides of the posterior tongue
187
• What are taste buds?
o Onion-shaped structures consisting of 50-100 taste receptor cells; each cell has microvilli that project through the “taste pore” and respond to specific chemicals or chemical combinations
188
• What was the original concept of 4 tastes? More current?
o Sweet, sour, salty, bitter perceived in different parts of the tongue
o The list is always increasing, now including astringency, pungency, fat, starchy, metallic and umami (MSG)
189
• How do receptor cells respond to the tastes?
o Have receptors for most taste sensations, but are tuned primarily to one
190
• What is the new model of taste regions?
o Instead of taste-specific regions (old model), one region will have groups of taste buds each tuned to a specific taste
191
• What are supertasters?
o People with heightened response to taste; women are more likely to be supertasters, as are Asians, Africans, and South Americans. Only 25% of European descent; cause may be increase fungiform papillae (?)
192
• What are tastants?
o Taste stimuli; molecules that interact with either ion channels or membrane receptors that trigger 2nd messengers
193
• How are taste receptors expressed?
o Selectively, in subsets of cells, so different taste cells respond to different categories of tastes
194
• So how can we perceive 4 or 5 taste modalities at a time?
o Activation of 4 or 5 different cell types on the tongue that transmit activation along labeled lines to the brain
195
• What do taste neurons respond to?
o Have several receptor types, so respond to multiple taste stimuli (sweet, salty, sour, bitter, etc); but usually respond most strongly to one type
196
• What can modulate taste reception?
o Local peptides; GLP-1 and its receptor are released from taste cells in response to food; alters cell responsivity to taste (ex: enhances sensitivity to sweet, decreases umami, etc); GLP-1 usually associated with intestinal activity
197
• What cranial nerves are responsible for taste in different areas of the tongue?
o Facial- anterior 2/3; glossopharyngeal- posterior 1/3; vagus- palate and epiglottis
198
• Where do taste neurons project to?
o NTS in medulla -> ipsilaterally to ventral posterior medial nucleus (VPL) of thalamus -> limbic cortex
199
• What is the involvement of the insula in taste?
o Primary gustatory cortex; taste identification and intensity (discriminative aspects of taste); damage (like stroke) leads to inability to ID tastes
200
• What is the orbitofrontal cortex (OFC) involvement in taste?
o Secondary gustatory cortex; receives input from insula (primary); appreciation of flavor, food reward, feeding control; site of integration for taste, olfactory and visual cues for eating; decision to ingest or reject a food
201
• What are the 2 regions of the skull?
o Neurocranium and viscerocranium (face and anterior neck)
202
• What are the types of bones of the skull and how are they formed?
o Cartilaginous bones- endochondral ossification
o Membranous bones- intramembranous ossification (bones form directly from mesenchyme)
o Cartilages of larynx
203
• What types of bones are in the neurocranium? Examples?
```
o Membranous: vault bones
o Cartilaginous (chondrocranium): cranial base bones (basicranium)
```
204
• What are the vault bones?
o Interparietal part of occipital, parietal, frontal, squamous temporal
205
• What are fontanelles?
o CT sutures; span the vault bones prior to fusion
206
• What types of bones are in the viscerocranium? Examples?
o Cartilaginous: ossicles, hyoid bone
| o Membranous: face bones
207
• From what are the skull bones and cartilage derived from?
o Mostly outer epithelial layers; local mesodermal somites/ somitomeres; neural crest cells migrating in from neural tube area
208
• How is the eventual shape of the skull formed?
o By soft tissues (brain, CT, muscle)
209
• How are the cranial base bones formed?
o Cartilage islands fuse to form the chondrocranium
| o Endochondral ossification forms the ethmoid, sphenoid, petrous temporal and occipital bones
210
• Where are synchondrosis type joints found in the cranial base?
o join frontal, ethmoid, sphenoid and occipital bones for longitudinal and lateral growth
211
• What joints of cranial base close in mid-teens?
o Spheno-ethmoidal and spheno-occipital joints; ends longitudinal growth of the skull
212
• How is the TMJ formed?
o Temporal and sphenoid bones grow laterally to determine the width of the skull; they pull the TMJ outward with them
213
• How is the cranial base angle b/w occipital and sphenoid bones formed? Significance?
o Remodeling of sphenoid bone (clivus) congruent with the cephalic angle of neural tube
o Predicts the position of the mandible and susceptibility to malocclusions
214
• When does the spheno-occipital synchondrosis fuse? What do large or small angles mean?
o 15-17 years
o Large: associated with square jaws and overbite malocclusions
o Small: wide angled mandibles and mandibular protrusion type of malocclusions
215
• What are the pharyngeal arches?
o Condensations of mesenchyme and neural crest cells; each associated with CN (V, VII, IX, X), an artery (aortic arch), and cartilage
216
• What may happen to the cartilage of the pharyngeal arches?
o May remain cartilage (thyroid, cricoid, etc) or become surrounded with intramembranous bone (eg mandible, maxilla)…(ossicles are formed endochondrally)
217
• What do pharyngeal arches give rise to?
o Many of the structures of the anterior neck and face (viscerocranium)
218
• What happens to cartilage?
o Regress and replaced by intramembranous ossification or endochondral ossification
219
• How do neural crest cell interact with the pharyngeal arch mesenchyme?
o Migrate through, to form the bones, cartilage, skin, arteries and nerves of the face
220
• What do pharyngeal arches develop into?
o The viscerocranium
221
• What are the CNs associated with the pharyngeal arches?
o Mandibular arch (CN V, trigeminal); Hyoid arch (CN VII, facial); 3rd Arch (glossopharyngeal, CN IX); 4th and 6th Arch (vagus, CN X)
222
• What are the bones/cartilage associated with the pharyngeal arches?
o Mandibular (mandible, maxilla, zygoma, malleus, incus, squamous temporal); Hyoid (styloid process, hyoid, stapes); 3rd arch (hyoid); 4th and 6th Arch (larynx)
223
• What are the muscles associated with the pharyngeal arches?
o Mandibular (masticator, anterior digastric, tensor tympani, tensor palate); Hyoid (facial expression, posterior digastric, stylohyoid, stapedius); 3rd Arch (stylopharyngeus); 4th and 6th Arch (pharynx, larynx)
224
• What does the top pharyngeal groove form into?
o External acoustic meatus
225
• What do the pharyngeal pouches form into?
o Top (tympanic cavity/auditory tube) 2nd (palatine tonsil); 3rd (thymus and parathyroid migrate down into neck); 4th (parathyroid and C cells of thyroid migrate down into neck)
226
• What is the normal development of the thyroid?
o Thyroid descends from base of tongue through foramen cecum, thyroglossal duct, anterior to hyoid bones and larynx
227
• What are abnormalities in thyroid development?
o Ectopic thyroid tissue and cysts along thyroglossal duct
228
• What is pyramidal lobe?
o Thyroid tissue that has not quite reached the target area
229
• How do pharyngeal arches develop into the face?
o 1st arch expands and fuse to form a complex of bones, muscles and CT
o MEDIAL migration and fusion of maxillary, mandibular (EARLY), nasomedial and nasolateral processes
230
• How is a clef lip formed?
o Failure of normal fusion (maxillary and medial nasal prominences normally fuse to form continuous upper lip
231
• How is cleft palate formed?
o Failure in fusion of palatine processes (of maxilla, which normally fuse with septum to separate oral from nasal cavities, palate formation)
232
• What are facial characteristics of fetal alcohol syndrome?
o Due to incorrect closure of maxillary and nasal prominences (smooth philtrum, thin upper lip, eyes wide apart)
233
• What are other problems with fetal alcohol syndrome?
o Stunted physical and emotional development; memory and attention deficits; tendency to impulsive behavior; inability to reason from cause to effect; failure to comprehend the concept of time; difficulty telling fantasy from reality; inability to control sexual impulses; apparent lack of remorse
