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An4003 > Lecture 3: Sensory Systems – Dr Derryck Shewan > Flashcards

Lecture 3: Sensory Systems – Dr Derryck Shewan Flashcards

1
Q

Exteroreceptors

A

Receptors for external stimuli

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2
Q

Photoreceptors

A

Receptors responsible for vision

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3
Q

Hair cells

A

Mechanoreceptors located in various regions of the body, rapidly adapting to vibration or tickle

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4
Q

Olfactory receptors

A

Receptors responsible for the sense of smell

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5
Q

Skin receptors

A

Various receptors in the skin, including Meissner’s corpuscles, Merkel cells, and Ruffini’s corpuscles

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6
Q

Nociceptors

A

Pain receptors found in all skin layers, sensitive to pressure or sharp objects

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6
Q

Mechanoreceptors

A

Receptors responding to mechanical stimuli, including Meissner’s and Ruffini’s corpuscles

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7
Q

Thermoreceptors

A

Receptors sensitive to temperature changes, including cold and warm receptors

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8
Q

Muscle reflexes and body position

A

Most reflexes at the spinal level, conscious awareness is secondary

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8
Q

Proprioceptors

A

Receptors providing information about body position and movement

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9
Q

Joint receptors

A

Slow-conducting receptors relaying positional information

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10
Q

Equilibrium pathways

A

Project to the cerebellum and cortex via the thalamus, vestibular nerve transmits equilibrium impulses

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11
Q

Sensory information processing

A

Higher brain centers modulate perceptual threshold, inhibitory modulation allows the brain to decide what is necessary to fully perceive

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12
Q

Gustation

A

Provides information on food quality, quantity, flavor, and overall appreciation; involves sweet, salty, bitter, sour, and umami tastes

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13
Q

Taste pores

A

Located on the tongue, containing taste bud sensory cells; different papillae (circumvallate, foliate, fungiform) detect various tastes

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14
Q

Taste transduction

A

Different taste receptors, such as T1Rs, T2Rs, and T-mGluR4, involved in detecting various stimuli

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15
Q

Taste receptor activation

A

Sodium salts and acids cause depolarization, amino acids involve cAMP decrease and intracellular calcium rise, sugars may directly cause depolarization or increase cAMP-dependent PKA function

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16
Q

PKA Activation

A

PKA activation inhibits basolateral potassium conductance, leading to neuron depolarization.

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17
Q

Sugar and IP3 Activation

A

Sugars can activate IP3, causing an increase in intracellular calcium, enabling neurotransmitter release at the synapse.

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18
Q

Bitter Flavors

A

Bitter substances like quinine or divalent cations can directly depolarize neurons. Others may decrease cAMP, leading to increased intracellular calcium and neurotransmitter release.

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19
Q

Taste Sensation and Brain Connections

A

Taste sensation is intricately connected to other sensations and moods. Cranial nerves innervate brainstem nuclei, with further projections to the gustatory cortex and orbitofrontal cortex.

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20
Q

Gustatory Processing Complexity

A

Complex networks within and between brain regions, coupled with input from somatosensory and visceral systems, contribute to taste perception and can lead to ‘fads’ depending on various factors.

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21
Q

Olfactory Transduction Overview

A

Odorant molecules activate receptors on olfactory receptor neurons (ORNs), leading to depolarization and signal propagation to glomeruli in the olfactory bulb.

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22
Q

Odorant Receptor Binding

A

Odorant receptors bind odorants of a specific stoichiometry. Each ORN expresses only one type of receptor.

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23
Q

Glomeruli in Olfactory System

A

Glomeruli, composed of ORN axons and postsynaptic mitral cells, allow ‘like’ ORNs to converge, contributing to the convergence of odorant signals.

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23
Q

Olfactory Cortex Sensitivity

A

Bidirectional input allows directional sensitivity of smell, with convergence and lateral inhibition enhancing olfactory signal specificity.

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24
Q

Lateral Inhibition in Olfactory System

A

Stimulated glomeruli and mitral cells can inhibit neighboring structures through periglomerular and granule cells, contributing to odorant signal sharpening.

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25
Q

Mitral Cell Projection

A

Mitral cells project to the olfactory cortex, innervating pyramidal cells and contributing to bidirectional input from the olfactory epithelia.

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26
Q

Odorant Transduction Mechanism

A

Chemical binding to odorant receptors activates adenylate cyclase, leading to cAMP production, calcium influx, and depolarization.

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27
Q

Feedback Mechanism in Olfactory Transduction

A

Feedback mechanisms involving calmodulin, adenylate cyclase phosphorylation, and sodium/calcium exchange maintain membrane potential in olfactory receptor neurons.

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28
Q

Cochlear and Vestibular Apparatus

A

The inner ear comprises the sensory apparatus of the cochlea and vestibular apparatus, innervated by the cochlear nerve.

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29
Q

Middle Ear Ossicles

A

The middle ear links the eardrum to the cochlea via tiny bones (ossicles: malleus, incus, and stapes), contributing to sound transmission.

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30
Q

Sound Wave Transmission

A

Sound waves travel down the ear canal, causing vibrations in the tympanic membrane (eardrum), initiating the process of hearing.

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31
Q

Ossicle Vibration

A

Vibrations from the tympanic membrane cause the ossicles (malleus, incus, stapes) to vibrate, with the stapes transmitting vibrations to the fluid of the cochlea.

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32
Q

Cochlea Canals

A

The cochlea is divided into three main canals: tympanic, vestibular, and middle. These canals play a crucial role in transmitting and processing sound vibrations.

33
Q

Basilar Membrane

A

The basilar membrane in the cochlea separates the tympanic and middle canals. It responds differently to high and low-pitched sounds, contributing to the perception of pitch.

34
Q

Organ of Corti

A

The organ of Corti, located on the basilar membrane, consists of sensory hair cells, supporting cells, and auditory nerve endings. It plays a vital role in hearing.

35
Q

Hair Cell Cilia

A

Hair cells in the organ of Corti have cilia in contact with the tectorial membrane. Movement of these cilia in response to sound vibrations leads to sensory transduction.

36
Q

Stereocilia and Tip Links

A

Hair cells extend stereocilia into the endolymph fluid, connected by tip links. Sound waves cause cilia displacement, leading to force production and ion channel opening.

37
Q

Mechano-Electrical Transduction (Met) Channel

A

The opening of Met channels in hair cells, triggered by cilia movement, allows potassium influx, depolarization, and subsequent neurotransmitter release.

38
Q

Prestin

A

Prestin is a molecular motor identified at the lateral membranes of hair cells, crucial for maintaining cell length and proper function.

39
Q

Prestin Deficiency

A

Mice deficient in prestin display variations in cell height. Heterozygous mice, with one copy of the gene, show intermediate characteristics compared to wild type and completely deficient mice.

40
Q

In Situ Hybridization

A

In situ hybridization is a technique used to detect mRNA expression. It was employed to identify prestin deficiency in knockout mice and heterozygotes.

41
Q

Hair Cell Depolarization

A

Unlike chemosensory and somatosensory cells, hair cells do not depolarize. Calcium influx, triggered by sound-induced movements, leads to neurotransmitter release at the presynaptic membrane.

42
Q

Apical Surface of Hair Cells

A

The apical surface of hair cells, including the characteristic v-shaped cilia, appears normal in structure even in cases of prestin deficiency.

43
Q

Hair Cell Comparison

A

Individual hair cells from wild type, knockout, and heterozygote mice were compared in vitro, revealing differences in cell height and characteristics.

44
Q

Calcium Influx and Neurotransmitter Release

A

Calcium influx in hair cells, induced by sound waves, leads to neurotransmitter release from vesicles at the presynaptic membrane, contributing to auditory signal transmission.

45
Q

Neurotransmitter Release

A

Neurotransmitters released in the synapse bind to postsynaptic receptors, causing ion channels to open, depolarizing the cell, and propagating an action potential.

46
Q

Synaptic Ribbon

A

Vesicles in hair cells are attached to an electron-dense body called the synaptic ribbon or synaptic body, approximately 400nm in diameter.

47
Q

Vestibular Apparatus

A

The vestibular apparatus, connected to the cochlea, includes semicircular canals that detect head movements in different planes and hair cell receptors in maculae and ampulla.

48
Q

Cristae

A

Ampullar organs in the vestibular apparatus containing hair cells are called cristae, detecting rotational head movements.

49
Q

Maculae

A

Macular receptors in the vestibular apparatus detect linear movement and head position, with an additional component other than cilia.

50
Q

Otoliths

A

Macular sensory organs contain otoliths, crystals on the surface of the endolymph, sensing head tilting through displacement.

51
Q

Sensorineural Deafness

A

Sensorineural deafness involves damage to the transduction mechanism or conduction down the auditory nerve, often due to hair cell damage.

51
Q

Hair Cell Displacement

A

Hair cells in cristae increase firing when cilia move in one direction during head rotation, allowing us to sense the direction of head movement.

52
Q

Conductive Deafness

A

Conductive deafness blocks sounds from reaching the inner ear’s transduction mechanism, often caused by issues like wax, pressure, inflammation, or abnormal bone growth.

53
Q

Hair Cell Regeneration

A

Hair cells in mammals do not regenerate, but research in birds shows that damaged hair cells trigger surrounding cells to behave like stem cells, potentially leading to regeneration.

54
Q

Causes of Conductive Deafness

A

Causes of conductive deafness include wax, eustachian tube pressure, inflammation, eardrum perforation, and abnormal bone growth affecting sound conduction.

55
Q

Limitations of Human Hair Cell Regeneration

A

Research aims to uncover why human hair cells lack the regeneration mechanism found in birds, potentially offering molecular remedies for inducing hair cell regeneration.

56
Q

Stem Cell Research

A

Stem cell research holds promise for replacing damaged hair cells with stem cells, which can differentiate to form new functioning hair

57
Q

Nerve Deafness

A

Nerve deafness results from damage to the auditory nerve, impacting the transmission of signals from the hair cells to the brain.

58
Q

Challenges in Sensorineural Deafness

A

Sensorineural deafness challenges include damage to hair cells due to endolymph fluid buildup, head injury, age-related wear and tear, infections, or drugs, as hair cells in mammals do not regenerate.

59
Q

Tinnitus

A

Tinnitus is the continuous or intermittent ringing in the ears, often associated with the degeneration of the organ of Corti, external or middle ear problems, head injury, age, infection, or conditions like Ménière’s disease.

60
Q

Retinal Ganglion Cells

A

Activation of photoreceptors leads to the depolarization of bipolar cells, which then activate retinal ganglion cells (RGCs). RGC axons converge on the optic nerve head for signal transmission to the brain.

60
Q

Hereditary Deafness

A

Hereditary deafness exhibits diverse phenotypes, ranging from profound, congenital deafness to slowly-progressing adult onset. Over 100 mutant genes contribute to hereditary deafness.

60
Q

Eye Anatomy

A

Light enters the eye through the cornea, iris, and lens, with the ciliary muscles changing the lens shape for focusing. The iris regulates light entry. The retina, containing photoreceptor cells like rods and cones, captures focused light.

60
Q

Photoreceptor Cells

A

Rods and cones, located at the rear of the retina, detect light. Rods contain rhodopsin, while cones have pigments (red, blue, or green) absorbing light at different wavelengths.

60
Q

Vision Correction

A

Vision correction involves appropriately curved lenses to ensure precise focusing on the retina. Convex lenses are used for long-sightedness, and concave lenses for short-sightedness.

61
Q

Blind Spot

A

The optic nerve head (ONH) or optic disc is a blind spot as it lacks photoreceptor cells. Convergence of signals, lateral inhibition, and receptor density contribute to the formation of a receptive unit for light.

62
Q

Pigment Activation

A

Activation of pigments in rods and cones, such as rhodopsin in rods and red, blue, or green pigments in cones, leads to hyperpolarization, altering the firing rate in postsynaptic bipolar cells.

63
Q

Receptor Density

A

Acuity is achieved by receptor density, with the fovea being the most sensitive spot on the retina, containing only cones and having the densest population.

64
Q

Membranous Discs

A

Membranous discs in the outer segments of photoreceptors contain visual pigments and contribute to the phototransduction process.

65
Q

Optic Nerve

A

The optic nerve transmits light signals from the retina to the brain. Convergence of signals onto fewer retinal ganglion cells occurs due to synapsing onto fewer bipolar cells and lateral inhibition.

66
Q

Tonotopic Organization

A

Tonotopic organization refers to the spatial arrangement of neurons in the auditory system based on their preferred frequency of sound.

67
Q

Somatosensory System

A

The somatosensory system is responsible for processing sensory information related to touch, temperature, pain, and proprioception.

68
Q

Cross-Modal Plasticity

A

Cross-modal plasticity refers to the brain’s ability to adapt and reorganize in response to changes in sensory input, leading to enhanced performance in remaining sensory modalities.

69
Q

Plasticity in the Brain

A

Brain plasticity refers to the brain’s ability to reorganize itself by forming new neural connections throughout life, adapting to experiences, learning, and recovery from injuries.

70
Q

Pigment Activation

A

Pigment activation triggers a cGMP-mediated reduction in neurotransmitter release, leading to a decrease in postsynaptic activation of bipolar cells.

71
Q

Bipolar Cell Diversity

A

Bipolar cells exhibit diversity, with light-on bipolar cells being inhibited in the dark and activated in the light, while light-off bipolar cells show the opposite pattern. Activation depends on the neurotransmitter receptor expressed by the bipolar cells.

72
Q

Visual Processing

A

Visual processing begins in the retina, where light-on bipolar cells activate RGCs in the light, and light-off bipolar cells inhibit ganglion cells in the light, contributing to the perception of contrast in light emitted by objects.

73
Q

Inverted Image

A

Light entering the eye is inverted by the lens, requiring re-inversion when projected to the LGN to prevent perceiving the world as upside-down.

74
Q

Scotoma

A

A scotoma is a defect in the central visual field. Blind spots can cause natural scotomas. Lesions at the fovea result in the greatest loss of visual acuity.

75
Q

Retinal Lesions

A

Retinal lesions can be caused by occlusion of blood vessels, optic nerve issues, vitamin B12 deficiency, retinal detachment, or glaucoma, affecting vision.

76
Q

Glaucoma

A

Glaucoma leads to increased intraocular pressure and can impact vision. Each eye contributes information to both sides of the brain, reducing the likelihood of complete vision loss from injury to one part of the visual pathway.

77
Q

Trauma to Optic Chiasm

A

Trauma to the optic chiasm is serious and can affect all contributions to the brain. Causes include trauma, compression by tumors, atherosclerosis, or edema.

78
Q

Colour Blindness

A

Colour blindness, more prevalent in males due to its X-linked inheritance, results in the absence of one pigment. Trichromats possess blue, red, and green pigments, while dichromats lack one and monochromats are extremely rare and totally colour blind.

An4003 (4 decks)

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