H6 Smell, taste, pain, hearing and psychophysics Flashcards

1
Q

How can the process of sensation be described as a chain of three different kinds of events?

A
  1. Physical stimulus: matter/energy of phsycial world that impinges on sense organs.
  2. Physiological response: pattern of chemical/electrical activity that occurs in sense organs, nerves and brain as a result of stimulus
  3. Sensory experience: subjective/psychological sensation or perception experienced by individual whose sense organs have been stimulated
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2
Q

What are sensory neurons?

A

Neurons that carry information from sensory receptors to CNS

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3
Q

Where are the primary taste area, primary olfactory area, primary auditory area, primary visaul area and primary somatosensory area located?

A

Taste: insula, in between frontal and temporal lobe
Olfactory: front temporal lobe
Auditory: upper part temporal lobe
Visual: occipital area, achterste gedeelte
somatosensory: parietal lobe, grenzend aan frontal lobe

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4
Q

In general, how do physical stimuli produce action potentials in sensory neurons?

A

Through transduction: neural process by which the receptor produces an electrical change in response to physical stimulation, which is carried forward by sensory neuron

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5
Q

In general, how do sensory systems code information about the amount and kind of stimulus energy?

A

Quantity: the stronger the sitmulus, the larger the receptor potentials, which leads to a higher frequency of action potentials in sensory neurons.
Quality: qualitatively different stimuli activate different sets of sensory neurons

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6
Q

What is the value of sensory adaptataion? Does adaptation occur in receptors or neurons in the CNS?
What is the effect of lack vs continuous stimulation?

A

Saving energy: not getting stimulated as much by every sensation, only by new sensations.
Lack of stimulation increases sensitivity, continuus stimulation decreases sensitivity.

Both.

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7
Q

What is psychophysics?
What are 2 measures of sensitivity within the field of psychophysics?
What does Weber’s law state?

A

Study relationships between physical chracteristics of stimuli and the sensory experiences produced by those stimuli.1
1. Absolute threshold: Faintest detectable stimulus. Serve as a measure of a person’s sensitivity.
2. Difference threshold/just noticable threshold: minimal difference between 2 stimuli that person can detect.
Weber’s law: just noticable threshold is a constant proportion of the magnitude of original stimulus

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8
Q

What does the signal detection theory state?

A

That the detection of a stimulus does not only rely on the physical properties (such as strength of stimulus) but also on psychological state (such as motivation).

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9
Q

How do transduction, qualitative coding and quantitative coding occur for the sense of smell?

A

Transduction: chemicals bind to receptors of olfactory sensory neurons in olfactory epithelium> action potentials
Qualitative: different sensory neurons have different sensitivity to different odor molecules. Sensory neurons form synapses on glomeruli (to do this, the axons go into the olfactory bulb). The total pattern of which sensory neurons and which glomeruli are stimulated determine the qualitative coding.
Quantitative: amount of odor molecules

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10
Q

How do we smell foods that are already in our mouths and what evidence indicates that smell contributes greatly to flavour?

A

Mouth has connection to olfactory bulb: odor molecules go through nasal pharunx to nasal cavity.
We can’t distinguish flavours with shut nostrils.

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11
Q

How do sex, age, genetic differences and experience affect sensitivity to smell?

A

Sex: women are more sensitive
Age: younger people are more sensitive
Genetic: genetic variations affect production of specific olfactory receptors
Experience: stimulation of receptors can increase or decrease sensitivity

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12
Q

From an evolutionary perspective, why might mice prefer to mate with others that smell most different from themselves?

A
  1. Less likely to be close relatives
  2. More genetic variation to mix of disease fighting cells: 50 highly variable genes, collectively: major histocompatibility complex (MHC)
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13
Q

What are 3 functions of pheromones? And what is the vomeronasal organ?
Do humans have it?

A

Serve functions as sexual attraction, territorial marking and regulation of hormone production. This organ contains receptors specialized in pheromones. Most mammals have it. Ours is vestigial, unsure if it’s entirely vestigial. We were unable to find human specific secretion that consistently attracts members of opposite sex. From evolutionary perspective, humans do not need sex-attractant pheromones.

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14
Q

How does transduction occur in taste?

A

Sensory receptors are not directly on taste neurons, like with smell.
Taste molecules bind to the receptors of taste receptor cells in the fusiform papillae that contain taste buds > electrical change > action potentials in gustatory neurons

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15
Q

From an evolutionary perspective what is the function of each of the primary tastes? Why does bitter sensation increase in women during pregnancy?
Why do so many chemically diverse substances taste bitter?

A
1. Sweet: energy
Salt: homeostasis
Sour: Decay
Bitter: toxic
Umami: protein: tissue building and restoration
Fat: energy and tissue building

Because each is able too bind to one or another of the approximately 25 different types of receptor sites located on t bitter receptor cells

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16
Q

In what ways is pain a body sense, an emotion and a drive?

A
  1. Body sense: comes from within the body instead of external
  2. Emotion: strong pain can overwhelm the conscious mind
  3. Drive: avoid things that cause pain
17
Q

Are the receptor cells separate from sensory neurons or not when it comes to pain?

A

Receptor cells are sensory neurons. Their sensitive terminals, called free nerve endngs, are not encased in special capsules or end organs, as are the endings of touch and temperature receptors.

18
Q

What is the anatomical basis for the distinction between first and second pain?
Where do the neurons terminate?

A

First: A delta fibers, thick, myelinated fast
Second: C fibers, thin, unmyelinated, slow.
Terminate in brainstem on interneurons > reflexes and info put forward to thalamus

19
Q

What are the 3 different components of pain experience and with which areas are they associated?

A
  1. Sensory: somatosensory cortex; sensation, intensity and qualities, location
  2. Primary emotional and motivational: cingulate and insular cortex; motivation to escape pain
    3 Secondary emotional and motivational: prefrontal; worry about future or about meaning of pain
20
Q

What is the gate control theory of pain?

A

Explains Interpersonal variability in sensitivity to pain. It says that the experience of pain depends on the degree to which input from pain sensory neurons can pass through a neural gate and reach higher pain centers in the brain.
Volgens de gate-control theory is er een informatiepoort in de hersenstam (voor pijnprikkels van boven de nek) en in het ruggenmerg (voor pijnprikkels vanuit de rest van het lichaam) die de pijnprikkel doorgeeft aan het centrale zenuwstelsel en vervolgens aan de hersenen. De mate waarin pijn wordt ervaren is afhankelijk van in hoeverre de input van sensorische neuronen voor pijn kan worden doorgesluisd naar de pijntransmissieneuronen die de informatie doorgeven aan de hogere hersengebieden. De C fibers en A-delta fibers zijn de sensorische neuronen voor pijn die de pijnstimulus waarnemen en doorgeven aan het centrale zenuwstelsel. Bij de poort in het centrale zenuwstelsel (in hersenstam of ruggenmerg, afhankelijk van waar de pijnprikkel wordt waargenomen) eindigen de axonen van deze sensorische neuronen voor pijn en geven deze neuronen de input door aan de pijntransmissieneuronen. De mate waarin deze pijntransmissieneuronen reageren op de sensorische neuronen voor pijn is afhankelijk van de input van pijn-exciterende en pijn-inhiberende neuronen. Deze pijn-exciterende en pijn-inhiberende neuronen krijgen informatie van hogere hersengebieden (denk aan de invloed van emoties, verwachtingen en selectieve aandacht) en kunnen de pijntransmissieneuronen meer of minder ontvankelijk maken voor het reageren op de input van de sensorische neuronen voor pijn. De “pain-inhibiting” neuronen zijn dus de neuronen die de poort ‘sluiten’ en de “pain-enhancing” neuronen die de poort ‘openen’. Wanneer de poort gesloten is, wordt pijnperceptie geïnhibeerd (geblokkeerd), zelfs als een pijnbron aanwezig is.

21
Q

How does injury produce a localized increase in pain sensitivity?

A

Changes in free nerve endings of C fibers and A delta fibers that are induced by chemicals released from damaged cells.

22
Q

How can pain input be inhibited at its entry into the CNS and how (name the area) might endorphins be involved in pain inhibition?

A

PAG: paeriaqueductal gray is a neual center for pain inhibition in midbrain > increased acitivty > reduced pain.
Endorphins act on PAG and at places where pain carrying neurons enter the spinal cord and lower brainstem.

23
Q

What is analgesia? Is it mediated by endorphins?

A

Decreased pain sensitivity that accompanies stressful situations. Is taken away by giving endorphine blocking substances.

24
Q

What is the sound’s amplitude vs frequency?

A

Amplitude: intensity, loudness, dB
Frequency: sound’s pitch, Hz

25
Q

What are functions of the outer, middle and inner ear?

Describe what the middle ear looks like.

A

Outer: funnel for receiving sound and transporting it inward
Middle: increase amount of pressure that sound waves exert on inner ear; contain 3 little bones: hammer, anvil, stirrup, linked to eardrum at one end (outer ear) and to another membrane (oval window) at the other end (inner ear)
Inner: transduction

26
Q

How does transduction occur in inner ear?

What is the difference in high pitch and low pitch sounds?

A

Vibrations of bones in middle ear against oval window initiate vibration in fluid in outer duct of cochlea. Vibration leads to up and down waving motion of basilar membrane (super flexible), on which receptor cells for hearing are located: hair cells. Tectorial membrane on other end of hair cells does not move. Therefore, hair cells bend > tiny channels open op in hair cell’s membrane > change in electrical charge across membrane > neurotransmitters are released upon auditory neurons > action potentials.

High pitch: rapid firing neurons proximal end of membrane
Low pitch: distal end

27
Q

How do 2 kinds of deafness differ in their physiological bases and in possible treatment?

A
  1. Conduction deafness: ossicles rigid > hearing aid
  2. Sensorineural: damage to hair cells in cochlea/damage to auditory neurons. cochlear implant only works for damaged hair cells.
28
Q

How does the travelling wave theory explain the pattern of hearing loss that occurs as we get older?

A

Cells coding high frequencies are acted upon by all sounds, while those coding low frequencies are acted upon by only low frequency sounds

29
Q

How does the timing of action potentials code sound frequency? How do cochlear implants produce perception of pitch?

A

Burst of action potentials each time a sound wave peaks> frequency of bursts contributes to perception of pitch.
THey use both place and timing.

30
Q

How is tone frequency represented in the primary auditory cortex?

On what area does the capacity to distinguish pitch also depend on?

A

Tonotopically: each neuron is maximally responsive to sounds of a particular frequency, arranged from high to low.
Capacity to distinguish pitch depends also on intraparietal sulcus: involved in music perception and visual space perception

31
Q

What are phonemes and phonemic restoration?

A

Indiviual vowel and consonant sounds that make up words.

People hear phonemes that have been deletec from words or sentences as if they were still there.

32
Q

Hoe wordt in het boek fantoompijn verklaard? Probeer uit te leggen hoe dit een beperking vormt van de gate-control theory.

A

In het boek wordt aangegeven dat het gebrek aan sensorische input, vanwege een verwijderde ledemaat, fantoompijn kan verklaren. Het boek beschrijft op p210 hierover: ‘This suggests that the brain’s mechanism for experiencing pain and assigning it to a particular body location can be activated without sensory input from that part of the body. In fact, the lack of sensory input might trigger phantom-limb pain by removing a source of inhibition to the pain mechanisms of the brain.’

De gate-control theory beschrijft hoe input vanuit de pijnzenuwen (A-delta en C-vezels) wordt doorgegeven aan pijntransmissieneuronen en hoe interneuronen deze pijntransmissieneuronen meer of minder responsief kunnen maken en hiermee kunnen zorgen voor een verschil in pijnbeleving. In deze theorie staat dus de input van de pijnzenuwen centraal en wordt een mechanisme beschreven dat verklaart in welke mate dit pijnsignaal wordt doorgegeven aan hogere hersengebieden.

Fantoompijn kan echter optreden zonder een pijnprikkel vanuit de omgeving (want juist een gebrek aan sensorische input lijkt een oorzaak te zijn van fantoompijn). Fantoompijn vormt hiermee een beperking van de gate-control theory. Fantoompijn laat immers zien dat stimuli uit de omgeving (bijv. een speldenprik) niet de oorsprong zijn van de pijnbeleving (want dan zou met het amputeren van een ledemaat geen pijn meer gevoeld moeten worden want dan is er geen sensorische input meer vanuit dit deel van het lichaam). Stimuli uit de omgeving zouden dan eerder als trigger dan als oorsprong opgevat moeten worden van de pijnbeleving.

Merk op dat deze vraag en terugkoppeling daarop verder gaan dan de informatie uit het boek. Het boek is tentamenstof. De relatie tussen fantoompijn en in hoeverre dit wel/niet verklaard kan worden door de gate-control theory staat niet beschreven in het boek en vormt daarmee geen tentamenstof. Merk verder op dat de formulering van deze vraag (en de terugkoppeling daarop) is aangepast. Aangezien deze vraag en terugkoppeling daarop geen tentamenstof vormen, heeft dit geen consequenties voor het tentamen.