Exam 3 Flashcards

1
Q

Wavelengths of the visible spectrum

A

400-700 nm

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2
Q

Scotopic range

A

Rod vision
Low light intensity
Dark-adapted

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3
Q

Photopic range

A

Cone vision
Higher light intensities
Perception of color

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4
Q

Cornea

A

bends light that forms image on retina

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5
Q

Pupil

A

allows light to enter the eye

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6
Q

Retina

A

surface inside eye that contains photoreceptors

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7
Q

Iris

A

Provides opening for pupil

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8
Q

Lens

A

Focuses light with help of ciliary muscle

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9
Q

Fovea

A

The area of the retina with the highest density of photoreceptors

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10
Q

Projected image in the eye

A

Focused, but inverted and reversed

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11
Q

Order of cells from the retina out

A

Pigmented epithelium
Rods and cones
Bipolar cell layer
Ganglion cell layer
Optic nerve fibers

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12
Q

Optic nerve

A

formed from axons of ganglion cells

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13
Q

Both rods and cones contain:

A

stacks of discs that absorb light, triggering changes in membrane potential

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14
Q

Rhodopsin

A

In membranes of discs
visual pigment found in rod photoreceptor cells in the retina

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15
Q

Phototransduction

A

11-cis-retinal is sensitive to light

becomes all-trans-retinal when it absorbs a photon

all-trans-retinal activates a G-protein (transducin) that mediates change in membrane potential

returns to 11-cis-retinal, and is photoreceptive again

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16
Q

transducin

A

G-protein activated by all-trans-retinal in photoreception in the rhodopsin molecule

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17
Q

Distributions of rods and cones across the retina

A

Most cones in the fovea
Rods are kind of opposite

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18
Q

Pupils increase in size in:

A

dim light

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19
Q

Retino-geniculo-cortical pathway

A

Optic nerve
Optic tract
Optic chiasm (where tracts cross)
Lateral geniculate nucleus
Optic radiation
Striate cortex

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20
Q

Lateral geniculate nucleus

A

Part of the retino-geniculo-cortical pathway

6 layers
Termination of the optic tract
Thalamic nucleus
Begins visual processing

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21
Q

Receptive field

A

Area where cones detect photons

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22
Q

Two types of bipolar cells

A

Off-center
On-center

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23
Q

On-center bipolar cells
Response to LIGHT

A

Inhibited by glutamate

MGluR’s

Decreased NT release from light detection causes depolarization (disinhibition)

Increases NT release from bipolar cell

Increases firing rate of ganglion cell

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24
Q

Off-center bipolar cells
Response to LIGHT

A

Excited by glutamate

Ionotropic receptors

Decreased NT release from light detection causes hyperpolarization

Decreases NT release from bipolar cell

Decreases firing rate of ganglion cell

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25
On-center bipolar cells Response to DARK
Inhibited by glutamate MGluR's Increased NT release from dark causes hyperpolarization (due to inhibition) Decreases NT release from bipolar cell Decreases firing rate of ganglion cell
26
Off-center bipolar cells Response to DARK
Excited by glutamate Ionotropic receptors Increased NT release from dark causes depolarization (due to activation) Increases NT release from bipolar cell Increases firing rate of ganglion cell
27
Simple cortical cell
receives input from a row of on-center ganglion cells, and so responds better to a bar of light (in a specific orientation) than any single spot of light Other orientations will activate off-center cells and reduce activation of that specific cortical cell
28
Complex cortical cell
receives input from a row of simple cortical cells, and so response better to a bar of light MOVING across the retina than to any stationary bar of light. The bar must still have a particular orientation
29
Spatial-frequency model of vision
The visual system analyzes the number of light-dark (or color) cycles in any stimulus Cortical neurons detect light-dark cycles and respond maximally to repeating bars of light Cortical neurons respond differently to repeating patterns of light than to single bars, and each cell fires best to patterns of a particular orientation
30
Primary visual cortex (V1)
Respond to illusory boundaries and complex relations among the parts of their receptive fields Axons project to V2, V4, and the interior temporal lobe (IT)
31
Areas involved in the perception of form
V2, V4, and IT
32
V4 area
Strong response to frequency gratings and concentric, radial, or color stimuli
33
V5 area
(MT) - Medial Temporal Area Respond to motion Different cells for each direction
34
Three dimensions of color perception
Brightness Hue Saturation
35
Brightness
varies from dark to light
36
Hue
varies throughout all colors
37
Saturation
Varies from full color to gray
38
Trichromatic hypothesis of color perception
Three types of cones Each responds to a specific, different part of the spectrum Each has a separate pathway to the brain Color recognized based on which receptors are activated
39
Trichromatic hypothesis cone types
S cones - 420 (blue) M cones - 530 (green) L cones - 560 (yellow) In daylight, almost any object stimulates at least two types
40
Opponent-Process hypothesis of color perception
Four unique hues Three opposed pairs of colors Three processes with opposed positive and negative value are the basis of color vision Black dot gray image example
41
Spectrally opponent (color-opponent) cells
Opposite firing responses to different regions of the spectrum Ganglion and LGN Cells Fire in response to some wavelengths, inhibited by others
42
Spectrally opponent ganglion cells
Receive input from two or three different types of cones via bipolar cells Excited by some wavelengths, inhibited by others Record difference in stimulation of different types of cones
43
Why can't spectrally opponent cells be called color cells?
Send outputs to higher circuits for detection of form, depth, and motion Also, detect brightness and darkness
44
Two main processing streams that origination in the primary visual cortex
Ventral Stream - objects Dorsal Stream - location
45
Ventral stream
From primary visual cortex Identifying objects Damage causes problems in perceiving faces and objects
46
Dorsal Stream
from primary visual cortex assessing the location of objections and guiding movement toward them Damage causes optic ataxia
47
Frequency of sound waves
Detected as pitch
48
Optic ataxia
Due to damage of dorsal stream from primary visual cortex Difficulty using vision to reach for and grasp objects
49
Amplitude of sound waves
Detected as loudness
50
Sound
mechanical force transduced into neural activity
51
Pinna
Collects sound waves
52
Parts of the external ear
Pinna and ear canal
53
Organ of Corti
Part of scala media that holds structures that respond to vibrations Has outer and inner hair cells Framework of supporting cells Terminations of auditory nerve fibers Tectorial and basilar membranes Converts sound into neural activity
54
Basilar membrane
Different parts respond to different frequencies
55
High frequencies and basilar membrane
Greatest effect at the base of the basilar membrane, where it is narrow and stiff
56
Low frequencies and basilar membrane
Greatest effect near the apex of the basilar membrane, where it is wider and more flexible
57
Hair cells
Outer and inner hair cells Have cilia that project into tectorial membrane Mechanoreceptors
58
IHC Afferent hair cell connections
Convey action potentials that provide sound perception to the brain
59
Efferent hair cell connections
From the brain Control responsiveness of IHC's allow brain to modify stiffness of basilar membrane
60
Inner Hair Cells
IHC Afferents are 95% of fibers leading to the brain Sound perception to the brain
61
What cells do not convey sound information?
OHC afferents
62
Vestibulocochlear Nerve (Cranial Nerve VIII)
Fibers from this nerve contact the base of hair cells
63
Outer hair cells release:
acetylcholine
64
Inner hair cells release:
glutamate
65
Tip links of stereocilia
Different lengths of cilia Movement opens ion channels permeable to K+ and Ca+ Direction of cilia movement influences membrane potential
66
Direction of cilia movement vs membrane potential (hair cells in auditory system)
Depolarization when they move toward the longest one Hyperpolarization when they move toward the shortest one
67
Primary auditory cortex
AKA A1 Dorsal area of the temporal lobe
68
Main auditory pathway
Contralateral (opposite side of brain) Cochlea CN VIII (vestibulocochlear nerve) Inferior Colliculi Medial geniculate body Acoustic radiation to A1
69
Minor auditory pathway
Ipsilateral (same side of brain) Cochlea CN VIII (vestibulocochlear nerve) Olivary nuclei Nuclei of lateral lemniscus Inferior Colliculi
70
Tuning curves of auditory nerve cells
neurons have preferred frequencies from which they fire the most, but they will respond to a spectrum of frequencies (like cones' responses to wavelengths)
71
Sounds vs speech processing in brain
Pure sound activates A1 mainly Speech sounds activate other auditory cortical regions as well as A1
72
Duplex theory of sound localization
Disparities in sound intensity and time of arrival aid in localization (sound shadow causes another ear to hear things later and less)
73
Differences in perceived intensity of sound are greater at ________ frequencies
Higher (we can distinguish differences better at higher frequencies)
74
Sensorineural deafness in the cochlea
Severe noise damage causes the stereocilia in the organ of Corti to become crushed and flattened
75
Touch and pain type of pathway
labeled line
76
Merkel's Discs
Touch receptors edges and isolated points
77
Meissner's Corpuscle
Touch receptors Changes in light touch stimuli
78
Pacinian Corpuscles
In hypodermis Respond to vibration and pressure (textures) When membrane is stretched, ion channel opens and depolarizes the cell
79
Ruffini Corpuscles
In hypodermis Respond to stretch
80
Receptive fields
Found with sensory neurons Touch in center of field excites Touch outside of field has no effect Touch right around center inhibits
81
Phasic receptors
Display adaptation (i.e. Pacinian corpuscles, action potentials slow and steady after quickly firing at the beginning)
82
Somatosensory Cortex 1 (Primary Somatosensory Cortex) S1
Contains somatosensory map Areas with more sensation (hand) have more "real estate" Where sensory information goes in the brain
83
Somatosensory pathway
Travels through DORSAL root ganglia Crosses the midline in the medulla Goes through thalamus S1
84
Pain in the periphery (pathway to the dorsal root ganglia)
Damaged cells release excitatory substances Causes blood vessels and mast cells to produce inflammation Info enters dorsal root ganglia Pain fibers release glutamate and Substance P in the spinal cord Travels up spinal cord
85
NT's involved in pain
Serotonin K+ Prostaglandins Leukotrienes Substance P
86
Nocireceptors
Peripheral receptors on free nerve endings that respond to painful stimuli
87
Two types of nocireceptors
Transient receptor potential vanilloid Type (TRVP1) Transient receptor potential type (TRPM3)
88
Transient receptor potential type (TRPM3)
Nocireceptor A delta fibers Large diameter Myelinated Quick, immediate pain response
89
Transient receptor potential vanilloid Type (TRVP1)
Nocireceptor C fibers Thin Unmyelinated Slower, long-lasting, delayed aches
90
Spinothalamic ascending pain pathway
Glutamate and substance P released by A delta fibers and C fibers Cross the midline at the spinal cord Carry info through periaqueductal gray (opioid receptors) Goes through thalamus Then to S1
91
Gate control theory
Spinal "gates" (modulation sites) control the signal that goes to the brain
92
Analgesia
Absence of or reduction in pain Opiate drugs and endogenous opioids bind to receptors in the brain to reduce pain
93
Types of pain relief
Psychogenic Pharmacological Stimulation
94
Motor neurons
Sent AP's down axons to innervate muscles Release ACh (acetylcholine)
95
Proprioceptor
Responds to position and movement
96
Two types of proprioceptors
Muscle spindles Golgi tendon organs
97
Muscle spindles
Type of proprioceptor Capsule buried in other muscle fibers, contains intrafusal fibers Respond to stretch
98
Golgi tendon organs
Type of proprioceptor Respond to shortening (tension)
99
Primary pyramidal system
Motor pathway Leaves primary motor cortex (M1) Travels down the pyramid of medulla Cross to the opposite side in the medulla (contralateral projection) Travel down VENTRAL corticospinal tract
100
Primary Motor Cortex
Located in the precentral gyrus Larger areas have more motor capabilities (i.e. hand)
101
Supplementary motor cortex
Anterior to motor cortex Initiation of movement sequences
102
Premotor cortex
Anterior to motor cortex Guides motor sequences, particularly in response to external events and cues
103
Motor cortex damage
Plegia or paresis of voluntary movements Apraxia
104
Mirror neurons
Located in a subregion of premotor cortex (F5) Same neurons fire before making a movement as when observing another individual make the same movement
105
Extrapyramidal motor systems
Other axon pathways outside the pyramids of the medulla May go through spinal cord and brainstem (reticular formation)
106
Damage to extrapyramidal motor systems
Interferes with spinal reflexes and systems that fine tune motor behavior
107
Extrapyramidal motor systems examples
Basal ganglia Cerebellum
108
Basal ganglia
Extrapyramidal system Controls amplitude and direction of movement, initiation of movement, muscle memory
109
Cerebellum
Extrapyramidal system Guides movement through inhibition Fine-tune skilled movements Muscle memory
110
Cerebellar damage
abnormal gait and posture, especially ataxia (loss of coordination) of the legs
111
Wernicke-Korsakoff Syndrome
Loss of white matter in cerebellum and corpus callosum Loss of purkinje neurons in cerebellum Due to thiamine deficiency form alcohol consumption
112
Symptoms of Wernicke-Korsakoff Syndrome
Amnesia and cognitive dysfunction Posture and balance instability Ocular motor abnormalities Ataxia
113
Parkinson's Disease
Loss of dopaminergic cells in the substantia nigra
114
Parkinson's symptoms
tremors in the hands and face rigid posture reduced facial expression slowed and lack of movement
115
Treatments of parkinson's
Deep brain stimulation l-DOPA (precursor or dopamine)
116
Huntington's disease
Highly genetic (defective dominant gene HTT) Begin showing symptoms at age 30-50 Progressive damage to the basal ganglia, especially caudate, putamen, globus pallidus
117
Huntington's disease symptoms
Clumsiness and twitches of the fingers and face Excessive movement Uncontrolled movement Forgetfulness and impaired judgement
118
Difference between Parkinson's and HD
Parkinson's eventually leads to a reduction of movement, where HD has increasing excessive movement
119
Split brain studies
Split brain individuals are able to verbally report only words presented to the left hemisphere This is because the left hemisphere is the only one that has language areas necessary for verbalizing what they saw
120
Dichotic presentation of sound
Sound from the left ear takes longer (has to go to the right brain, then back to the speech zone in the left brain Right ear is faster because it goes to the left brain and the language center is already there
121
Right ear advantage
Right-handed people identify verbal stimuli delivered to the right ear more easily
122
Planum temporale
Activated when we hear speech rather than sounds larger in the left hemisphere, even in infants before the development of language
123
Perception of music
Right hemisphere mediated
124
Perfect pitch
Left hemisphere mechanisms
125
Congenital amusia
Tone Deafness
126
Wada test
Anesthetize one hemisphere of the brain Barbiturate injected into carotid artery helps figure out what side of the brain is important for different language and memory functions
127
Left hemisphere functions
Speech Understanding language Influenced by handedness
128
Right hemisphere functions
Processing spacial stimuli Object recognition Face perception
129
Left-handedness is...
hereditary
130
Agnosia
Inability to recognize objects
131
Associative agnosia
perceive objects, but cannot identify them
132
Astereognosia
inability to recognize objects by touch
133
Simultanagnosia
can perceive the basic shape of an object, but unable to perceive more than one object at a time
134
Prosopagnosia
Inability to recognize faces, including one's own
135
Hemispheres involved in recognizing faces
Both hemispheres Bilateral damage causes complete prosopagnosia
136
Damage of _____________ causes prosopagnosia
fusiform gyrus in inferotemporal cortex
137
Neurons needed to encode the shape and basic appearance of a face
~200 neurons in the medial temporal lobe
138
Phonemes
Basic speech sounds
139
morphemes
simple units of meaning
140
Syntax
words are assembled into meaningful strings with rules
141
Pragmatics
contextual information
142
Prosody
emotional tone and emphasis
143
aphasia
impairment in language ability, to varying degrees, caused by brain injury, especially in the left hemisphere
144
Paraphasia
substitution of a word by a sound, incorrect word, or unintended word
145
Most patients with aphasia also exhibit:
Agraphia, Alexia, apraxia
146
Agraphia
impairment in writing
147
alexia
impairment in reading
148
apraxia
motor impairment: difficulty making sequences of movements for speech
149
Broca's area
region of the left inferior frontal region involved in speech production
150
Broca's area is near:
the motor cortex
151
Broca's aphasia
Nonfluent aphasia Difficulty producing speech but not with comprehension many people with this also have hemiplegia
152
hemiplegia
often associated with Broca's aphasia paralysis of one side of the body, usually the right side
153
Wernicke's area
region of the left posterior temporo-parietal cortex involved in perception and production of speech
154
Wernicke's aphasia
Fluent Aphasia Meaningless speech accompanied by many paraphasias and minimal language comprehension unable to repeat words or phrases may also include anomia word deafness word blindness
155
Anomia
often associated with Wernicke's aphasia Difficulty naming objects or finding words spontaneously
156
Global aphasia
total loss of the ability to understand or produce language Widespread left hemisphere lesions affecting all speech zones Often accompanied by other neurological impairments
157
Connectionist model of aphasia Speaking a heard word
First sound info goes to primary auditory cortex sent to Wernicke's area then transmitted via the arcuate fasciculus to Broca's area then sent to motor cortex
158
Connectionist model of aphasia Speaking a written word
Visual cortex analyzes info Transmits info to angular gyrus Angular gyrus decodes info to recognize the word, then sends this to Wernicke's area Then same as speaking a heard word (arcuate fasciculus to Broca's, then motor cortex)
159
Diffusion tensor imaging (DTI)
shows the arcuate nucleus and how it terminates in the precentral gyrus
160
Conduction aphasia
consequence of damage to the superior temporal cortex, not white matter tracts
161
Motor theory of language
Anterior and posterior left-hemisphere language zones are motor control systems Aphasia is observed in people who use sign language following brain imagery in the left hemisphere
162
PET Scan activation for passively viewing words
posterior area within the left hemisphere
163
PET Scan activation for passively hearing words
temporal lobes
164
Event-related potentials (ERPs) and language processing
N400 errors and P600 errors Shows that a word with an error in meaning is processed more quickly than an error in grammar
165
N400 potential
Error in meaning Negative potential Processed faster
166
P600 potential
Error in grammar Positive potential Longer to process
167
Dyslexia
mild to severe difficulty with reading attributed to brain impairment
168
Acquired dyslexia
Alexia sudden dyslexia after brain damage, usually to the left hemisphere
169
Deep dyslexia
patients read one word as another, related word
170
Surface dyslexia
patients are restricted to the regular sound rules of letters
171
Developmental dyslexia
unique to written language Associated with neurological abnormalities
172
Left hemisphere sites with decreased activity in dyslexia patients
Left inferior parietotemporal region Left inferior fusiform region
173
Is dyslexia a cognitive deficit?
No
174
Plutchik's Eight basic emotions
Joy/sadness Affection/disgust Anger/fear Expectation/surprise
175
Folk psychology theory of emotion
Stimulus Perception/Interpretation Emotion Autonomic arousal
176
James-Lange theory of emotion
Stimulus Perception/Interpretation Autonomic arousal Emotion
177
Cannon-Bard theory of emotion
Stimulus Perception/Interpretation Autonomic arousal and emotion happen simultaneously
178
Schachter's Theory
Stimulus Perception/Interpretation Autonomic arousal COGNITIVE appraisal of CONTEXT Emotion
179
Ekman's Universal facial expressions
Anger Sadness Happiness Fear Disgust Surprise Contempt Embarrassment
180
Hemisphere involved in emotion
Right hemisphere
181
Side of face that is more emotionally expressive
Left side (right hemisphere)
182
Medial forebrain bundle
tract that rises from the midbrain throughout the hypothalamus brain site that supports positive self-stimulation and mediates positive emotions
183
Limbic system
Proposed subcortical circuit for emotion Includes amygdala and hippocampus
184
Kluver-Bucy Syndrome
Dramatic reduction of fear and anxiety following bilateral amygdala damage
185
Amygdala and emotional learning
Fear-provoking stimuli either take the high road or low road to the amygdala
186
High Road
Fear-provoking stimulus Thalamus Sensory cortex & Hippocampus Amygdala Allows for slower conscious perception that can integrate with the higher-level cognitive functions of learning and memory
187
Low road
Fear-provoking stimulus thalamus Directed immediately to amygdala
188
Different parts of the brain involved in emotion
Insula cingulate cortex prefrontal cortex
189
Physical stress
caused by traumatic events, illness, injury
190
Psychological stress
has an emotional and mental aspect (fear, anxiety, grief)
191
Claude Bernard
Introduced the concept of milieu interieur
192
Walter Cannon
Coined the term "homeostasis" to describe physiological reactions that maintain a steady state in response to external challenges
193
Hans Selye
irrespective of the nature of a stressor, the physiological response is similar General Adaptation Syndrome
194
General Adaptation Syndrome
Alarm Stage Arousal/resistance Exhaustion
195
Two systems triggered by stress
Sympathetic nervous system Hypothalamic-Pituitary-Adrenal (HPA) Axis
196
Sympathetic nervous system stress response
Epinephrine and norepinephrine form the adrenal medulla Boosts HR, Resp rate, BP, etc.
197
HPA Axis stress response
Cortisol from adrenal cortex Promotes energy use through the body by increasing proteins and enzymes of glucose and lipid metabolism
198
Noradrenergic changes in response to social stress
Epinephrine and Norepinephrine increase
199
HPA Axis process that leads to cortisol release
Parvocellular neurosecretory cells in Hypothalamus release CRH Enters to anterior pituitary through hypophyseal portal circulation Anterior pituitary releases ACTH ACTH activates adrenals
200
Cortisol feedback
Negative feedback loop
201
Chronic stress on HPA Axis
Chronic stress alters negative feedback of the HPA Axis
202
Cortisol type of hormone
Steroid
203
Activity of cortisol at glucocorticoid receptors
Affects genes involved in endocrine, immune, and metabolic functions: -CRH (regulates HPA axis) -Leptin (energy homeostasis) -Cytokines (immune/inflammatory response)
204
Stress and immune function
Dental students give mouth wound The wound healed 40% more slowly during an exam period
205
Behavioral medicine
social factors that cause, or influence the progression of illness
206
Psychoneuroimmunology
how the immune system interacts with psychological and neurological processes
207
Stress effect on learning and memory
Can impair memory (during an exam) Can improve memory (embarrassing experience)
208
Stress effect on areas of the brain
Decreases the volume of the hippocampus and prefrontal cortex
209
Things that increase volume of prefrontal cortex and neuron number
Exercise (volume and number) Cognitive Behavioral Therapy (prefrontal cortex volume)