FOUNDATIONS OF COGNITIVE PSYCHOLOGY AND NEUROSCIENCE I
LESSON 1
Some history:
The Egyptians believed the brain was useless, it was just there to ll the skull. Aristotle believed it was there
to cool down the blood. At last, Galen (150 CE) gured that consciousness and intelligence would reside in
the brain. Fast-forward to Descartes, who neatly separated the body (a tangible machine that functions based
on the four humours, which could be properly studied) from the mind (intangible, can’t be studied) (cartesian
dualism). Even though these were some pretty intelligent guys, they were led astray by the poor technology
and the batshit crazy scienti c misconceptions of their time. We all agree that the Enlightenment was a really
cool time for science, but still, Phrenology was a thing. Even though it suggested that certain areas of the
brain do certain things (which is kind of true), the theory that a more developed function would determine a
bump in the skull is just bullshit. Fun fact: Phrenology was debunked by Napoleon. Basically, a smart guy
(Gall) into phrenology said like: “judging by the shape of his head, Napoleon is a very pragmatic person, not
that intelligent though”. Napoleon was offended and hired a smarter guy (Flourens) to debunk phrenology.
Flourens came up with the aggregate elds theory: different brain regions work together in order to
accomplish a speci c function.
There are a few people who contributed to linking certain brain areas to speci c functions: John Hughlings
Jackson, who noticed that seizures tend to follow a speci c pattern; good old Phineas Gage, whose PFC was
absolutely devastated, with severe consequences on his social behaviour, Broca and Wernicke, who studied
different forms of speech impairment caused by brain damage and Galvani, who gured out (by accident)
that brain activity has an electrical nature and has nothing to do with the humours. But one of the most
important contributors to the development of neuroscience is Ramon y Cajal. Based on Golgi’s silver stain,
he theorized that the brain was not just a single, big, messy network, but was made out of individual cells,
called neurons (Neuronal doctrine). Also, Hubel and Wiesel (1959-62) were among the rst to record the
activity of a single neuron (a single unit recording of a V1 neuron from a monkey).
Hubel and Wiesel recorded a single cell, but you can also record multiple at the same time (since nearby
neurons like to re in unison), in a so called “local eld potential” (LFP). And if you record thousands and
thousands at a time, they create such a strong electrical eld that you can record it from the scalp. Boom,
you’ve got electroencephalography (invented by Hans Berger in 1924). EEG can record oscillations and/or
ERP (neuron activation in response to an external stimulus, but to get a clear signal you need to average
many many trials to rule out the noise). Even though EEG has a killer temporal resolution, it has a really bad
spatial resolution, you can barely guess where the signal came from. MEG (magnetoencephalography) is
much much better: better temporal and spatial (still, not amazing) resolution, much cleaner signal, but it costs
an arm and a leg. EcoG (electrocorticography) has fantastic temporal and spatial resolution, but you can do it
on very few subjects (because you need to split their head open and apply the electrodes directly on the
brain).
Onto a brief history of psychology and its methods:
We started studying psychological phenomena via introspection, which is a really shitty method because it is
extremely subjective. James (functionalism) gured that in order to study the mind, we must nd a way to
measure it, and that’s what behaviourism did. Thorndike, Skinner, Watson and friends studied the behaviour
as an objective, measurable response to a stimulus, who cares about the mind? Not me. Cognitivism does,
because not everything can be learned through conditioning and not everything can be studied through the
behaviour. Cognitivism was inspired by the emerging computer science. Finally, Neuropsychology was born
as a marriage between neurology and cognitive psychology. It wanted to study how the brain affects the mind
(mainly by studying broken brains).
Strengths of Neuropsychology: it’s causal; natural experiments (?)
Weaknesses: Idiosyncratic (the same damage may cause different symptoms in different subjects); plasticity
(a damaged brain will do its best to x himself by reorganizing structure and functions); brain damage is
more prevalent in certain regions.
Onto some brain stimulation and imaging:
TMS is a cool way to stimulate the brain, before (of ine TMS) or during (online TMS) a task. But the real
star of the show is fMRI. It has a good spatial resolution but an awful temporal resolution (it measures
blood ow, not neuron activity). The invention of fMRI gave origin to a lot of studies that were simple but
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, extremely important. Nowadays we still have plenty of studies being published at a really high speed, but
what about the quality?
LESSON 2
Inside the neuron you’ve got a negative charge (resting membrane potential), because most of the
Na+ is outside. There are, however, some ionic channels which allow the Na+ to rush inside the
cell, depolarizing it and causing an action potential, which always travels from the axon hillock to
the presynaptic terminals, never the opposite.
A postsynaptic potential (PSP) is a temporary change in the electrical membrane potential of a
postsynaptic neuron (the neuron receiving a signal) that occurs in response to neurotransmitters
released by a presynaptic neuron (the neuron sending the signal) at a synapse.
The terminals will release some neurotransmitters to the post-synaptic neuron, causing a graded
potential which goes from the dendrites to the nucleus. From here (actually, from the hillock), if a
speci c threshold is reached, an action potential is triggered and so on.
For the anatomy of the brain, check the slides.
Can you not do anything? Nope, even when you think you’re doing nothing, your brain is working,
namely, the default mode network (DMN), which is comprised of mPFC, MTL, lateral temporal
cortex, precuneus/retrosplenial cortex and lateral parietal cortex. And what if you are doing
something? The task positive network is working. However, if you’re doing a mind wandering task,
the DMN is on.
TO CLEAR THINGS UP
The differences between postsynaptic potential (PSP), action potential (AP), and graded
potential (GP) lie in their mechanisms, characteristics, and roles in neural signaling. Here’s a
breakdown:
1. Postsynaptic Potential (PSP)
• De nition: A change in membrane potential that occurs in the postsynaptic neuron in response to
neurotransmitter binding at a synapse.
• Types:
◦ Excitatory PSP (EPSP): Depolarizes the membrane (makes it less negative).
◦ Inhibitory PSP (IPSP): Hyperpolarizes the membrane (makes it more negative).
• Location: Occurs on the dendrites or cell body (soma) of the postsynaptic neuron.
• Amplitude: Graded; depends on the amount of neurotransmitter released and the number of
receptors activated.
• Summation: PSPs can sum both temporally (over time) and spatially (from different synapses),
leading to either a cumulative depolarization or hyperpolarization.
• Function: Modulates the likelihood of generating an action potential in the postsynaptic neuron but
does not itself cause an action potential.
2. Action Potential (AP)
• De nition: A rapid, all-or-none electrical signal that propagates along the axon of a neuron when
the membrane potential reaches a critical threshold.
• Location: Generated at the axon hillock (initial segment of the axon) and propagates along the axon
to the synaptic terminals.
• Amplitude: Always the same (all-or-none) once the threshold is reached, regardless of the stimulus
intensity.
• Propagation: Self-propagating and does not degrade over distance; travels in a unidirectional
manner along the axon.
• Threshold: Requires the membrane potential to depolarize to a speci c threshold (usually around
-55 mV) for initiation.
• Function: Transmits information over long distances within the nervous system, allowing for
communication between neurons and effector organs (muscles, glands, etc.).
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, 3. Graded Potential (GP)
• De nition: A localized change in membrane potential that occurs in response to stimuli, but its
amplitude varies with the strength of the stimulus.
• Location: Occurs primarily in the dendrites and cell body of neurons, and can also occur in sensory
receptors (like in the skin or retina).
• Amplitude: Variable; depends on the intensity of the stimulus. The stronger the stimulus, the larger
the graded potential.
• Propagation: Decremental; the potential decreases as it moves away from the site of initiation,
meaning it fades over distance.
• Summation: Like PSPs, graded potentials can summate both temporally and spatially to in uence
the generation of an action potential.
• Function: Acts as the initial step in neural signaling by causing small, localized changes in
membrane potential, which can either trigger or inhibit an action potential.
Charact Postsynaptic Action Potential
Graded Potential (GP)
eristic Potential (PSP) (AP)
Neurotransmitter Threshold
Trigger Stimulus (e.g., sensory input)
binding depolarization
Amplitu
Graded, variable All-or-none ( xed) Graded, variable
de
Propaga Self-propagating,
Local, decremental Local, decremental
tion non-decremental
Locatio Dendrites, soma, sensory
Dendrites, soma Axon
n receptors
Summat Yes (temporal,
No summation Yes (temporal, spatial)
ion spatial)
Functio Modulate action Long-distance Localized potential change,
n potential likelihood signaling modulates AP likelihood
In summary:
• PSPs are speci c types of graded potentials generated by synaptic activity and can lead to or
inhibit action potentials.
• Action potentials are uniform, long-distance signals that transmit information within
neurons.
• Graded potentials are variable, local changes in membrane potential that can summate and
trigger an action potential if they reach threshold.
LESSON 3
Vision
The pupil and iris (which contains circular muscles) control the aperture of your eye, allowing the
right amount of light inside. The light then goes through the lens (to focus) which, being curved,
projects and upside image on the retina. The dead center of you retina is called fovea (which
contains many cones and few rods for a really high resolution) and the periphery is called parafovea
(with many rods and few cones, lower resolution but high sensitivity to motion). The retina has
many layers. You’ve got a layer of cones (for chromatic vision) and rods (for b/w vision); they send
signals to a layer of bipolar cells; they send signals to a layer of ganglion cells (with a few amacrine
cells in between). The ganglion cells form the optical nerve which pokes through your parafovea
(leaving a blind spot), splits in two (L/R visual elds) at the optic chiasm and goes to the LGN
(lateral geniculate nucleus, but a small portion of the visual signals goes through the superior
colliculus instead of the LGN) in the thalamus and into your primary visual cortex (V1).
fi fi fi fi fl
, Light causes a chemical reaction that makes a photoreceptor more likely to re. Cones will respond
differently depending on the wavelength of the light, so basically they like a speci c color between
red, green and blue. The thing is, green and red have similar wavelengths, so it’s possible that cones
respond to the wrong color. This problem is solved by the ganglion cells, they too have color
preference, namely blue/yellow and red/green. This double layer of color-speci c cells allows to
better discriminate colours. Also, color resolution gets better the higher you go in the visual
hierarchy, you get a lot more shades.
Lateral inhibition happens when excited photoreceptors inhibit the neighboring photoreceptors.
Opponent-process theory (ganglion cells): It explains color perception through specialized
ganglion cells that process signals from cone photoreceptors. These signals are organized into
opponent channels:
1. Red-green channel: Compares input from medium (M) and long (L) wavelength cones. Red
excites one side, green excites the other.
2. Blue-yellow channel: Compares input from short (S) cones to the combined input of M and
L cones. Blue excites one side, yellow excites the other.
3. Light-dark (luminance) channel: Combines all cones to detect brightness.
Ganglion cells have opponent receptive elds: stimulation in one region excites a response (e.g.,
red), while stimulation in the opposing region inhibits it (e.g., green). This antagonism prevents the
simultaneous perception of certain color combinations (e.g., reddish-green).
This theory explains phenomena like afterimages (e.g., staring at green causes a red afterimage)
and enhances color contrast by detecting edges and color changes.
Every cell in the visual system has a receptive eld, a portion of space represented by the cells. The
RFs get bigger the higher you go in the hierarchy. Ganglion cells have an excitatory region in the
centre of the RF and an inhibitory region in the periphery of the RF. If the stimulus falls in the
middle, the cell is excited; if it falls in the periphery, it is inhibited; if it falls in between, + and – try
to cancel each other out.
V1 cells like lines, and each cell has a favourite orientation of such lines. The “line” signal is
actually the combined signals of many ganglion cells, whose excitatory regions in their RFs have
been stimulated by an external stimulus. V1 cells that like the same orientation of a line are
organized in orientation-selective cortical columns. These columns are then organized in left and
right-eye columns. A cortical module is a piece of cortex that contains all the orientation columns
for the left and right eye.
Ocular dominance columns (V1): The
primary visual cortex (V1) processes visual
information through a highly organized
structure. Visual input from each eye is
separated into ocular dominance columns,
which are vertical bands of neurons that
respond preferentially to either the left or right
eye. Within these columns are orientation
columns, where neurons are tuned to detect
speci c line orientations, enabling the brain to
identify edges and contours in the visual eld.
Scattered among these are blobs, circular
regions specialized for processing color
information, while the rest of the column
handles contrast and brightness. Together, these
elements form cortical modules, which are functional units in V1. Each module contains all the
necessary information—line orientation, color, and intensity—for processing a small portion of the
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LESSON 1
Some history:
The Egyptians believed the brain was useless, it was just there to ll the skull. Aristotle believed it was there
to cool down the blood. At last, Galen (150 CE) gured that consciousness and intelligence would reside in
the brain. Fast-forward to Descartes, who neatly separated the body (a tangible machine that functions based
on the four humours, which could be properly studied) from the mind (intangible, can’t be studied) (cartesian
dualism). Even though these were some pretty intelligent guys, they were led astray by the poor technology
and the batshit crazy scienti c misconceptions of their time. We all agree that the Enlightenment was a really
cool time for science, but still, Phrenology was a thing. Even though it suggested that certain areas of the
brain do certain things (which is kind of true), the theory that a more developed function would determine a
bump in the skull is just bullshit. Fun fact: Phrenology was debunked by Napoleon. Basically, a smart guy
(Gall) into phrenology said like: “judging by the shape of his head, Napoleon is a very pragmatic person, not
that intelligent though”. Napoleon was offended and hired a smarter guy (Flourens) to debunk phrenology.
Flourens came up with the aggregate elds theory: different brain regions work together in order to
accomplish a speci c function.
There are a few people who contributed to linking certain brain areas to speci c functions: John Hughlings
Jackson, who noticed that seizures tend to follow a speci c pattern; good old Phineas Gage, whose PFC was
absolutely devastated, with severe consequences on his social behaviour, Broca and Wernicke, who studied
different forms of speech impairment caused by brain damage and Galvani, who gured out (by accident)
that brain activity has an electrical nature and has nothing to do with the humours. But one of the most
important contributors to the development of neuroscience is Ramon y Cajal. Based on Golgi’s silver stain,
he theorized that the brain was not just a single, big, messy network, but was made out of individual cells,
called neurons (Neuronal doctrine). Also, Hubel and Wiesel (1959-62) were among the rst to record the
activity of a single neuron (a single unit recording of a V1 neuron from a monkey).
Hubel and Wiesel recorded a single cell, but you can also record multiple at the same time (since nearby
neurons like to re in unison), in a so called “local eld potential” (LFP). And if you record thousands and
thousands at a time, they create such a strong electrical eld that you can record it from the scalp. Boom,
you’ve got electroencephalography (invented by Hans Berger in 1924). EEG can record oscillations and/or
ERP (neuron activation in response to an external stimulus, but to get a clear signal you need to average
many many trials to rule out the noise). Even though EEG has a killer temporal resolution, it has a really bad
spatial resolution, you can barely guess where the signal came from. MEG (magnetoencephalography) is
much much better: better temporal and spatial (still, not amazing) resolution, much cleaner signal, but it costs
an arm and a leg. EcoG (electrocorticography) has fantastic temporal and spatial resolution, but you can do it
on very few subjects (because you need to split their head open and apply the electrodes directly on the
brain).
Onto a brief history of psychology and its methods:
We started studying psychological phenomena via introspection, which is a really shitty method because it is
extremely subjective. James (functionalism) gured that in order to study the mind, we must nd a way to
measure it, and that’s what behaviourism did. Thorndike, Skinner, Watson and friends studied the behaviour
as an objective, measurable response to a stimulus, who cares about the mind? Not me. Cognitivism does,
because not everything can be learned through conditioning and not everything can be studied through the
behaviour. Cognitivism was inspired by the emerging computer science. Finally, Neuropsychology was born
as a marriage between neurology and cognitive psychology. It wanted to study how the brain affects the mind
(mainly by studying broken brains).
Strengths of Neuropsychology: it’s causal; natural experiments (?)
Weaknesses: Idiosyncratic (the same damage may cause different symptoms in different subjects); plasticity
(a damaged brain will do its best to x himself by reorganizing structure and functions); brain damage is
more prevalent in certain regions.
Onto some brain stimulation and imaging:
TMS is a cool way to stimulate the brain, before (of ine TMS) or during (online TMS) a task. But the real
star of the show is fMRI. It has a good spatial resolution but an awful temporal resolution (it measures
blood ow, not neuron activity). The invention of fMRI gave origin to a lot of studies that were simple but
fl fi fi fi fi fi fi fi fifl fi fi fi fi fi fi fi
, extremely important. Nowadays we still have plenty of studies being published at a really high speed, but
what about the quality?
LESSON 2
Inside the neuron you’ve got a negative charge (resting membrane potential), because most of the
Na+ is outside. There are, however, some ionic channels which allow the Na+ to rush inside the
cell, depolarizing it and causing an action potential, which always travels from the axon hillock to
the presynaptic terminals, never the opposite.
A postsynaptic potential (PSP) is a temporary change in the electrical membrane potential of a
postsynaptic neuron (the neuron receiving a signal) that occurs in response to neurotransmitters
released by a presynaptic neuron (the neuron sending the signal) at a synapse.
The terminals will release some neurotransmitters to the post-synaptic neuron, causing a graded
potential which goes from the dendrites to the nucleus. From here (actually, from the hillock), if a
speci c threshold is reached, an action potential is triggered and so on.
For the anatomy of the brain, check the slides.
Can you not do anything? Nope, even when you think you’re doing nothing, your brain is working,
namely, the default mode network (DMN), which is comprised of mPFC, MTL, lateral temporal
cortex, precuneus/retrosplenial cortex and lateral parietal cortex. And what if you are doing
something? The task positive network is working. However, if you’re doing a mind wandering task,
the DMN is on.
TO CLEAR THINGS UP
The differences between postsynaptic potential (PSP), action potential (AP), and graded
potential (GP) lie in their mechanisms, characteristics, and roles in neural signaling. Here’s a
breakdown:
1. Postsynaptic Potential (PSP)
• De nition: A change in membrane potential that occurs in the postsynaptic neuron in response to
neurotransmitter binding at a synapse.
• Types:
◦ Excitatory PSP (EPSP): Depolarizes the membrane (makes it less negative).
◦ Inhibitory PSP (IPSP): Hyperpolarizes the membrane (makes it more negative).
• Location: Occurs on the dendrites or cell body (soma) of the postsynaptic neuron.
• Amplitude: Graded; depends on the amount of neurotransmitter released and the number of
receptors activated.
• Summation: PSPs can sum both temporally (over time) and spatially (from different synapses),
leading to either a cumulative depolarization or hyperpolarization.
• Function: Modulates the likelihood of generating an action potential in the postsynaptic neuron but
does not itself cause an action potential.
2. Action Potential (AP)
• De nition: A rapid, all-or-none electrical signal that propagates along the axon of a neuron when
the membrane potential reaches a critical threshold.
• Location: Generated at the axon hillock (initial segment of the axon) and propagates along the axon
to the synaptic terminals.
• Amplitude: Always the same (all-or-none) once the threshold is reached, regardless of the stimulus
intensity.
• Propagation: Self-propagating and does not degrade over distance; travels in a unidirectional
manner along the axon.
• Threshold: Requires the membrane potential to depolarize to a speci c threshold (usually around
-55 mV) for initiation.
• Function: Transmits information over long distances within the nervous system, allowing for
communication between neurons and effector organs (muscles, glands, etc.).
fi fi fi
, 3. Graded Potential (GP)
• De nition: A localized change in membrane potential that occurs in response to stimuli, but its
amplitude varies with the strength of the stimulus.
• Location: Occurs primarily in the dendrites and cell body of neurons, and can also occur in sensory
receptors (like in the skin or retina).
• Amplitude: Variable; depends on the intensity of the stimulus. The stronger the stimulus, the larger
the graded potential.
• Propagation: Decremental; the potential decreases as it moves away from the site of initiation,
meaning it fades over distance.
• Summation: Like PSPs, graded potentials can summate both temporally and spatially to in uence
the generation of an action potential.
• Function: Acts as the initial step in neural signaling by causing small, localized changes in
membrane potential, which can either trigger or inhibit an action potential.
Charact Postsynaptic Action Potential
Graded Potential (GP)
eristic Potential (PSP) (AP)
Neurotransmitter Threshold
Trigger Stimulus (e.g., sensory input)
binding depolarization
Amplitu
Graded, variable All-or-none ( xed) Graded, variable
de
Propaga Self-propagating,
Local, decremental Local, decremental
tion non-decremental
Locatio Dendrites, soma, sensory
Dendrites, soma Axon
n receptors
Summat Yes (temporal,
No summation Yes (temporal, spatial)
ion spatial)
Functio Modulate action Long-distance Localized potential change,
n potential likelihood signaling modulates AP likelihood
In summary:
• PSPs are speci c types of graded potentials generated by synaptic activity and can lead to or
inhibit action potentials.
• Action potentials are uniform, long-distance signals that transmit information within
neurons.
• Graded potentials are variable, local changes in membrane potential that can summate and
trigger an action potential if they reach threshold.
LESSON 3
Vision
The pupil and iris (which contains circular muscles) control the aperture of your eye, allowing the
right amount of light inside. The light then goes through the lens (to focus) which, being curved,
projects and upside image on the retina. The dead center of you retina is called fovea (which
contains many cones and few rods for a really high resolution) and the periphery is called parafovea
(with many rods and few cones, lower resolution but high sensitivity to motion). The retina has
many layers. You’ve got a layer of cones (for chromatic vision) and rods (for b/w vision); they send
signals to a layer of bipolar cells; they send signals to a layer of ganglion cells (with a few amacrine
cells in between). The ganglion cells form the optical nerve which pokes through your parafovea
(leaving a blind spot), splits in two (L/R visual elds) at the optic chiasm and goes to the LGN
(lateral geniculate nucleus, but a small portion of the visual signals goes through the superior
colliculus instead of the LGN) in the thalamus and into your primary visual cortex (V1).
fi fi fi fi fl
, Light causes a chemical reaction that makes a photoreceptor more likely to re. Cones will respond
differently depending on the wavelength of the light, so basically they like a speci c color between
red, green and blue. The thing is, green and red have similar wavelengths, so it’s possible that cones
respond to the wrong color. This problem is solved by the ganglion cells, they too have color
preference, namely blue/yellow and red/green. This double layer of color-speci c cells allows to
better discriminate colours. Also, color resolution gets better the higher you go in the visual
hierarchy, you get a lot more shades.
Lateral inhibition happens when excited photoreceptors inhibit the neighboring photoreceptors.
Opponent-process theory (ganglion cells): It explains color perception through specialized
ganglion cells that process signals from cone photoreceptors. These signals are organized into
opponent channels:
1. Red-green channel: Compares input from medium (M) and long (L) wavelength cones. Red
excites one side, green excites the other.
2. Blue-yellow channel: Compares input from short (S) cones to the combined input of M and
L cones. Blue excites one side, yellow excites the other.
3. Light-dark (luminance) channel: Combines all cones to detect brightness.
Ganglion cells have opponent receptive elds: stimulation in one region excites a response (e.g.,
red), while stimulation in the opposing region inhibits it (e.g., green). This antagonism prevents the
simultaneous perception of certain color combinations (e.g., reddish-green).
This theory explains phenomena like afterimages (e.g., staring at green causes a red afterimage)
and enhances color contrast by detecting edges and color changes.
Every cell in the visual system has a receptive eld, a portion of space represented by the cells. The
RFs get bigger the higher you go in the hierarchy. Ganglion cells have an excitatory region in the
centre of the RF and an inhibitory region in the periphery of the RF. If the stimulus falls in the
middle, the cell is excited; if it falls in the periphery, it is inhibited; if it falls in between, + and – try
to cancel each other out.
V1 cells like lines, and each cell has a favourite orientation of such lines. The “line” signal is
actually the combined signals of many ganglion cells, whose excitatory regions in their RFs have
been stimulated by an external stimulus. V1 cells that like the same orientation of a line are
organized in orientation-selective cortical columns. These columns are then organized in left and
right-eye columns. A cortical module is a piece of cortex that contains all the orientation columns
for the left and right eye.
Ocular dominance columns (V1): The
primary visual cortex (V1) processes visual
information through a highly organized
structure. Visual input from each eye is
separated into ocular dominance columns,
which are vertical bands of neurons that
respond preferentially to either the left or right
eye. Within these columns are orientation
columns, where neurons are tuned to detect
speci c line orientations, enabling the brain to
identify edges and contours in the visual eld.
Scattered among these are blobs, circular
regions specialized for processing color
information, while the rest of the column
handles contrast and brightness. Together, these
elements form cortical modules, which are functional units in V1. Each module contains all the
necessary information—line orientation, color, and intensity—for processing a small portion of the
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