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Interested in the nature of consciousness

-i.e. of the nervous system,

-its one of the big unknowns
-Humans are aware of, and can tell others, about our thoughts, our perceptions, our
memories and our feelings.
-We are aware of our own state and can communicate that with other people, i.e. I dont
feel good language concept involved
-All consciousness is language based
-If you cant talk or cant communicate then youre not conscious
-Limited definition, i.e. animals?
-Figure: skeleton contemplating himself
Clinical examples that illustrate how language is an important part of conscious
1. Blindsight phenomenon: person has a brain injury to a visual part of brain/visual
a. Report that they cant see anything or that theyre blind because of that
b. However they do experience some sight but its sight that they arent aware
c. Eyes and brain have to be seeing something but hes not consciously
aware that hes seeing anything
d. Walk them around a room and they avoid objects or catch a ball thrown at
e. Report that they cant see anything
f. Damage directly to visual cortical area of the brain
g. Figure 1.2 damage of people with blindsight is to mammalian system but
they can walk around and see because the primitive visual system isnt
damaged itself
2. Split brain: epileptic seizures that are uncontrollable, part of the brain becomes
overactive and spreads to other parts of the brain, unconscious, fall down, injure
themselves, etc.
a. Treated today with drugs
b. In the old days, if drug therapies didnt work, desperate method took place
prevent overactivity from spreading
c. Corpus collosum (fiber pathway that goes from one part of brain to
another hard body in between two hemisphers of the brain)
d. Cut the corpus collusum because cut the connecting pathway between
hemispheres can no longer transmit inactivity to between hemispheres of
the brain
e. Functionally we dont see any differences, two eyes see things at the same
f. However, there were differences functionally when discussing corpus
g. Smelling with a split brain body is aware of something that you cannot

h. Plug left nostril, smell with right nostril sends smell to right
hemisphere left side controls speech but cannot speak that they smell it
i. THEREFORE you are only conscious of things that you can verbally
3. Unilateral Neglect : Parietal lobe on both hemispheres
a. Damage right lobe you arent conscious of things that happen to your left
b. Ask a woman to draw a flower, but she only draws half aka the right side
of a flower. Demonstrates their unawareness of the left side of things
c. Draw only right side of clock
d. Ask them to describe a familiar location describe everything on the right
e. Seeing with both sides but left side is ignored (connected to right lobe)
4. Rubber hand illusion
a. See figure 1.6
b. Parietal lobe
c. Premotor cortex
Chapter 2
1. Construction and physiology of the nervous system
2. Neurons
a. Integrate information
b. Send information to other parts of the nervous system
c. Refamiliarize with parts of neuron
3. Types of synapses
a. presynaptic element and the post synaptic element
b. Synapses can be found on dendrites, on cell body, from one terminal to
another terminal directly
c. Figure 2.27
i. Presynaptic specialization
ii. Postsynaptic specialization
iii. Look up jobs
d. 2.28
i. terminal has a bunch of vesicles which migrate to synapse, fuse,
gap, migrate to neurotransmitters
e. 2.29
i. first evidence that showed that synaptic vesicles come to
presynaptic membrane, fuse, release into snaptic space, and
interact with postsynaptic membrane omega
f. 2.30
i. release of neurotransmitter. Presynaptic membrane becomes larger
and larger because keep adding material to it
g. 2.32
i. recycling of the membrane of synaptic vesicles
ii. fusion where release neurotransmitter, becomes larger, release
h. 2.33

i. neurotransmitter fits into receptor and activates, causes that

receptor to open channel allowing ions from outside of neuron to
inside of dendrite or particular neuron
ii. neurons normally slightly negative, action potential, need to let in a
lot of positive ions
iii. resting neuron -70 millivolts
1. Fast acting, short lived
2. Presynaptic and postsynaptic (dendrites) very close to one
i. 2.34
i. surface of a cell body is studied
ii. lavender interacts with neurotransmitter
iii. when interacts with light blue allows
1. Change the state of the neuron, so that its biased to be more
or less likely to fire
2. Longer time period, seconds or minutes of behaviors
3. Gap is longer between elements (pre/post synaptic
4. May just bias the neuron
5. Bias for several minutes
v. Action potential to occur on a long term basis
j. Hormonal receptors
i. Inside neuron have receptors for those hormones
ii. Can act on receptors on membrane of neuron, in cytosol, in
nucleus, to change expression of the genetic material
iii. Take longer to act, and when they begin acting they act longer
iv. Farther apart
v. Travel through bloodstream andactivate receptors in cytosol in
nuclear membrane
vi. Take longer to be effective and further to travel, but when they
activate they are in long term action
k. Figure 2.35
i. Can have an exchange of ions across the membrane
ii. -70 mV in potential
iii. neutrotransmitter
iv. Action potential occurs when lots of channels open allowing
positive ions into post synaptic membrane when neurotransmitter
attaches to binding site
v. Kicks out potassium ions (+) neuron becomes more negative and
becomes closer to resting potential
vi. Open chloride channels (-) alloing negative charges inside neuron
driving it to negative state
vii. Reaches resting potential





viii. Calcium (+) facilitates migration, diffusion, and release of

neurotransmitters of cell
ix. Calcium channels also found in dendrites of cell bodies very
important in changing structure of the dendrite
Figure 2.36
i. Three mechanisms for removing neurotransmitters from synaptic
1. Diffusion
2. For some neurotransmitters there is an enxyme looking for
neurotrans. And when enxyme finds it it degrades into
component parts. Presynaptic membrane will pick up these
parts, repack it in membrane and send it out again.
3. Active mechanism for seeking neurotransmitter reuptake
picks up and brings neurotrans. Back into the neuron
4. Enhance reuptake mechanism
5. Block mechanism of reuptake and leave neurotransmitter
so that it can attach to another receptor again and prolong
this action
Figure 2.37
i. Excidatory effects
ii. Excidatory post synaptic potential (EPSP) have enough can get to
threshold so that theres an inhibition in the nervous system
1. Second image: red (excidatory EPSPs eventually add up
to an action potention) and blue (inhibitory IPSPs)
2. Inhibitory action allows potential to lower to even -72 or
-75 mV making it even harder for firing to take place
Figure 2.38
i. Synapses happen between terminals and dendrites and terminals
and terminals
ii. Homosynaptic effect
iii. Heterosynaptic effect
1. When two terminals are attached while third connection is
main to dendrite
2. Can have inhibitory or excitatory
iv. Dendrites can release neurotransmitters that can affect receptors
that are own their OWN dendrites
v. Calms neuron down
vi. Autoreceptors are when dendrite affects its own neuron
Figure 2.39
i. Gap junctions are rare, four places

Chapter 3
1) Figure 3.1
a) Naming conventions
b) i.e. lateral geniculate nucleus (LGN) - visual
c) Median geniculate nucleus (MGN) auditory
2) Table 3.1

a) Central nervous system encased in bone

b) Peripheral nervous system not encased in bone
3) Figure 3.7
a) Neural plate development
b) Neural tube
i) Creates brain and spinal cord
c) Developing neural streak, cells enlarging to creat invagination
d) Center part comes together and fuses in middle
e) Zips up on both sides to create enclosed neural tube, one end brain, one end spinal
f) Recognizable structure on brain
4) Figure 3.8
a) Brain development
b) Identifiable components to the nervous system
5) Table 3.2
a) Major division
i) Forebrain
(1) Cerebral cortex, basal ganglia, limbic system
(2) Thalamus, hypothalamus
ii) Hindbrain closest to spinal cord
(1) Anterior = rostral (towards nose)
(2) Posterior = caudal (towards tail)
iii) Midbrain
b) Figure 3.9
i) Cortical development
ii) Nervous system overproduces neurons to ensure that we have enough, but
need to get rid of spare
(1) Program cell death apoptosis
(2) Figure 3.10
(a) Effects of learning on neurogenesis
(b) Learning new things allows you to develop new neurons after youre
(c) New area of research
iii) 3.11
(1) cross sections of brain
(2) grey matter
(a) Gyrus and sulcus
(3) White matter
(a) Corpus collusum
(4) Limbic system
(a) Singular cortex
(5) Amygdala
(a) Fears
(b) Acquired fears in your lifetime
(c) emotions
(6) Hippocampus




(a) Really important for memories

(7) Basal ganglia
(a) Really important for motor functions
(b) Really important in thought processes -> parkinsons thoughts slow
Figure 3.12
i) Left and right hemisphere
ii) Lateral fissure
iii) Central sulcus
iv) Central lobe
(1) Mostly involved in motor functions
v) Pre frontal cortex
vi) Frontal lobe
vii) Parietal cortex is behind the central sulcus
viii) Occipital cortex is associated with visual function
ix) Temporal load
x) Association cortex
xi) Rhineacephalon
Figure 3.13
i) Lateral
ii) Medial
iii) Ventral (down)
Fgure 3.15
mid- saginal
i) medial view of brain
i) FOREbrain
(1) HypothalamusL only 0.5% of total brain volume
3.20 hindbrain
i) cerenbellum
i) pretty complex structure relatively small in comparison
ii) everthing needs to go through ti
iii) tube having a small demarcation
(1) everything above the line is sensory in nature
(2) anything below the line is motor in nature
(3) upper part is known as the roof of the midbrain
(a) tectum
(b) superior colliculus visual in nature (not part of conscious experience)
(c) inferior colliculus auditory in nature
(4) tegmentum is bottom
(a) substantia nigra

1) FIGURE 4.4 very important to study

a) Drug effects on synaptic transmission

b) Can make a lot of communication between pre and post synaptic mechanisms
c) Agonist facilitates from one element to another, communicates between pre and
post synaptic element
d) Antagonist interferes
i) No ingredients to make neurotransmitter
ii) Could make sure its not put into vesicles
iii) Put into degrading vescibles
iv) Vesicles dont dock with neurotrans
v) Dont release neurotrans
vi) Uptake mecahnis is effective so that neurotransmitter is taken up too fast
vii) Drugs that block the receptor blocker
e) Makes a snapse more effective so that he learns better or worse
2) Figure 4.5
a) Direct effect
b) Direct agonist
i) Open a chanel
c) Direct antagonist
i) Close a channel
d) Second neurotransmitter can indirectly facilitate the opening of a channel so that
when second neurotrans comes it easily opens up the channel
e) Or can have the opposite effect closes in antagonistsic effect
f) Direct or indirect effects
3) Fig 4.6
a) Heterosynaptic connection
b) Neuron above influences the activity of middle terminal to release its
c) Modiefies the calcium channels
i) Can allow opening or closing of channels
4) Fig 4.7
5) Not going to be tested on things below
6) Acetylcholine
7) Dopamine
8) Neuropenefrine
9) Gludamate
10) Ceratonin
11) Can figure out distribution
12) The nature on whether or not a chemical is excitatory or inhibitory is entirely
dependent on receptor on post synaptic membrane
13) two inhibitory (-) neurons cancel each other out and excite the third neuron (+)
14) inhibition of an inhibitory neuron is called disinhibition
15) odd and even numbers are dependent, same as basic pos and neg multiplication
-Know where parts of the brain are, anterior or posterior parts/organs
Chapter 5

Every technique has its advantages and disadvantages

Figure 5.22
1) Chronic microelectrodes
2) Connect connecters to amplifies that enhance electrical signal on electrodes monitor
a) Firing rate of the cells in that area while the animal is doing the behavior of
b) Chronic recording long term
i) For behaviors of interests study
c) Acute recording only during the surgery
d) Single unit recording
i) Similar to what may be done in acute experiment
ii) Animal is asleep, put recording electrode directly into the neuron of interest
iii) Small electrode required, made with small glass pipettes microelectrodes
iv) Type of recording typically seen in textbooks within neurons
v) See picture on phone
e) Internal spaces of the brain create cerebral spinal fluid in which the brain in
f) Prevent electrode from staying in place when the animal is awake
g) Instead of using intracellular electrode (as above) use extracellular recording
i) Electrode outside of several neurons
ii) Multiple unit recordings many neurons at the same time
iii) However, able to record single neuron from extracellular electrode by
touching electrode to neuron itself
iv) Make it really large, can record from 50 or 100 neurons at the same time
within cell
v) Spike from 0 line above and below is rapid change in action potential and
action potential itself7
Figure 5.23
1) EEG
2) Looking at average of many action potentials happening at the same time or not at the
same time
3) If theres a lot of activity large action potential/ vs. small uncoordinated peaks
Figure 5.24
1) MEG
2) Recording magnetic changes
4) Super magnets are very sensitive to picking up magnetic changes originating from the
brain itself
Figure 5.25
1) Rat brain stained for

2) Brain consumes oxygen and glucose

3) If radioactively labeled glucose, inject into rat that is behaving, neurons pick it up,
able to see which parts of the brain are activated
4) 2-deoxyglucose, an alternative form of glucose
a) brain cells recognize
b) take into cells
c) want to metabolize
d) 2-deoxyglucose however cannot be metabolized so it stays in the cells
e) going to pull in a lot of the glucose if its very active
f) able to see which parts of the brain are very active
g) only inject small amount of 2-dg so they can maintain themselves with other
glucose in body
h) accumulate 2-dg
i) after behaves in certain way, take animals brain, slice it, juxtapose and x-ray film
j) corpus collosum didnt pick up radioactivity
k) basal ganglia (important for motor functions, parkinsons, operative conditioning,
i) labeled in control animals as well
ii) difference seen by arrow
iii) identify area of interest
iv) unusual amount of radioactivity not seen in control animal
(1) part of hypothalamus
(2) mammillary nucleus
(3) has to do with memory functions
Figure 5.26
1) FOX
2) Called immunocytochemistry
3) Looking for genetic expression
4) Fox becomes active to facilitate expression of gnese
5) C-fox
6) Radioactively label
7) Immunological reaction
a) Add to some chemical that is going to react to a foreign substance
b) Light up and tell us where C-fox is expressed
c) Early genes
d) When become active, call to action to activate certain genes
e) More involvement of c-fox to show that happening
f) Dark spots show activation
i) Lots of activation in medial amygdala
ii) Amygdala unlearned natural fears and learned fears/phobias of life
Figure 5.27
1) PET scan
2) Radioactively labeled something, inject into people, while theyre doing something
behaviorally interesting, wait for it to show up

3) Engaging right hand activity lights up in motor control areas

4) Label glucose, oxygen, neurotransmitters (see what parts of the brain activate for
neurotransmitter usage)
5) PET scans tell us something functional, when hes doing something
6) fMRI techniques, pet scans are not as good
7) too general, looking at an area that do not show differences in resolution terms
a) location/spatial resolution
b) temporal resolution (time wise)
8) most of the time make it radioactive for a few minutes but its too short and
radioactivity becomes negligible
9) have to have experiment set up next to cyclotron
a) expensive big machines
b) severe requirements
1) fMRI functional magnetic resonance imaging
2) spatial resolution is 1 mm, better than pet
3) time is a couple sec, better again
4) advantages for sure
5) put magnet that aligns the spin of the electrons and positrons of the brain so that they
are spinning in the same direction
6) send in radio signal to perturb axis of signals
7) detects flow of blood into particular region
a) tells you that the location must be very active, pulling in oxygen and glucose
8) male brain is active on one side vs both sides for female brain
a) male brain unilateral
b) female bilateral
9) different images
a) place control and experimental on each other
b) see difference between before and after
c) group of individuals as well
10) structural fMRI
a) gives a good idea of what the brain looks like
11) fMRI
a) before and after that tells you the difference in activity
1) cannula (syringe)
2) expose neurotransmitter blocker to one particular area of the brian
3) chronic cannula
a) outer and inner cannula
b) inner goes slightly past outer
c) need to be careful about damaging nucleus of interest during surgery
d) inner cannular is 2 mm longer that outer to deliver drug

e) able to do an injection while hes behaving

f) or withdraw the fluid to see whats being used at the time
1) photostimulation
2) recognize that dendrites and receptors of neurons
3) identify genetic code for creating channels and receptors
4) inject coding into neuron/group of neurons
a) in viral form (inject code for the channel and the receptor)
b) deliver genetic material into region
c) not there previously
d) however, attach to the coding fluorescent coding light sensitive element
e) cause channels to open up
f) postiviely charged ions enter into the neuron
g) makes it more positive
h) action potential
i) activate area by shining light that gives instruction to open channels
j) blue light tags and yellow light
i) blue light positive
ii) yellow light negative, i.e. chloride ions
iii) or turn on or off neuron activity
5) sophisticated technique uses cannula to reach deeper area of interest
6) take thin fiberoptic cable through cannula and deliver part of the brain
7) stimulate part of the brain to activate channels instead of injecting neurochemicals
8) see how basal ganglia works
1) cause a magnetic field to occur outside of animal
2) change electromagnetic field of area stimulate response
3) TMS
4) Stimulate part of the brain can be overly stimulated and turn off area
5) How to turn on or off certain area?
a) Vary parameters, intensity, etc.
6) Magnetic stimulation of this sort, or imaging techniques have big advantages in that
you dont need to open up brains to see whats going on
7) Non-invasive techniques
8) Invasive techniques can cause infections
Chapter 6
Table 6.1
1) Rods are peripherally located on the retina, turned to the side of the retina.
a) On cell type
b) Changes of light that may exist
c) Related to this is motion and direction that something is moving

d) Peripheral vision
e) Receptors along margins of retina itself for side vision
2) Rods are ON type bipolar cells (Schiller et. al. study using APB to block ON bipolar
a) Detect spots that get brighter
b) Vision in dim light
3) Cones
a) Fovea pit in the center of the retina
i) High concentration of cones
ii) Acuity how easy we can see something
Figure 6.8
1) Photoreceptors (light affects/rods/cones)
2) Bipolar cell second element, intermediator
a) Two protrusions one dendritic extension, one is an axon with associated
3) Ganglion cell receives information from photo/bi cell
a) Axons of cell make up optic nerve, second cranial nerve itself
4) Interior of the eye are way too the right
5) If light is absorbed to ganglion cell the light is absorbed and you cant see
6) Therefore its not directly behind structure, somewhat offset
7) Eye can collect a lot more light than we need to see
8) Transduction property of all sensory systems
a) Some sort of receptive elements designed to convert some kind of energy or
movement into an electrical signal that the nervous system can eventually
b) Cant see without transductive elements
i) Flash of light for long time, blind for some time
ii) Exhausted all the material needed for this process
iii) Regenerates quickly, unless you damage the cells by looking at the sun
c) Photoreceptor: look at neurotransmitter it uses
i) Uses glutamate neurotransmitter
(1) Excitatory neurotransmitter normally
(2) But in this case it inhibits the bipolar cell
(a) Glutamate receptors in bipolar cell are inhibitory in nature
ii) In the dark photoreceptors leak out glutamate and therefore are constantly
inhibiting bipolar cells
(1) Called the dark current
(2) Measurable
(3) Communication stops vision
(4) When photon of light comes in however, photoreceptor closes positive ion
channels (sodium ie) and as a result bipolar cell is released from inhibition
(5) Remove suppression by light, remove inhibition by bipolar cell, so that it
can undergo some activity

(a) Can in turn excite ganglion cell in turn exciting central nervous
9) Neurons with axons vs. without axons
a) Signal travels along axon itself
b) Long distance neuron communication requires axon
c) If neuron is very close to cells of interest doesnt need axon doesnt need
action potential associated with it
i) Action potential if one photon of light hit photoreceptor it would turn off the
inhibition proportionally. Two photons of light effect x2. Etc
(1) Coding amount of information by amplitude of the signal
(2) Action potentials always the same size
(3) Cells with axons code for magnitude based on action potential
ii) Graded potential
(1) Bipolar cell exposed to light
(2) Depolarizing membrane potential
(3) Intracellular recording
iii) Ganglion exposed to disinhibited bipolar cell
(1) Increased rate of firing
10) In fovea close to 1:1:1 relationship for photoreceptor bipolar ganglion
11) Normally its much higher ratio, i.e. for peripheral vision
Figure 6.9
1) Cortex
2) Lateral geniculate nucleus
a) Part of the thalamus (sensory relay area of brain)
b) In human brain
i) Different layers
ii) Layers 2 +4
iii) Layers 4 + 5?
iv) Layers represent which eyeball info is coming from right or left
v) Ipsilateral = same side as eyeball
vi) Contralateral = opposite side eyeball
vii) Retinotopic map
(1) Topographical map for what we see with the eye
viii) When signal sent from lateral geniculate nucleus to cortex preserve map =
called geniculo striate
(1) First name refers to where it started
(2) Second to where it ends up
c) Striate cortex
i) Cortex has six layers to it
ii) Striate cortex is synonymous with primary visual cortex
iii) Visual in nature extra striate cortex
(1) Refers to secondary and tertiary visual cortical areas
(2) Figure 6.10

Figure 6.11
1) Visual Field
2) Eyeball overlap in visual field allows stereopsis detect distances of objects
3) Cells in cortex getting info from both eyes
4) Left and right visual field
5) Right field ends up in left hemisphere and vice versa
6) Combine these two things by corpus collosum
Figure 6.12
1) Central visual area precise, 1:1:1
2) Peripheral visual field gross vision
a) Many receptors vs. just one
b) No way of telling which elements detected the light
c) Only know that somewhere in the visual field you saw something
3) Cones have detailed visions = fine detail detection = acuity
Figure 6.13
1) If light is in center of central peripheral field, ganglion can become active
2) If spot of light is off to the side, inhibit ganglion cell
3) Allow to detect more finely, more acuity
4) Off or on ganglion cell
5) On center off surround
6) Off center on surround
7) Allows for greater detail in peripheral vision
8) Processing is preserved in all levels
Color vision
Figure 6.17
1) Three kinds of color cones in eyes
a) Red
b) Green
c) Blue
d) Individuals born without red photoreceptor
e) Trichromatic color theory
i) Red green blindness
ii) Lacking red
iii) Called protanopia
iv) Deuteranopia (lacking green)
v) Tritanopia (lack of blue receptors - blue/green blindness)
f) Can detect stimuli if you have the photoreceptor
g) Limited to the kinds of sensory receptors
2) Figure 6.18
a) Opponent processing theory
i) Explains why we cannot see certain combinations of color
3) Figure 6.19
a) Theoretical understanding

b) When we see red, red light hits red cone, excites ganglion cell
c) Ganglion cell is either excited by red or inhibited by green
4) Organization of retina fulfill the trichromatic theory (see certain colors), but why we
can only see certain color combinations is due to
Figure 6.24 (not tested)
Dorsal stream
-important for detecting where image happened and is it moving
-identifying basic shape
-low freq.
Ventral stream of the cortex necessary to identify objects
-depends on spaces between lines
-interested in identify that im looking at a person and distinguishing them from someone
-high spatial freq.
Figure 6.25
1) Low spatial frequency on the left (fewer sine waves than in high spatial freq.)
a) Magnocellular form
i) Cares about movement vs. precise nature of it
ii) Large axons to them
(1) Send information very quickly in the visual system
(2) Milenated
(3) Its more important to react to begin with in a defensive manner than
recognizing, defense and survival factor
(4) Without necessarily knowing why
(5) Fast, for brightness changes
(6) Form of the object
b) Overall shape and form of object, not specifics or particulars about the object (not
distinguishable faces)
2) High spatial freq.
a) Specifics and distinguishable faces
b) Parvocellular detail (small cell)
i) Smaller axons, not nearly as fast at sending information as you get from
ii) Detailed information
iii) Associated with ventral visual pathway
(1) Includes projections coming from parvocellular system
(a) V1,v2, etc.
(b) Koniocellular refers to cells that exists in between layers, related to
blue visual component
(c) Cones in the eye
Change in illumination is an edge Abe Lincoln pictures

Figure 6.27
1) Spatial filtering
Figure 6.29
2) Small section of primary visual cortex, lots associated with it
a) Modular processing fine detail analysis of information that you see in in
b) Stereopsis visual cortex has cells that detect information from specific objects
Figure 6.31
1) Higher visual processing
2) How we actually make perceptions
3) Perception of an object depends on background
Hierarchical organization
Color constantly constancy
achromatopsia without color vision TEO
1) Cortical color blindness
TE appreceptive visual agonosia
2) Cant necessarily see things to count them but visual experience is lost
3) Summary of many visual cortical areas that we have
4) Looking at right hemisphere from a backward idrectiion
5) Calcarine sulous
Table 6.2
Figure 6.36
1) Fusiform face area
a) Temporal lobe fusiform face area becomes active when you see various objects
b) Slightly activated, typical to see areas activated outside of the area
c) These areas are important in detecting categorization of faces
d) Damage to this area called prosopagnosia
i) Lack of being able to tell the difference between faces
ii) Strokes, other injuries
iii) Farmer could no longer recognize cows
e) Born with the ability to distinguish faces
f) General area where learning of facial recognition occurs, throughout lifetime
theres plasticity that allows us to learn how to recognize categories of things

g) Is it specifically there to detect faces? Or is the flexible face area, meaning you
can learn a lot of things from this area
Figure 6.41
1) Activation for child is less than adult for fusiform face area
2) Develop over time
3) Right side more active, hemispherical differences?
Figure 6.42
1) Infants spent more time looking at things that are face like in there correct orientation
2) Evolutionary advantage for kids to recognize faces early on, identify caregivers etc.
a) In young infants, magnocellular is the first to develop in people
3) Some individuals born early with prosopagnosia
a) Can recognize that there is a person/face
b) Magnocellular is developed, less developed is parvocellular
4) Some people born with cataracts, clouded lens
a) Test between 9-21 shows people are able to distinguish people from objects but
not individuals, parvocellular system not as developed
5) People born with only one cataract
a) Left eyeball to right hemisphere, and vice versa when youre younger
b) Cataract in left eyeball
i) People are most impaired with prosopagnosia
c) Cataract in right eyeball
i) Can recognize faces early, can recognize individuals, as adults
ii) Fusiform face area right side is more important than the left side for
detecting individuals in temporal cortex
What is the function of the FFA, born detecting the outline of faces but we have to
develop the recognizable ability to faces themselves
-autistic children arent social and miss social interaction that people give by facial
expression themselves b/c dont look in the eye
Figure 6.35
1) Lateral occipital cortex (LOC)
a) Tools, kinds of tools, animals
b) Letters and numbers is important in the left hemisphere (as are most visual areas)
2) Man could identify man but not the objects or vegetables and flowers and things that
make up the man
a) Damaged LOC
Figure 6.38
1) FFA is activated by faces and implied faces
2) Extrastriate body area (EBA) activated by headless bodies and body parts
a) Specialization of different area for face vs. parts of the body
b) Posterior to FFA
c) Activated by photos, silhouettes, drawings

3) TMS (transcranial magnetic stimulation)

a) Directly stimulate EBA, they lose perception of body parts, its disrupted
b) Stimulate FFA and lose ability to recognize faces
c) Stimulate and lose ability to categorize objects
4) Parahippocampal place area
a) Coretex just next to the hippocampus
b) Important for detecting locations youre at
c) Natural or manmade scenery or background
d) Activate this area
Figure 6.39
1) PPA
2) Associative visual agnosia
Ventral what is it that I'm looking at, perceptual experiences, specialization for face
knowledge and categorization of
ST- superior temporal cortex
Middle temporal gyrus
all the same place
Optic flow (V5)
Intraparietal sulcus
Figure 6.47
1) Anterior interparietal sulcus (AIPS or aIP)
a) Important (location) because it tells us where and object is and how to acquire that
particular object
b) Reach for bottle, anterior part becomes activated for grasping an object and
making sure that hand is in correct orientation for grasping that object of interest
c) Have to know location, have to know orientation hand should be in from this area
2) Point at object vs. picking it up
a) Ventral part of interparietal sulcus
b) Important for pointing


Medial part reaching for object youve pointed to

Central part is important for stereopsis (depth perception)
ALL PART OF DORSAL STREAM (answers the question
Ventral stream answer the question where is it and how do I interact with it?

Eyeball and muscles are not important

Chapter 7
Figure 7.5
1) Bottom picture
a) Sound comes in through external auditory maileus
b) Humans are very sensitive to sound
c) Little bones in ear help to amplify signal being picked up by ear drum,
mechanical advantage, final bone therefore vibrates even more in amplitude
d) Oval window attached to
e) Wave itself deflects and pushes down on central structure called organ of corti
7.4 organ of corti
1) Oval window on top
2) Round window on bottom
3) Base and roof and transducting elements are in between, where you find the receptors
for hearing
a) Roof
i) Tectum
ii) Receptor elements in between
iii) Basiliar membrane
iv) Roof collapses at preferred frequency for particular sound that runs into
receptor elements for hearing:
(a) Outer hair cells (not receptor elements but effector element efferents)
(b) 3x as many outer hair cells as there are inner hair cells
(c) attached between tectum and basiliar membrane, when they contract
they pull elements together.
(i) Afferent (information coming into a particular location) vs.
efferent (where does this nucleus project to, a motor function,
output for a particular brain region)
(d) Selective hearing
(e) Can contract outer hairs cells along outer membrane, activate inner
hair cells, detect very small sound
(f) Motor in function
(2) Inner hair cells (afferent structures/in terms of hearing, are the transducing
elements themselves; detect sound)
(a) Only attached to basiliar membrane
(b) Sensory in function
v) Nerve 8, primary associated with hearing coming from inner hair cells

Wave passes through structure, depress roof to run into receptor elements
How they react where there is depression results in change of hearing, see figure 7.5
Large frequencies result in depression by oval window
Lower frequencies of sound results in depression towards tail, receptor elements
towards tail end are the ones who react

8) High 20,000 Hz at base

9) Low 200 Hz at apex low frequency location
10) Tonotopic map
11) Wherever there is deformation
12) Rate coding (200-20 Hz) membrane vibrates
13) Damage to inner hair cells cant be regained
14) Place stimulating electrodes on membrane to stimulate structure and produce
rudimentary sound, learn that the thing youre hearing is a sound
a) Adding an auditory prosthesis so that a person can hear
1) Cilia on inner hair cells, vary in sizes
2) No sound is happening whatsoever, little tension in connections
a) Mechanical deformation of the channels that are found on cilia
b) Allows positive ions to come into the receptor element
c) Positivity leads to an action potential, or a graded potential
d) More that you have open at the same time, more positive, inner hair cells release
neurotransmitter (glutamate, actually excitatory) and is interpreted as excitatory
and send signal to central nervous system
3) Bend hair cells in direction towards larger cilia, pull open and mechanically deform
channels and cause more positive ions to enter inner hair cell potassium and
4) Push towards smaller cilia relaxes tension on channels and they close, little positive
charge comes on no activity whatsoever
5) Hearing something, tectum is pushing down and vibrating hair cells, lots of
deformation and positive charges, lots of glutamate released
6) Intentional plaques attached to channels, kind of receptor called TRP (Transient
Receptor Potential)
a) Associated with hearing is called TRPA1 receptors
b) Found in other sensory systems touch temp and taste
1) Basiliar end (oval window) higher frequencies vs. apex is lower
2) Tonotopic map there is a physical representation on basiliar membrane that
represents sounds
a) Represented at many levels of nervous system
b) Cochlear nuclei dorsal and ventral cochlear nucleus
i) Have a tonotopic representation
c) Superior olivary complex
i) Also has tonotopic rep.
ii) Multiple nuclei as well
iii) Complex of structures with tonotopic reps
d) All structures are close to where auditory nerve comes in area of brain stem

e) Two structures above send projections to midbrain to inferior colliculus (auditory

in nature)
i) In turn projects up to the thalamus (major sensory relay to cortex) medial
geniculate nucleus projects to primary auditory cortex
f) Olivary structure has superior and inferior olive
i) Superior/inferior olivary complex/nucleus
ii) Send to cochlea which sends to auditory hair cells amplified perception but
also selective attention controlled by superior olive
iii) Olivocochlear bundle - goes from superior olive and ends up in cochlear
membrane making synaptic connections with outer hair cells
Depending on how much deformation there is we have the perception of loudness
-large deformation sounds loud
-smaller deformation
-individual inner hair cells have a range of responding for detecting tones if the tone is
loud there are many action potentials for that particular frequency
-when you have a loud sound and deform basiliar membrane, you deform neighbors and
activate more of the inner hair cells at the same time
-loudness based on number of action potentials activated but also deformations
-pitch and loudness
1) Tuning curves
2) Put recording electrode into inner hair cell (intracellular recording)
3) Set range of sounds
4) Three different inner hair cells with different preferences
5) Blue will respond to a range of frequencies on either side
6) If reacts to certain frequency, turn down the volume
7) See that with a very low intensity of the stimulus, still reacting with 500 Hz
8) Certain cells require different intensities
9) So you are interested in frequencies and intensities
10) Can then inactivate or poison outer hair cells red is very sharp line, if you poison it
loses its sensitivity
11) Selectively amplify
12) Damage causes loss of sensitivity
1) Thalamus, cortical strucures
2) Further down, take another section, horizontal to the ground (horizontal or transverse
3) Auditory or 8th cranial nerve has projections that go to the dorsal/ventral cochlear
a) Projects to the opposite side, in one ear and ends up on opposite side
b) Also projects to the trapezoid body and the superior olivary complex
c) Superior olivary complex has projections on same and different sides

d) Superior olivary nucleus sends information on the same side to the inferior
e) Immediately crosses over but some stays on the same side
f) Its difficult to tell which ear the information came from
g) Diagram only represents what happens with one ear
h) Both ears cross very early
i) Superior olive is getting information from BOTH EARS
i) One side is faster than the other
(1) Object must be to the side
ii) If source of sound is in front, hears at same time
(1) Superior olives recognize same time sound, therefore object in front must
be in front
iii) Mandatory relay, regardless of sides there is a synapse
iv) Lateral fissure on sides in cortex
(1) Temporal gyrus of auditory cortex
1) Primary auditory cortex to anterior parts of the temporal lobe = ventral stream
2) Other direction = dorsal auditory stream
3) Similar to ventral and dorsal functions to visual system
4) Anterior or ventral hearing system asks, what is it that im hearing
5) Dorsal or posterior system asks where is the sound coming from, how do I respond in
terms of location, and can this help me navigate through environment
a) i.e. blind people hear echos
6) medial geniculate nucleus goes to core (primary auditory cortex, A1) projects to
area immediately surrounding area aka the belt or A2 ventral stream projects to the
frontal cortex as well; premotor cortex; prefrontal cortex (decisions about the nature
of that sound) dorsal stream asks where was it that I heard it; goes to parietal
cortex (understanding location and space); sends projections to anterior regions as
7) damage to primary auditory cortex and belt region one thinks they cant hear
anything, but they can actually hear things they just arent sure what or where the
sound came from
a) train animals to do an action with different tones, how sensitive are animals to
detecting similar sounds
b) damage primary and secondary auditory cortex they lose the abilty to discriminate
between sounds and they lose the action that they are expected to have
c) parabelt region below is sensitive to environmental sounds: legit sounds you
would hear in the environment (animals, wind, trees, etc.); growl vs. purr as well
d) reactions to primary auditory cortex for same sounds, both regions become
activated if you play the sound. If you play the sound backwards the primary
auditory cortex still reacts, but the parabelt region no longer reacts has to be
meaningful for the region to react appropriately
e) agnosia (lack of understanding)
f) auditory agnosia would be caused by parabelt region damage (couldnt
recognize sound)

g) associative auditory agnosia associate particular sound with label, thats joe,
i) something that has been learned to attach label to sound
ii) primarily due to the anterior regions of the temporal cortex, and sometime
frontal cortex damage
h) music
i) in young infants present sounds and record brains 1-3 year olds show altered
brain activity when they hear sounds that dont go together
ii) musicians have well developed system, larger auditory representations and
regions are more active
(1) better you are the more active your regions are
iii) music has pitches, timbres (complex of frequencies occurring at the same
time, various pitches, rhythm, simultaneous notes pleasant/unpleasant, aspect
of intervals, pauses, melodies)
iv) parts of the cortical area
(1) inferior frontal cortex particularly important in recognizing harmonies
(2) auditory frontal cortex drum beat
(3) right cortex- emotional music/character
(4) left cortex rhythm that exists, repeating patterns
(5) structures like cerebellum and basal ganglia important for understanding
motor movements and timing in music
(6) musical training changes the activity of all of these places
(7) Amusia - people born without being able to appreciate music
(a) I.R. patient extensive damage, had normal hearing, could understand
speech, converse, environmental sounds but couldnt sing, think of
music in her hear, but she insisted that she enjoyed listening to music,
particularly because of right hemisphere
(b) Some people born with it = congenital amusia, about 4% of the
(c) Genetic basis for loss of function passed on from generation
(d) Close genetic relatives are likely to have similar kinds of problems
v) Figure 7.16
(1) Coincidence detectors that are detecting from phase
(2) Determination of right from left?
vi) Figure 7.15
(1) Low frequencies are easier for ear to detect which side sound came from
(2) Left ears hear out of phase
(3) Right ears hear in phase
(4) Superior olivary nucleus/complex
(5) High frequency sounds can be distinguished by right or left
(a) Tell us things about right and left
(b) And up and down
(6) Ears fixed top part of the ear will result in a lower sound than sound that
hits bottom part of the ear in lower canal itself
(7) Blind people have a harder time distinguishing up from down
8) Figure 7.18

a) Humans are different than cats. For humans

i) Discriminating right/left and up/down
(1) Phase differences (low freq.)
(2) Intensity differences (high freq.)
(3) Less intense on opposite side, means it had to come from louder side
(4) Same cues for up and down in humans, due to shape of the ear
ii) Discriminating front and back
(1) Timbre differences (like a cat)
9) Figure 7.19
a) Damage in higher auditory systems results in agnosia (without knowing or
without knowledge)
i) Apperception auditory agnosia not able to perceive, recognize that you
heard a sound but cant recognize where the sound came from or the nature of
that sound
ii) Associative agnosia connect verbal label to what you had heard, recognize
its a voice but sue or joe unsure
b) Ventral
c) Dorsal (not posterior)
10) Figure 7.10
a) Left hemisphere identify what
b) Right identify where
11) 7.21
a) Infants are sensitive to music
b) Amusia congeaital
12) 7.25
a) cutaneous sense touch coming from the skin
i) pressure
ii) vibration
iii) heat/cold
iv) pain
b) senses for body position
(1) i.e. joints kinesthetic senses
c) organic senses sense of muscle linings and gastrointestinal senses
d) auditory sense trpA1 type receptor
e) trpC1 receptor for cutaneous senses
f) Types of receptors that can be identified vary depending on these properties
variables for receptive fields:
i) adaptation fast/slow
(1) fast adapting only interested in changes of touch
(2) slowly adapting touch part of the skin, immediately recognizes that its
being touched, lots of activity recognizes how long youre being
ii) receptor field small/large in nature

(1) have a hard time localizing where im being touched if same receptor
remains active tested with a two point discrimination: if you can touch
points of the skin and can still recognize that its two points = receptive
field must be very small
(a) i.e. finger tips detailed information
(2) two points, but continue to separate and you still cant recognize that its
two points = large receptive field
iii) borders diffuse/sharp
(1) whether or not there is overlap of receptive fields
(2) diffused borders lots of overlap between them, share some of the same
skin, touch that area both receptors are activated at the same time
(3) sharp able to distinguish
g) see pictures
h) Rullfini corpuscle
i) Static force/stretch
ii) Slow
iii) Large
iv) diffuse
i) Merkels disks
i) Form of objects that youre touching
ii) Smooth or rough
iii) Slowly adapting receptors
iv) Small receptive fields
v) Sharp borders
vi) Finger tips
j) Meissners corpuscle
i) Rapid
ii) Small fields
iii) Sharp borders
iv) Contours of objects
v) Rapidly adapting have to be changes
vi) Important for reading brail
vii) Esp. fingers: edges, contours, brail
k) Pacinian corpuscle
i) Rapidly adapting interested in changes vibrations
ii) Large
iii) Diffused borders
iv) Extension (tools)
v) Know where the hammer will hit the nail, idea of distances, elongated tool
l) Free nerve endings
i) Pain
ii) Temp
iii) Hair movement
iv) Caress/limbic massages, petting an animal
v) Dont have specialized receptor elements
13) Two categories

a) Free nerve endings Figure 7.26

i) Temperature cold and heat
ii) Trp receptors (transient receptor potential)
iii) TRPA1 plays a role in reaction to temperature, esp. cold temperature
(1) Cold receptor as well
(2) Most active around 11/12 less active as you get warmer
(1) Warm receptor
vi) 13 deg C
(1) differences in activity at different levels
(2) cold and heat receptor overlap at 20 deg C
vii) TRP receptors originally identified in the tongue
viii) Also found in other places for other senses
ix) TRP names
(1) A auditory
(2) M menthol
(3) V vanilloid (e.g. capsaicin)
x) What you need to know:
(1) Several different receptors
(2) Pattern of activity due to overlap of receptors
(3) Some respond to heat vs. cold
(4) Found in mouth, others found in ear?
b) Specialized receptors
c) Categories are carried into spinal cord and remain separated in nervous system to
some degree
14) Table 7.1
15) Figure 7.27
a) Detecting touch
b) Is that cold or not
c) Painful or not
d) See picture
e) Fast ones
i) Associate with specialized receptors
f) Free nerve endings are slower kind
g) Cortex perception
i) Cross sections of the nervous system
ii) Two different colored axons
(1) Pain and temperature
(2) Spino where it originates and where it ends
(3) Red neuron thalamus synaptic connection continues to cortex
(4) So its the slower system
(1) Touch
(2) Kinesthetic sense

(3) Limbic touch

(4) Specialized receptors
(5) Comes from looking at spinal cord itself long elongated structure, with
columns on backside (dorsal) = dorsal columns
(6) Blue axon in dorsal column
v) Both pathways follow a rule as soon as there is a synapse, then there is
immediately crossing over to the other side
(1) Unipolar neuron from cell body
(2) Single pole coming off of it
(3) Divides
(4) Part of the axon goes to periphery
(5) Part goes to spinal cord itself
(6) Neural signal follows red axon to central nervous system, past cell body
(7) Action potentioal gets to subterminal fields synaptic connection
(8) Second neuron immediately crosses over and goes to spinal cord to brain
(9) = contralateral representation
(a) crossing over from one side to other on spinal cord
vi) unipolar neuron
vii) action potential continues on into the spinal cord
viii) no synapse for connection
ix) gets to nedulary levels where there exists the synaptic connection
x) immediate crossing to the other side, contralateral representation
xi) red and blue are now on opposite sides
xii) ventral posterior nuclei in thalamus
xiii) project to somatosensory cortex
xiv) DECUSSATION = crossing to the other side
xv) Midbrain connections, and connection in thalamus (ventral posterior nuclei)
still segregated in somatosensory cortex
xvi) Move up or down the spinal cord achieve a map
xvii) So different cells activated in somatosensory cortex
16) 7.28
a) appreceptive agnosia
i) left parietal
ii) drawings would not show what youre feeling
iii) no perception of what youre feeling
iv) Patient EC
b) associative tactile agnosia
i) bilateral angular gyrus
ii) patient MT
iii) draw what youre feeling but when feeling not able to recognize it
17) 7.29
a) ascending pain pathways
b) mechano receptors
i) nociception perception of pain
ii) sharp, alittle faster in the nervous system, associated with quick withdrawl

iii) only felt for duration of contact with the stimulus

c) TRPV1 receptors
i) Free nerve endings reacting to extremes of heat or extremes of acids
ii) Originally identified in the tongue
iii) i.e. capceasin
iv) dull pain experiences
v) burning sensation
vi) pain but cant identify exactly where that pain was
vii) remove the burning stimulus, pain persists and lasts for a long time
d) ATP
i) Receptors on neurons themselves
ii) Detect free floating ATP
iii) Energy substance for cells
iv) Damaged cells that leak out ATP, receptors that detect that ATP has been
e) Cutaneous stimuli
i) Touch
ii) Temperature
iii) Pain
iv) Itch
(1) Not going to be tested
v) Somatosensory pathways
(1) Higher pathways that are associated with pain
f) Suggests that different experiences are associated with pain
i) Hurts
ii) Emotional reaction to the pain can last for longer too
iii) Prefrontal cortex areas remember painful experiences that changes how we
react to life in general
g) Nociceptive information from spinal cord
i) DM or VPL body/VPM face
ii) Sm1
(1) Not only sensory in nature, but also some motor function as well
iii) Sm2
iv) Insula + ACC = unpleasantness
(1) Can be considered to be part of limbic system (unpleasantness of pain
perception we have)
v) PFC
(1) Long term emotional consequences
18) Figure 7.30
a) fMRI
i) individuals experiences painful stimulation (shock, cold, etc.)
ii) primary somatosensory cortex becomes active
iii) normal patient see limbic areas
(1) anterior cingulate cortex becomes very active
iv) hypnotize subject
(1) primary somatosensory cortex are similar

(2) hypnotic suggestion reduces pain perception and activity in ACC

v) without hypnosis, just suggesting its a good idea, or making it a contest
(1) normal people can keep their hands in longer than someone with hypnosis
vi) how are you individually suppressing it?
19) 7.31
a) ascending pain pathway
i) spinal cord to cortex
b) descending pain pathways
i) how to hypnosis/suggestion work
ii) suppress systems with pain like function
iii) interact with opiate systems
iv) body has receptors for opiats and creates recpetors
c) DLPFC (dorsal lateral prefrontal cortex)
d) PAG midbrain (between tectum and tegmuentum)
i) Inhibiting an inhibitory neuron results in a release of inhibiton and activates
PAG neurons
e) At spinal cord level you block painful information from being sent from spinal
cord to the cortex
i) Block asending pain pathway
ii) i.e. acupuncture
iii) counter irritation
f) implant a stimulating electrode into PAG to suppress pain perception
i) do this kind of psychosurgery in desperate situations/chronic pain
ii) i.e. someone with cancer
g) discovered by accident i.e. frontal lobotomy
i) cut themselves and dont care cause dont feel pain
ii) pre frontal cortex
h) opiates are most common use for pain perception, however not good for
suppressing long term or chronic pain because we develop a tolerance for the
i) generally have patient awake for surgery so they can assess pain differences
j) some people immune to pain = chronic congenital (born with it) pain insesntivity
i) born without receptors for pain detection
ii) genetic?
iii) Can be acquired tumor or stroke damages pain pathways
iv) Damage to spinal cord itself
v) i.e. patient could no longer feel sharp pain lower half of spinal cord dorsal
vi) upper spinal cord sensations still there
20) Figure 7.32
a) Placebo effect (inert pill or chemical)
b) Psychological effect of placebo
c) Opioid receptors become very active in nucleus accumbens and anterior cingulate
d) NAC (nucleus accumbens) most active
i) Pleasure center or brain

ii) Placebo causes pleasurable experience

21) 7.33
a) placebo effect based on expense of medication
b) less pain perception for regular price
c) more pain perception for low price
d) placebo effect quite powerful
e) since 1970 all studies in psych journals have to have a control group accound
for placebo effects
f) ubiquitous effect
22) 7.34
a) placebo effect activates PAG (periaqueductal grey)
23) phantom limb pain is something very difficult to get rid of
a) somatosensory cortex has map of body
b) area can still be active and give you the impression/perception that the limb still
c) even though cells are no longer receiving signals from those cells

Figure 7.24
1) Color coated to indicate different smells
2) Colors become segregated in the brain
3) Olfactory bulb
4) Smells originally scattered all over the place but comes together in one location
5) Own place in the brain
6) Segregation very early in representation of smell on cortical surfacing
7) Basic smells
Figure 7.44
1) Fifth lobe
2) Primary olfactory cortex allows smells to combine
3) 10,000 different smells we are capable to detecting
4) Activation of multiple regions at the same time
5) Patterns of activities is very important for all of cortical processing