Lecture 1: Neurons

1.1. Neurons and Glia

Cell membrane
- protein channels in the membrane permit a controlled flow of water,
oxygen, sodium, potassium, calcium, chloride, and other important
chemicals
Mitochondria
- have genes separate from those in the nucleus of a cell  differ from
one another genetically

Dendrites
- surface is lined with specialized synaptic receptors  receives
information from other neurons
- The greater the surface area of a dendrite, the more information it can
receive
- Many dendrites contain dendritic spines  short outgrowths that
increase the surface area available for synapses

*Invertebrate axons do not have myelin sheaths

An afferent axon: brings information into a structure
An efferent axon: carries information away from a structure
 Every sensory neuron is an afferent to the rest of the nervous system, and
every motor neuron is an efferent from the nervous system

Sensory & motor neurons

- 3 types of neurons
o Sensory: senses
o Motor: receive command from brain  send out signals to muscles
o Inter-neuron: not sensory/motor
- Structure: imagined as a long link
o One end: sensory neuron  pass signal to inter-neuron  another end
is motor neuron (has soma in spinal cord) to command the muscle
 - Motor neurons
o Need longer axon  need to send signal to more distant location from
the soma
- Brain neurons
o Most neurons are inter-neuron  responsible for processing
information
Glia
- Neurons need nutrition, oxygen, mechanism to remove waste when it is
working, synchronizing mechanism
- Neurons need to migrate from one place to another  Gila leads neurons to
migrate to location that is needed

1.2. Blood-brain Barrier

Blood-Brain-Barrier
- Main purpose is for protection
- Maintain intact cognitive abilities
1.3. Actions potentials: 5 steps
Action potential
- NA+ come from salt; K+ come from food
- Migration of neurons causes action potential
- Influx of sodium ions causes action potential

AP voltage
- Absolute level of the inside and outside voltage does not matter
- Difference in voltage matters! (=inside - outside)

STEP1: Resting potential

- The NA+, K+ ions channel is closed
- The pump will move the ions back inside after the AP is done
Inside the neuron:
- Negative charge during resting stage
- Difference between electric potential inside and outside = electric gradient
 - Other ions (other than NA+, K+) present leading to the negative charge inside
the neuron
- How to know when is positive/negative?
o Look at 5 Steps in AP  charges are reversed in different states

STEP 2: Depolarization
Pump VS ion channels
- Why still increase in NA+ ions?
 Rate of moving in by the ion channels > rate of move out thr the pump
Gated channels
- If drug blocks the channel, AP cannot be fired

STEP 4: Peak of AP
- NA+ channels completely shut down
- Migration of ions depends on concentration gradient (concentration of that ion
in the particular location) & electrical gradient (same charges repel  K+
tends to move to outside)
o Both gradient push the K+ out
o NA+ also move out thr the pump

STEP 5: Refractory period

- Hyperpolarization  prevent the next AP from occurring
- After refractory period, action potential is regarded as complete  return to
esting state

1.4. Actions potential propagation

Saltatory conduction
- AP only occur in the node of ranvier (only nodes have sodium channel)
- Signal is passed from 1 node to another node
- Diffusion of ions goes in same direction as action potential
o Concentration gradient: Higher concentration of NA+ in 1 node 
gradually move to less concentrated node
 o When there is enough NA+  fires another AP in the node
- The stimulus causes the NA+ to rush in (depolarization in the membrane) 
NA+ channel opens cuz it’s voltage sensitive  ions will diffuse to the
neighboring axon node
- Saves energy as sodium ions are only admitted at the nodes (compared to
regenerating AP at every point of the axon)
(Process: After an action potential occurs at a node, sodium ions enter the
axon and diffuse, pushing a chain of positive charge along the axon to the
next node, where they regenerate the action potential. This flow of charge
moves considerably faster than the regeneration of an action potential at
each point along the axon.)

Length of the myelin sheath

- The length is guided by the gila  related to DNA information
- If it is too long, the voltage will gradually decrease during saltatory conduction
 the current cannot diffuse from one node to the next while still remaining
above threshold
 no signal passed to next node
- If too short, the sodium ions have to jump many times  waste of energy 
slower transmission of signal

1.5. Neural coding

Neural coding (how information is encoded by neurons)
Firing rates
- ONE neuron: fires  firing rate represents likeliness of being a face
- Population coding  signal is represented by a group of neurons
o Collectively fire
o E.g. primary visual cortex  a group of neurons is representing a point
of visual field  responsible for diff orientation (degrees of tilt) by
firing for one orientation
Graded potential
- No ions channels involved
- Some neurons can generate action potential, some generate graded potential
- The change of electrical gradient  pass thr axons  gradually reduce, but no
 ion channels to produce action potential to pass the info
- E.g. some neurons on our eyeball  e.g. photo inceptor cell?
1.6. Lecturer’s questions
1. Axon with myelin sheath transmit signal faster
- Action potential only occurs in the node of ranvier by the saltatory
conduction  axon no need to make AP at every single point of the
axon
2. Some useful chemicals pass thr BBB
- Active transport, e.g. vitamin
3. In 5 stages of AP, concentration gradient NEVER push NA+ out of the neurons
- Concentration of NA+ outside is very high
- Even in some situation, NA+ move in
- No situation that concentration gradient will push NA+ outside the
neurons
4. Not every situation to a neuron can trigger AP
- The stimulus is not strong enough  need to depolarize > threshold
5. When a signal passes thr an axon, more than 1 AP are generated
- Signals are propagated along the axon
- When one point of axon has AP  cause other AP in neighboring
position along the axon  pass from one end to another end of the axon
6. Amplitude of firing of AP is always the same

Lecture 2: Synapses
2.1. Synapse
Founders of modern neuroscience (need to rmb their names)
- Santiago Ramon y Cajal: neurons are separated
- Charles Sherrington: discovered synapses with behavioral observations
o He observed a reflex action of a dog
o Measured the speed of signal from body part to spinal cord
(velocity) < 40m/s (slower!!)
o Speed of signal transmitted along the axon = 40m/s
o Gap between neurons causing delay in the time

Synapses VS synaptic cleft

- Cleft: exactly the gap between the presynaptic and postsynaptic
neurons
o Allows diffusion for neurotransmitters
o Ensure one-direction of transmission
- Synapse: includes cleft and other areas in the presynaptic neuron and
membrane of the postsynaptic neuron

EPSP & IPSP

- Both decay over time
- If the summation cannot trigger AP, then the signal will be gone
- Inhibitory neurons, e.g. send out relax signals to muscles
An IPSP occurs when synaptic input selectively opens the gates for
potassium ions to leave the cell (carrying a positive charge with them) or for
chloride ions to enter the cell (carrying a negative charge).
Temporal summation of postsynaptic potentials (happening inside one neuron)
- Summation of membrane potential
- Dendrite will receive input  excitatory or inhibitory
- Before the first potential declines to 0, the second potential can join
and summed up
- What is actually summing up?
o potential = electric potential
o by ways like increase in positive ions or decrease in negative
ions
Graded potential can trigger AP (happens in the axon hillock) *but not related to
whether it is pre or postsynaptic neuron*
- Summation of graded potential is high enough then will trigger wide
open of sodium ion channels  trigger AP

2.2. Events at synapse

Chemical vs electrical synapses
- Chemical:
o Signals transmitted by neurotransmitters
o Most neurons are this
- Electrical
o Signals transmitted by ions

Vesicles
- membrane bound structure that contain the neurotransmitters
o Change in voltage brought by AP causes calcium channels to
open
o Influx of ions changes voltage in the postsynaptic neuron 
causes propagation of action potential in the postsynaptic
neuron  pass down the signal
Membrane potential vs graded potential vs action potential
- Membrane: (difference) how high or low the potential is at particular
membrane
- Graded, action: potential to give signal
o Graded: dendrite (input)
o Action: axon (output)  action potential only occurs along
axons
Sequence of chemical events at synapse:
1) The neuron synthesizes chemicals that serve as
neurotransmitters. It synthesizes the smaller
neurotransmitters in the axon terminals and
synthesizes neuropeptides in the cell body.
2) *Action potentials travel down the axon. At the
presynaptic terminal, action potential opens the Ca2+
ion channel and enables calcium to enter the cell. Influx
of Ca2+ makes the synaptic vesicles start to fuse with
the presynaptic membrane.
3) Exocytosis  Calcium releases neurotransmitters from
the vesicles and into the synaptic cleft, the space
between the presynaptic and postsynaptic neurons.
4) The released neurotransmitter molecules diffuse
across the synaptic cleft (<0.01ms), attach to receptors,
and alter the activity of the postsynaptic neuron.
Mechanisms vary for altering that activity.
5) The neurotransmitter molecules separate from their
receptors.
6) The neurotransmitter molecules may be taken back
into the presynaptic neuron for recycling or they may
diffuse away.
7) Some postsynaptic cells send reverse messages to
control the further release of neurotransmitter by
presynaptic cells, by releasing retrograde transmitters

2.3. Neurotransmitters
Other types of neurotransmitter (not in PPT)

Purines ATP, adenosine, maybe others

Gases NO (nitric oxide), maybe others

Ionotropic or metabotropic effect
- Each can be excitatory (EPSP) or inhibitory (IPSP)
- Some neurotransmitters always attach to either receptor  some
always give EPSP or IPSP, e.g. glutamate always give EPSP

Metabotropic effects
- G-protein was originally attached to the metabotropic receptor of the
postsynaptic neuron  activate other chemicals (“second
messengers”= other chemicals) to send out signals
- Influences larger area of the cell

Most synthesis of neurotransmitters happen in the presynaptic terminal, some

synthesize in the soma, e.g. neuropeptides

2.4. Hormones
Hormones VS neurotransmitters
- Neurotransmitters: direct message to specific, particular recipient
o Used in nervous system
o Sent from presynaptic neuron to postsynaptic neuron
- Hormone: broadcast the message  changes in larger area
o Transported by blood to circulate different parts of the body
2.5. Lecturer’s questions
- Between 2 neurons, there is no graded potential  only travel of
neurotransmitters (exocytosis triggered by AP travelling down the axon
in the presynaptic neuron)
- graded potential occurs after neurotransmitters bind to receptor in
the postsynaptic neuron  receptor will change the membrane
potential
- Some AP cannot trigger exocytosis  AP just end there
 Lecture 3: Nervous system

3.1. Peripheral nervous system

Reflex
- Somatic nervous system
- Can control contraction & relax of muscles
Unlike the ganglia in the sympathetic system, the parasympathetic ganglia
are not arranged in a chain near the spinal cord. Rather,
long preganglionic axons extend from the spinal cord to parasympathetic
ganglia close to each internal organ. Shorter postganglionic fibers then
extend from the parasympathetic ganglia into the organs themselves. 

Because the parasympathetic ganglia are not linked to one another, they act
more independently than the sympathetic ganglia do. 

3.2. Central nervous system

Spinal cord
- Sensory nerves connected to back of the spinal cord
- Motor nerves connected to the front of the spinal cord
o Information exit/flow out from the spinal cord
- Damage of spinal cord
o Severity of damages
 only dorsal part will be damaged (sensory)
 If removed in surgery, both sensory & motor part will be
damaged
White matter & grey matter
- White matter = myelinated area of the axon  white fatty substance)
- Grey matter = cell body
 Spinal cord Cerebral cortex
White Outside Inside
-myelinated axons are below
the cortex, since axon is
connected to the body
e.g. thr cranial nerves (cable
going from inside the brain)
Gray Inside Outside
-central part of the spinal cord -surface of the cerebral cortex
does the processing and receive
signal from the body

Place cell (under hippocampus)

- Hippocampus is responsible for semantic memory
- Place cell is the neuron help to remember locations by activation

Midbrain, occipital lobe

- Multiple parts of brain responsible for the same functions
- Vision: long pathway to process info
o E.g. higher level of processing like object recognition in temporal
lobe
Sensors thr thalamus
- We process visual info in PVC, smell in olfactory bulb
- Some info go thr relay station  projected to PVC for further
processing
- Smell directly go to olfactory bulb for processing (no relay station)
- Relay station  minimum processing by taking in the info and pass to
another part of the brain
Substantial nigra
- Structure covered by the tegmentum (slide 25-26)
3.3. Cerebral cortex
Laminae
 - Cortex is organized in 6 layers of cell bodies (=laminae)
- Parallel to the surface of the cortex
Blindsight (due to damage in the occipital lobe)
- PVC/V1 in the occipital lobe
- Normal person: light info received by the eye  sent to the back of the
brain  processed by V1
- Blindsight happens when V1 is damaged  Info can still be sent from
relay station to the brain
- No visual awareness  can still make an above-chance “guess” of
the object due to part of the info not going thr V1 but sent to the
brain
- If V1 damaged, cannot have visual images in dreams
- Opposite situation: damaged eyes
o Still have imagery when thinking or dreaming
Somatosensory & motor representations
- Motor: send out motor command/info
o Our brain has larger area to send out / process motor info for
the head, fingers
- Somatosensory: receive sensory info
o Larger brain area to receive sensory signal with head, hand,
fingers
- Both homunculus are not proportional to our body shape in real life
The postcentral gyrus includes four bands of cells parallel to the central
sulcus. Separate areas along each band receive simultaneous information
from different parts of the body. Two of the bands receive mostly light-
touch information, one receives deep-pressure information, and one
receives a combination of both. In effect, the postcentral gyrus represents
the body four times.
 Lecture 4: Genetics and Evolution

4.1. Genetics
DNA
- The last chain in the DNA  Sex chromosome
- DNA  the two ladders would separate  produce the RNA based on
the right part (DNA is the template  RNA is produced and detached
from the DNA for multiple times)
- Every 3 bases in the RNA  instruction for producing 1 amino acid
(produced according to the code in the RNA)
- Any protein consists of some combination of 20 amino acids
o Some protein from part of the structure of the body
o Some serve as enzymes that control rate of chemical reaction

DNA contains four “bases”—adenine, guanine, cytosine, and thymine

 The order of those bases determines the order of corresponding bases
along an RNA molecule—adenine, guanine, cytosine, and uracil.
 The order of bases along an RNA molecule in turn determines the order
of amino acids that compose a protein. 
e.g. if three RNA bases are in the order cytosine, adenine, and guanine, then
the protein adds the amino acid glutamine.

Epigenetics
- Whether the code of information in the DNA would be expressed in our
body (in diff stages in our body life or under diff environments)
- At a critical period (e.g. puberty)  some part of genes will be active 
determines how your body develops
- Related to diff environment we are in, e.g. lack of resources  different
expression
4.2. Heritability
Heritability
- Whether variance in some characteristics is related more to
genetics/environmental factors
- Methods to measure
o Unrelated children adopted in the same family  if they have
common characteristics  then the characteristics are more
related to environment
o Compare 2 pairs of children (adopted in the same fam VS 2
children in diff families)  environment?
4.3. Neural development
Neural development
- Goal-oriented to build the brain
- Synaptogenesis is related to memory formation  e.g. hippocampus 
how neurons connect to each other affect memory
Process of neural development:
The dorsal surface thickens and then long thin lips rise, curl, and merge,
forming a neural tube that surrounds a fluid-filled cavity. As the tube sinks
under the surface of the skin, the forward end enlarges and differentiates
into the hindbrain, midbrain, and forebrain. The rest becomes the spinal
cord. The fluid-filled cavity within the neural tube becomes the central canal
of the spinal cord and the four ventricles of the brain, containing the
cerebrospinal fluid (CSF). 

Stem cells
- The origin of every cell  can transform to diff cell types
- Before differentiation  cells only have cell body
4.4. Pathfinding by axons
Neural Darwinism
- Certain neuron is not active for a long time  gradually become
insensitive and eventually die out
Roger Sperry’s experiment
- Concentration of one chemical (3 times) on dorsal side  guide
pathfinding of axon
Fetal alcohol syndrome
- a condition marked by hyperactivity, impulsiveness, difficulty
maintaining attention, varying degrees of mental retardation,
motor problems, heart defects, and facial abnormalities.

4.5. Neural plasticity

Blind people
- Occipital lobe not in use (for visual input)
- Plasticity: occipital lobe will be used for processing other sensory info
Brain damage
- surviving parts have decreased activity  no activation from damaged
part
Stroke
- In ischemia, the neurons deprived of blood lose much of their
oxygen and glucose supplies. In hemorrhage, they are flooded
with blood and excess oxygen, calcium, and other chemicals. 
- increases pressure on the brain and the probability of
additional strokes
- impair the sodium–potassium pump, leading to an
accumulation of sodium inside neurons. The combination of
edema and excess sodium provokes excess release of the
transmitter glutamate  overstimulates neurons, damaging
both neurons and synapses
 
Collateral sprouting & denervation supersensitivity
- If after the new branches, less information
 still can supersensitivity
 Lecture 5: Vision

5.1 Eyes and light

Process
- light passes through the ganglion, amacrine, and bipolar cells en
route to the receptors. However, these cells are transparent,
and light passes through them without distortion

Fovea for detail perception

- blood vessels and ganglion cell axons are almost absent near
the fovea, it has nearly unimpeded vision
- tight packing of receptors aids perception of detail
- each receptor in the fovea connects to a single bipolar cell,
which in turn connects to a single ganglion cell that has an axon
to the brain. The ganglion cells in the fovea of humans and
other primates are called midget ganglion cells because each
is small and responds to just a single cone.
- each cone in the fovea has a direct route by its own ganglion
cell to the brain.
- Because the midget ganglion cells provide 70 percent of the
input to the brain, your vision is dominated by what you see in
and near the fovea

Photopigments
- Both rods and cones contain photopigments, chemicals that
release energy when struck by light.
 - Photopigments consist of 11-cis-retinal (a derivative of vitamin
A) bound to proteins called opsins, which modify the
photopigments’ sensitivity to different wavelengths of light.
- Light converts 11-cis-retinal to all-trans-retinal, thus releasing
energy that activates second messengers within the cell
5.2 Color perception
Trichromatic theory
- Observation of wavelength selectivity is consistent with trichromatic
theory  When an image is presented to the retina, all cones will be
activated  But some cones with preferred wavelength will react more
strongly than others
- More intense light increases the activity of all three cones
without much change in their ratio of responses  the light
appears brighter but still the same color. When all three types
of cones are equally active, we see white or gray
- Long- and medium-wavelength cones are far more abundant
than short-wavelength (blue) cones  easier to see tiny red,
yellow, or green dots than blue dots

Opponent-process theory
- Imagine a bipolar cell that receives excitation from a short-
wavelength cone and inhibition from long- and medium-
wavelength cones
-  increases its activity in response to short-wavelength (blue)
light and decreases it in response to yellowish light
-  After prolonged exposure to blue light, the fatigued cell
decreases its response
-  Because a low level of response by that cell usually means
yellow, you perceive yellow
5.3 Lateral inhibition
Lateral inhibition
- Consider info around the targeted location  functional advantage:
enhance signal  interaction/communication among info between
neighboring info [horizontal cell & amacrine cell]
- Occurs in diff parts of visual pathways, e.g. LGN, retina, V1
- Horizontal cell  send inhibitory info to bipolar cell
- Amacrine cell receive inhibitory info from bipolar cell  send info to
ganglion cell
- Function: to sharpen borders & create contrast

Hermann grid
- Neurons responsible for the intersection receive 4 inhibitory signal
(weaker signal for firing) from the neighboring neurons in the 4
corners  darker
- For other parts of the white line  receive 2 inhibitory signals
- The receptor excites both the bipolar cells and the horizontal
cell. The horizontal cell inhibits the same bipolar cell that was
excited (=net excitation) plus additional bipolar cells in the
surround (=net inhibition).

5.4 Retina
Retina: visual field (<=180 degrees)
- All information from right & left visual fields goes to both eyes
- Half of retina on each eye responsible for receiving info for left visual
field; half of retina for right visual field
- At optic chiasm  Half of each optic nerve, the part representing
the nasal half of the retina crosses to the contralateral
hemisphere at the optic chiasm
- After exchange  right hemisphere only receives info about left visual
field; vice versa
- If one eye is damaged, both info from left & right visual fields can be
sent to right & left hemisphere
- If one hemisphere, e.g. MT, is damaged  cannot perceive motion
Receptive field
- Receptive field of bipolar cell = Sum of the receptive fields of all the
rods and cones connected to it

Lateral inhibition x center-surround receptive fields

- Lateral inhibition  interconnection between neurons on the same
level
- Center-surround  receptive fields of neurons  in what situations the
neuron will fire, e.g. large receptive field  many location on visual
field affect activation of neurons
- Center-surround is a special form of receptive field  in a form of inner
circle and outer circle
- On-center, off-surround, e.g. light on centre, no light on surround 
neuron will fire
- Off-center, on surround, vice versa
- Combination of the signals  can be grouped in V1  help us detect
orientation

5.5 Primary visual cortex

Selectivity of V1 neurons
- Preferred stimuli  if certain stimuli is present  particular neuron
has high firing rates [property of the neuron]
- Lower-level neurons, e.g. on retina  preferred stimuli: simpler shape
- Higher-level neurons, e.g. on FFT  complex shape, e.g. face
- All neurons work tgt to help us detect features of objects

Optical illusion
- due to feedback from other cortical areas to change responses
in the primary visual cortex 
Simple cells VS Complex cells
- Simple cells: most have bar-shaped or edge-shaped receptive
fields; More respond to horizontal or vertical orientations than
to diagonals
- Complex cells: respond to a pattern of light in a particular
orientation (e.g., a vertical bar) anywhere within its large
receptive field; Most respond most strongly to a stimulus
moving in a particular direction—for example, a vertical bar
moving horizontally. 

5.6 “What” and “Where” pathways

Prosopagnosia
- In some people the right fusiform gyrus is significantly smaller
than average and has fewer than normal connections with the
occipital face area

Temporal cortex
- has specialized areas for perceiving places, faces, and bodies,
including bodies in motion
- Neurons in areas MT and the ventral part of MST respond
briskly if something moves relative to the background, but they
show little response if the object and the background both
move in the same direction and speed
 MT and MST neurons enable you to distinguish between the
 result of eye movements and the result of object movements
 You do not see your own eyes move because area MT and
parts of the parietal cortex decrease their activity during
voluntary eye movements, known as saccades

Motion blindness
- Ppl become motion blind shortly before and during a saccade
(voluntary eye movement), because of suppressed activity in
area MT

Blindsight
- V1 in occipital cortex is damaged  cannot depend on occipital cortex
- Apparently depends on connection from thalamus to the temporal
cortex
- Temporal cortex  recognizing object

Lecture 6: Audition and other senses

6.1 Ears and sound
Physical properties of sound
- Amplitude  height of sound waves
- From top to bottom = one cycle
- Narrower cycles  complete more cycles in one second  higher
frequency
- Timbre = quality of the sound, e.g. same note from piano and violin
sounds different

Audible frequencies
- Sounds important for survival are heard
- Range decreases with age  maybe due to depreciation of ear
- Bigger animal tends to hear sound with lower hertz (+produce!!)
- Absolute pitch
- Tone deafness (insensitive to diff of tones)

Pitch perception
- Frequency theory: produce action potential at the same rate of the
hertz (18 hertz in a second  18 APs in a second)
o refractory period of a neuron is typically about  1/1000

second, so the maximum firing rate of a neuron is about

1000 Hz, far short of the highest frequencies we hear.
 ideal for low frequencies
- Place theory: for high pitch sound, we cannot produce AP that fast
o each frequency activates the hair cells at only one place

along the basilar membrane, and the nervous system

 distinguishes among frequencies based on which
neurons respond
- Current view
o Low frequencies: the frequency of impulses identifies the

pitch, and the number of firing cells identifies loudness.

o Higher frequencies: a neuron might fire on some of the

waves and not others

 APs are phase-locked to the peaks of the sound waves;
 Other auditory neurons also produce APs that are
phase-locked with peaks of the sound wave  can be out
of phase with one another:
o Highest frequencies: each wave of a high-frequency tone

excites at least a few auditory neurons  high-pitched

sound sets up a traveling wave that peaks at some point
along the basilar membrane, and then stops. The point at
which it peaks identifies the frequency of the sound
 Near the base: highest frequency sounds vibrate hair
cells near the base
 Near the apex: lower frequency sounds
6.2 Primary auditory cortex
Tonotopic map
- each location in the auditory cortex responds to a preferred tone
Sound localization
- Time difference  the ear nearer to the source receives the sound
earlier
- Loudness difference  delay in time with decrease in loudness 
sound needs to go around the head to arrive the other ear [extra path]
- [additional info] Phase difference  due to time difference  left ear &
right ear not in sync  receives sound signal at diff phases
Sound localization under different conditions
- Head under water: you will have trouble localizing low- and
medium-frequency sounds.
 sounds travel faster in water than in air, so a sound arrives
at the two ears almost simultaneously and the phase
differences are small
- Different sizes of head:
o a small head  localizes sounds mainly by differences in

loudness because the ears are not far enough apart for
differences in onset time to be useful.
o a large head  localizes sounds mainly by differences in

onset time because its ears are far apart and well suited
to noting differences in phase or onset time

Vision VS Audition (advanced auditory processing)

Criteria Visual
Two pathways Vendral & dorsal
Pathways Earlier pathways of vision
before V1 process simpler,
basic features
V1  process more
complicated features, e.g.
shape, faces, motion
Audition
Identification & localization of
sound
Ear  process basic feature of
the sound
A1  identify the tones
A2  changes of sound, e.g. high
pitch to low pitch
outside A2  auditory objects
(uniquely produced by an object)

Primary Active during imagination and Active during imagination and

cortex dreams dreams
Superior Analyze visual stimuli Analyze auditory stimuli
temporal Damage  motion blindness Damage  motion deafness
cortex
 Impairment Intact eyeballs, damaged V1 Intact ears, damaged A1
 no visual consciousness but  impair perception for complex
can make accurate guess sounds but no deafness

6.3 Mechanical senses: vestibular

Vestibular system
- Compensatory movements: e.g. when you are reading a letter, your
head moves right, your eyes would move left to stay on the words
- 3 semicircular canals (change in tiltness)  movements produce
accelerations  movement of fluids push hair cells that produce AP
- Otoliths detect current tiltness of the head

6.4 Mechanical senses: somatosensation

Free nerve endings
- Related to pain, temperature
- For each (somato) sense: independent pathways from receptors to
brain
- Do not have special designs of receptors, in contrast to photoreceptors

Pain
- thicker and faster axons convey sharp pain
 - thinner ones convey duller pain, such as postsurgical pain. 
- Pathways
o A pathway to the thalamus, and from there to the
somatosensory cortex, conveys the sensory aspects of pain
o A separate pathway to the hypothalamus, amygdala, and
cingulate cortex (emotional aspect of sensation) produces the
emotional aspects
6.5 Chemical senses: taste
Sweetness, bitterness, and umami receptors
- resemble the metabotropic synapses  After a molecule binds
to one of these receptors (e.g. glutamate), it activates a G
protein that releases a second messenger within the cell.
- People have two types of sweetness receptors and two types of
umami receptors, each with somewhat different sensitivities

Bitter chemicals
- Also trigger receptors in the nose, provoking coughing and
sneezing if you happen to inhale them

A saltiness receptor
- detects the presence of sodium, simply permits sodium ions on
the tongue to cross its membrane. Chemicals that prevent
sodium from crossing the membrane weaken salty tastes
Sour receptors
- detect the presence of acids 

Taste coding in the brain

- From the NTS, information branches out, reaching the pons, the
lateral hypothalamus, the amygdala, the ventral-posterior
 thalamus, and two areas of the cerebral cortex
- One of these areas, the somatosensory cortex, responds to the
touch aspects of tongue stimulation.
- Insula: the primary taste cortex.
o The insula in each hemisphere of the cortex receives

input from both sides of the tongue

6.6 Chemical senses: olfaction

Olfactory receptors
- each olfactory cell has cilia (threadlike dendrites) that extend
from the cell body into the mucous surface of the nasal passage.
- Olfactory receptors are located on the cilia.

Olfactory coding in the brain

- Like metabotropic neurotransmitter receptors
- each of these proteins traverses the cell membrane seven times
and responds to a chemical outside the cell (here an odorant
molecule instead of a neurotransmitter) by triggering changes
in a G protein inside the cell
- The G protein then provokes chemical activities that lead to an
action potential. 

VNO
- VNO receptors continue responding even after prolonged
stimulation 
- Example: the timing of women’s menstrual cycles
o women who spend much time together find that their

menstrual cycles become more synchronized, unless they

are taking birth control pills
Lecture 7: Sleep
7.1 Endogenous Circadian Rhythm
Repeated adjustments of circadian rhythm
- Stress elevates blood levels of the adrenal hormone cortisol
- prolonged elevations of cortisol damage neurons in the
hippocampus  a brain area important for memory

Melatonin
- Signaling night time instead of sleep time  released at night for all
species
- Melatonin pills  received by receptors in the SCN  adjust biological
block  release melatonin earlier in the next day

What proves SCN produces circadian rhythm by itself?

- Even a single isolated SCN cell can maintain a circadian rhythm,
although interactions among cells sharpen the accuracy of the
rhythm

Photosensitive RGCs
- respond to light slowly and turn off slowly when the light
ceases  overall average amount of light, not to instantaneous
changes in light  exactly the information the SCN needs to
gauge the time of day

7.2 Sleep stages

Monitoring sleep
 - Blue: EEG  measure average electrical potential of the surrounding
neurons, of the position attached with electrodes
o Not measuring 1 neuron  but a group of neurons around that
electrode
o Measures the synchrony of electrical potential/neuronal signals
 big waves = high synchrony; straight line = low synchrony
(cancelled out electric potential, e.g. half + & half -)
- Red: eye movement
- Black: time

EEG waves
- Key difference: frequency
- Delta: lower frequency  take more time to finish one cycle (one up &
down)
- Theta: higher
- Alpha: highest

NREM Stage 2:
Sleep spindles
- increase in number after new learning
- number of sleep spindles correlates positively with
improvements in certain types of memory
 related to the consolidation of memory
K-complex
- “Complex” = Compose of different structures
- Upwards means negative; downward means positive
- Slower + wave  wider width = takes longer time
REM sleep:
PGO waves
- Frequency observed during REM sleep  related to dreaming
[activation-synthesis hypothesis]
- If it appears in other NREM stages  cause dreaming in those stages

Why REM state is contradictory

- It is deep sleep in some ways  consider muscle  relaxed
- But light sleep in some way  consider brain waves

Factors affecting sleep

- older adult has less slow-wave sleep and many more
awakenings during the night 
- frequency of awakenings correlates with loss of cells in the
hypothalamus, and with a tendency toward cognitive decline 

7.3 Brain mechanisms

Wakefulness
- These transmitters produce wakefulness partly by regulating
the levels of potassium and other ions that produce a constant
state of arousal
- After the ions are in a state that supports arousal, they tend to
remain at a stable concentration
 waking up is generally faster than falling asleep 

Without orexin?
- alternate between brief periods of waking and sleeping.
During sleep
- neurons in the thalamus become hyperpolarized  decreasing
their readiness to respond to stimuli  decreasing the
information they transmit to the cortex
- GABA interferes with the spread of info between neurons 
weaker connections between brain areas  inhibit behaviour
and promote slow-wave sleep (being unconscious)

Sleepwalking
- Sleepwalkers are asleep in much of the brain, but awake in the
motor cortex and a few other areas
- most of the brain is not alert enough to process information and
make reasonable decisions

Lucid dreaming
- much activity around 40 Hz (cycles per second) occurs in the
frontal and temporal cortex

7.4 Sleep disorders

Insomnia
- Coffee also phase-delays the circadian rhythm  causing a
delay in the release of melatonin 
7.5 Functions of sleep
Memory consolidation
- Certain synapses become weakened, enabling others to stand
out by contrast
7.6 Dreaming
Dreams
- 80-90% happen in REM sleep
- Can happen in NREM sleep, e.g. stage 1,2,3
Activation-synthesis hypothesis
- E.g. 1. Flying or falling dream
o While you are asleep, you lie flat, unlike your posture
for the rest of the day.
o Your brain in its partly aroused condition feels the
vestibular sensation of your position  flying or falling
dream
- E.g. 2 can’t move dream
o your motor cortex is inactive and your major postural

muscles are virtually paralyzed. That is, when you are

dreaming, you really cannot move, you feel your lack of
movement, and thus, you dream of failing to move

Clinico-anatomical hypothesis
- Parietal cortex
o activity is relatively high

o visuospatial perception

o Patients with damage here fail to bind body sensations

with vision. They also report no dreams.

- Areas of visual cortex other than V1
o Fairly high activity  presumably important for the

visual imagery that accompanies most dreams.

- Hypothalamus, amygdala, and other areas
o High activity

o important for emotions and motivations

 Lecture 8: Reproductive behavior

8.1 Sex Hormones

Sex hormones
- SRY genes [kick off] turn gonad into testes  Level of testosterone
[reinforce] will become more and more concentrated  encourage
other undifferentiated parts into male sex organ
- SRY gene does not affect development of female sex organ
- Ovaries & testes are major parts to produce sex hormones, but other
parts will also produce

Androgens
- cause the Wolffian ducts to develop into seminal vesicles (saclike
structures that store semen) and the vas deferens (a duct from the
testis into the penis)
- The testes also produce Müllerian-inhibiting hormone (MIH) that
causes the Mü llerian ducts to degenerate
- The final result is the development of a penis and scrotum

Absence of MIH
- The Müllerian ducts of the fetus develop into a female’s uterus,
oviducts, and the upper part of the vagina

Steroid hormones
- 1. they bind to membrane receptors, like neurotransmitters,
exerting rapid effects
 - 2. they enter cells and activate certain kinds of proteins in the
cytoplasm
- 3. they bind to receptors that bind to chromosomes, where they
activate or inactivate certain genes 

Progesterone
- prepares the uterus for the implantation of a fertilized ovum
- promotes the maintenance of pregnancy

8.2 Organizing effects

 Sensitive period
- As a male’s developing testes secrete testosterone, certain
enzymes convert it to dihydrotestosterone, which is far more
effective at promoting growth of the penis
- If levels of dihydrotestosterone are high enough  the tiny genital
tubercle grows and develops into a penis.
- If the levels are low  the tubercle develops into a clitoris
- Similarly, depending on levels of testosterone and
dihydrotestosterone, the embryo develops either a scrotum,
characteristic of males, or labia, characteristic of females.

Puberty
- The surge of hormones at puberty produces breast development
in women
- facial hair and penis growth in men, changes in voice
- male–female differences in the anatomy of certain parts of the
hypothalamus 
Sexual differentiation of hypothalamus

8.3 Activating effects

Pregnancy
- The burst of hormones during pregnancy produces temporary
effects on emotional arousal, aggressive behaviour, learning, and
cognition

Menstrual cycle
- Hormone affects mood changes
- Process:
o After the end of a menstrual period  the anterior pituitary
releases follicle-stimulating hormone (FSH)  promotes
the growth of a follicle in the ovary.
o The follicle nurtures the ovum (egg cell) and produces
several types of estrogen, including estradiol.
o Toward the middle of the menstrual cycle  the follicle
builds up more and more receptors to FSH, so even though
the actual concentration of FSH in the blood is decreasing,
its effects on the follicle increase.
o As a result, the follicle produces increasing amounts of
 estradiol. The increased release of estradiol causes an
increased release of FSH as well as a sudden surge in the
release of luteinizing hormone (LH) from the anterior
pituitary. FSH and LH combine to cause the follicle to
release an ovum.
o The remnant of the follicle (now called the corpus luteum)
releases the hormone progesterone, which prepares the
uterus for the implantation of a fertilized ovum.
Progesterone also inhibits the further release of LH. If the
woman is pregnant, estradiol and progesterone levels
continue to increase. If she is not pregnant, both hormones
decline, the lining of the uterus is cast off (menstruation),
and the cycle begins again.

Birth control pills

- Pills interrupt communication between brain and ovaries  should not
continue the cycle

Female sexual arousal

- **Estradiol increases the sensitivity of the pudendal nerve, which
transmits tactile stimulation from the vagina and cervix to the
brain  female’s main sex drive
- Administering testosterone can increase a woman’s sexual desire,
but only if administered at levels far above what a woman would
experience naturally

Non-sexual characteristics
- that testosterone interferes with attention to emotional
expressions
- estradiol increased men’s emotional responses to seeing a person
 in distress

8.4 Sexual orientation

Older siblings
- a mother’s immune system sometimes reacts against a protein in
a son and then attacks subsequent sons enough to alter their
development  later-born homosexual men tend to be shorter
than average //higher chance to be homosexual
Brain anatomy
- Brain size is not an accurate hint of sexual orientation

Lecture 9: Learning and memory

9.1 Engrams
Cerebellum
- Damage to the cerebellum impairs learning only when a
discrete response needs to be made with precise timing
 specialized for timing brief intervals.

Flashbulb memory
- highly emotional experiences arouse the locus coeruleus
 increases norepinephrine release throughout the cortex and
dopamine release in the hippocampus
- also increase the secretion of epinephrine and cortisol that
activate the amygdala and hippocampus

Working memory
- Storing WM during delay  occasional bursts of gamma
oscillations (45 to 100 Hz) occur in cells that responded to a
stimulus
- but the bursts alternate among cells instead of persisting
throughout the delay in any one cell.

9.2 Brain areas for learning

Hippocampus’ role
- Contextual learning: When people successfully retrieve an
episodic memory, activity in and around the hippocampus
synchronizes with activity in several parts of the cortex,
consistent with the idea that the hippocampus is providing the
connections that are necessary for recall 
- Recent memories with much contextual detail depend on the
hippocampus
 older, less detailed memories depend mainly on the cerebral
cortex with less contribution from the hippocampus 

Brain areas for explicit VS implicit learning

- Procedural memory depends on the striatum too!!

Korsakoff’s syndrome
- Prolonged thiamine deficiency leads to a loss or shrinkage of
neurons throughout the brain  dorsomedial thalamus (the
main source of input to the prefrontal cortex)

Alzheimer’s disease
 - People with Down syndrome, caused by an extra copy of
chromosome 21, almost always develop Alzheimer’s disease in
middle age.
- The genes controlling early-onset Alzheimer’s disease cause a
protein called amyloid-β to accumulate inside and outside
neurons and spread from cell to cell
 damages axons and dendrites, decreases synaptic input, and
decreases plasticity
 damaged axons and dendrites cluster into structures
called plaques that damage the cerebral cortex, hippocampus,
and other areas
- May also relates to the tau protein in the intracellular support
structure of axons
 High levels of amyloid-β cause more phosphate groups to
attach to tau proteins. The altered tau cannot bind to its usual
targets within axons, and so it starts spreading into the cell
body and dendrites
 The altered tau is principally responsible for tangles,
structures formed from degeneration within neurons 

9.3 Hebbian learning

- Only a theory  no conclusive findings to support the implementation

How it explains classical conditioning

- suppose axon A initially excites cell B slightly, and axon C
excites B more strongly
 If A and C fire together, their combined effect on B may
produce an action potential
 axon A as the conditioned stimulus and axon C as the
 unconditioned stimulus
 Pairing activity in axons A and C increases the future effect of
A on B
Hebbian synapse
- pairing the activity of a weaker (CS) axon with a stronger (UCS)
axon produces an action potential
- in the process strengthens the response of the cell to the CS
axon
- On later trials, it will produce a bigger depolarization of the
postsynaptic cell conditioned response

9.4 Habituation and Sensitization

- General phenomenon observed in sensory & motor neurons
- Not specific for some type of neuron/stimulus

Sensitization & LTP

- Two levels
- Sensitization: phenomenon level
- LTP: neuronal level  what happen in the neurons
- Both  about synapse between pre and postsynaptic neuron

9.5 Long-term Potentiation and Long-term Depression

AMPA and NMDA receptors before LTP

- Glutamate attaches to both receptors. At the AMPA

receptor, it opens a channel to let sodium ions enter. At
the NMDA receptor, it binds but usually fails to open the
channel, which is blocked by magnesium ions
- If one or more AMPA receptors have been repeatedly
stimulated, enough sodium enters to largely depolarize
 the dendrite’s membrane  displaces the magnesium
ions and enables glutamate to open the NMDA receptor,
through which sodium and calcium enter
- Stimulation of the NMDA receptors lets calcium enter the cell,
where it sets into motion a series of changes that build new
glutamate synapses or increase response to glutamate at
existing AMPA receptors  After LTP occurs, NMDA receptors
revert to their original condition

THE END
LIVE HAPPILY EVER AFTER