NEUROSCIENCE: DEFINITIONS / THEORIES

NEUROANATOMY

Directions Dorsal​: top of the brain, points upwards (also known as superior)
Ventral​: bottom of the brain (also known as inferior)
Rostral​: front facing direction
Caudal:​ backwards facing direction
Neck also has rostral (moving up the neck) and caudal (moving down)
directions.
Brain areas are also either lateral (towards outside) or medial (closer to
midline).

Sections Brain can be examined on three planes (can be sliced in three ways). Slicing is
used for an MRI or similar.
Sagittal​: midsagittal is directly through middle from looking down on top of
brain and lateral sagittal is more towards lateral surface.
Coronal​: brain is sliced parallel to long axis on body but at opposite to midline
Horizontal:​ sliced perpendicular to long axis on body

The Nervous Facilitates communication between the different parts of body and processes
System information. This communication is carried out by neurons which provide high
speed connections between body cells. Neurons also analyze sensory information
and plan actions (e.g touching a hot surface and removing hand). The brain is a
complex way of relating sensations to actions. Nervous system is split into
central (right) and peripheral (left). The central consists of the brain and spinal
cord. Peripheral runs all over the body and is split into somatic and autonomic
systems, of which both have afferent and efferent nerves. Somatic system is in
control of responses to sensation and autonomic regulates bodily functions like
heart rate. These regulations happen by the sympathetic or parasympathetic
systems which make up the autonomic system. Sympathetic is ‘fight or flight’
responses when sensing danger and increases heart rate, quickens breathing,
secretes adrenaline etc which prepares for survival. Parasympathetic is ‘rest or
digest’ responses which is a complementary system (not contrast) to flight or
fight. Connections are arranged differently and take more time as speed is not
necessary.

Protection of CNS CNS is encased in bone and covered by three membranes.

Dura mater​ membrane: tough outer membrane, difficult to penetrate, provides
protection for brain is skull is damaged, between skull and arachnoid mater.
Arachnoid mater​: web like membrane found under dura mater.
Pia mater​: innermost layer.
Blood clots can occur between layers due to the blood flow between layers, a
blood vessel can tear. Happens through external trauma.
Cerebrospinal fluid is found between arachnoid and pia maters, sits inside gaps
in these layers and serves as a cushion during a fall.

Divisions of The Main divisions: forebrain, midbrain and hindbrain.

Brain Forebrain includes telencephalon and diencephalon.
Telencephalon​ consists of cerebral cortex, hippocampus, amygdala and basal
ganglia, and is part of limbic system (involved in regulation memory and
emotion).
Diencephalon​ consists of thalamus (relay station for sensory info) and
hypothalamus (involved in homeostatic mechanisms to maintain normal state of
body).

Hindbrain includes metencephalon and myelencephalon and midbrain (also

known as mesencephalon).
Metencephalon​ is composed of many tracts and has the pons as its ventral
surface - pons controls breathing, brain communication and sensations. Also
consists of cerebellum which is involved in motor coordination / movement.
Myelencephalon​ is what medulla develops from and is composed largely of
tracts. It is the origin of the reticular formation which plays central role in
consciousness such as alertness and sleep.
Mesencephalon​ consists of tectum (dorsal), which has an inferior colliculus
(responsible for relaying auditory info) and superior colliculus (responsible for
relaying visual info) and also the tegmentum (ventral).

Cerebral Cortex Cerebral cortex is outermost part of forebrain. It analyses sensory information
and performs functions essential for survival. Folds and creases serve to increase
the surface area. There is a longitudinal fissure which separates right and left
hemispheres. Corpus callosum is largest tract which connects hemispheres.
Consists of frontal (important for motor execution/planning), parietal (receiving
sensory info from body), temporal and occipital lobes.

White and Gray Both consist of cells and fibres. Gray has more cell bodies than white. The two
Matter types allow for fast communication between brain parts.

NEURONS

Neurons The brain is an intricate network of neurons. Neurons are specialised cells
which receive and transmit electrochemical signals and come in many
shapes/sizes. Per neuron, there are 10 glial cells which support and insulate it.

Parts of a Neuron Neurons have dendrites which are tree-like projections which receive signals.
The messages start here and move through the neuron to the terminal buttons
where they are released.

How Neurons The axon is the long, narrow nerve fiber which projects from cell body and, at
Work the junction where this projects from, there is an axon hillock. This is where
electric potential becomes positively charged which triggers electric impulse.
Then the action potential travels down the axon to the terminal buttons where
the neurotransmitter (message) is released across the synapse to
receptors/dendrites of receiving neuron. This neurotransmitter causes excitatory
 (more positive) or inhibitory (more negative) potential in receiving neuron. If
sum of excitatory minus inhibitor potential is large enough then another action
potential is generated.

Communication Neurons communicate via the axon which enables rapid communication.
Messages are released and received between neurons via terminal buttons and
down the axon.

Cell Membrane Neurons have a cell membrane which is a lipid (fatty) bilayer which have ion
channels embedded in them. Ion channels are proteins which enable ions to pass
through.

Resting Potential The outside of the ion cells (which pass through the channels embedded in the
neuron) have a higher concentration of sodium ions and a lower concentration
of potassium ions. This means the outside is positively charged compared to the
inside which is negative. When the ion is at resting level, the outside is
positively charged, and this resting potential is maintained by the
sodium-potassium pump.

Sodium-Potassium These ‘pumps’ lay within the membrane. They are sodium-potassium
Pump transporters which are always at work, even at resting level of cell. They
transport sodium out of the neuron and potassium into the neuron.

Action Potential When the passing ions cause changes in the electrical potential of the cell.
The resting membrane of the cell is higher in charge on the outside than the
inside. For action potential to be generated, the electrical charge of membrane
must change from -70 to -55 or less.
The membrane potential peaks at around 40 and returns back to resting level -
but then goes beyond resting level and becomes more negative - eventually
returning to resting level.
The inside of the membrane being more positively charged triggers the sodium
channels to open - sodium ions rush into the axon and cause it to become more
positive (depolarisation). This depolarisation causes potassium channels to open
which allows positive potassium ions to flow out and release some positive
charge. This causes sodium channels to close and the electric potential is
reduced due to outflow of potassium. Returns to resting potential. There is a lag
in the closing of potassium channels which leads to hyperpolarization and cell
momentarily becomes more negative.
The body is always trying to maintain equilibrium, hence the opening and
closing of channels. This process speeds up the transmission of
neurotransmitters.

Resting Membrane The difference in charge of the inside and outside of the cell.
Potential

Synapse The neuron releases synaptic vesicles which contain neurotransmitter into the
synapse. Inside the synapse, neurotransmitter binds onto the binding sites of the
receiving neuron site.
 At the synapse, two processes occur:
Reuptake: transporter molecule takes neurotransmitter back into the axon.
Enzymatic Degradation: enzymes come into the synaptic cleft and break down
the transmitter remains which makes it inactive and ensures no overload.

Release of This process is known as exocytosis. The arrival of an action potential at the
neurotransmitter terminal of the neuron causes calcium channels to open due to the voltage. The
entry of calcium ions causes vesicles to fuse with the terminal membrane and
release their contents. The neuron which then receives the transmitter is known
as the presynaptic neuron. It is received at the postsynaptic (receptor site).

Receptors One type of receptor is ionotropic receptors which form a channel for ions to
pass. Some neurotransmitter molecules bind to these receptors. When this
happens, the channel opens or closes which alters the flow of ions into or out of
the neuron.

Post Synaptic There are different potentials of a neuron which depend on the type of ions
Potentials entering the cell.
EPSP: Excitatory Postsynaptic Potential. Change which occurs in membrane
voltage due to positively charged ions (sodium) entering the cell. Increases
neurons membrane potential and creates depolarization.
IPSP: Inhibitory Postsynaptic Potential. Change in voltage due to negative ions
(calcium and potassium) leaving the cell which creates hyperpolarization. Maes
neuron less likely to generate action potential.
Main difference: EPSP can initiate action potential whereas IPSP lessens the
chance of it.

PSYCHOPHARMACOLOGY

Psychopharmacology The study of drugs that affect the nervous system and behaviour. This studies
both drugs of abuse and therapeutic drugs. A drug is a substance produced
outside of the body that alters the function of cells within the body. They
affect communication between neurons usually by interfering with chemical
transmission across synapses.

Drug Actions Drugs can be agonosit (increasing/stronger postsynaptic effect of

neurotransmitter) or antagonist (decreasing). Each drug is designed to target
a certain transmitter of which there may be over a hundred - each one can be
affected in many different ways.

Agonistic Increases amount of precursor (makes more molecules available through

synthesis) and increases number of neurotransmitter molecules by destroying
enzymes.
Reduces degrading substance which leads to more neurotransmitter and can
increase amount released from terminal buttons.
Can block reuptake or degradation which is sometimes what gives desired
 effect of drug.

Antagonistic Reduces effect of neurotransmitter and the amount in axon.

Blocks synthesis/making of molecules - means less neurotransmitter available.
The drug can be destroyed by degrading enzymes.
Block release from terminal buttons.
Activate auto receptor, inhibiting release of neurotransmitters.

Neurotransmitter Main neurotransmitters for communication between neurons in brain are

Systems glutamate (excitatory) and GABA (inhibitory). Need both excitatory and
inhibitory to provide balance and equilibrium. Other transmitters have
modulating roles.
Alcohol is an indirect antagonist which reduces how likely glutamate is to
bind to receptor. This receptor involved in memory - may explain why
alcohol causes memory blanks.

Direct vs Indirect Direct: common for most drugs - binding site for neurotransmitter for agonist
and antagonist and is competitive binding as the drug takes place of the
neurotransmitter.
Indirect: binding to another site on channels so non competitive binding as
both can bind.

Glutamate and Begins with balance between inhibition and excitation.

Alcohol Small amount of alcohol leads to more inhibition (feeling more free, less
interfering thoughts).
Tolerance adapts so now alcohol is required for equilibrium.
High tolerance develops. Stop having it leads to not enough inhibition, too
much glutamate.
Normalcy has to be regained using drugs for addicts.

GABA and Valium GABA is main inhibitory neurotransmitter in brain.

Valium are indirect agonists for GABA meaning they increase affinity of
GABA for the channel where GABA is found in the nervous system. This
increases chance of binding and more inhibition.
Valium reduces anxiety as more inhibition reverses anxious effects. In high
doses can cause coma and death due to too much neural inhibition.

Dopamine and Dopamine is involved in motor function.

L-DOPA Loss of neurons which release it (from substantia nigra in basal ganglia)
causes tremors and difficulty executing movement (Parkinson’s disease).
L-DOPA is a precursor to dopamine so it increases the levels in the remaining
neurons which reduces symptoms.
More precursors leads to more neurotransmitters.

Parkinson’s Played a role in discovering drugs to treat schizophrenia.

In the 50s, two drugs found to have antischizophrenic effects after 3 weeks of
consumption and at this point also started to produce mild symptoms of
Parkinson’s.
 These results together lead to two findings: Parkinson’s disease is associated
with degeneration of a main dopamine pathway in the brain and dopamine
agonists produce a transient condition that resembles schizophrenia.
This suggests schizophrenia is caused by excessive activity at dopamine
synapses, hence dopamine antagonists would be effective in its treatment.

Dopamine and Dopamine: the neurotransmitter used in reward pathway.

Cocaine Cocaine: dopamine reuptake blocker.
Therefore there is an accumulation of dopamine in synapses of the reward
pathway which leads to overstimulation.

Addiction Human body acts to maintain state of equilibrium which can be disrupted by
drugs, leading to reaction to counteract these effects. This leads to dependence
on the drug to maintain equilibrium.
Repeated drug use leads to intolerance which then requires larger and larger
doses of the drug to produce same effect.
Main factor of addiction is not avoiding withdrawal but rather desire to
continue euphoria/reward feeling.

Addiction - Recovery Two factors to recovery:

1. Neural recovery - recovering from damage (e.g to brain cells). For
example, long term meth use leads to damage such as transmitter
changes, rewiring of brain’s reward system, brain cell death (in parts
of brain associated with self control such as frontal lobe and
hippocampus). This kind of damage leads to psychiatric symptoms
such as psychosis and dementia.
2. Behaviour recovery - for example effects on mental health.
Ability to recover from damage depends on length of drug use, regularity of
use and quantity.
Recovery from cell death not always possible.
Cases have shown within six to twelve months of recovery, there is
restoration of neurotransmitter activity, improvement in depression and
anxiety, improvement in focus and attention and reduction in emotional
rages.
Drug cravings may also not improve.

Steroids Anabolic steroids: synthetic derivative of testosterone. Abuse can lead to

hormonal imbalances and conditions such as infertility, liver damage and
depression.
Work differently than other drugs, do not have same short term effect on
brain. Most important difference is they do not trigger rapid dopamine release
(which causes usual ‘high’ from drugs). Long term abuse can still act on some
pathways and chemicals such as dopamine and serotonin. Can result in
significant effect on mood and behaviour.
They affect areas of CNS controlling mood, sexuality and aggression. 20-30%
of people abusing steroids show signs of psychiatric illness such as depression
and hallucinations. 30% exhibit aggressive behaviours and irritability.
 Cases have shown the hormones are responsible for impaired impulse control
which leads to previously stable people becoming violent.
Withdrawal from steroids includes mood swings, sleep problems, decreased
sex drive and depression.
Cerebrospinal fluid drawn out of the spine has shown to have altered levels of
monoamine metabolites, neurohormones and neuropeptides which are
involved in reward system. Changes in this fluid correlated to psychiatric
symptom scores.

Modafinil Drug licensed to treat narcolepsy but used as a ‘smart drug’ that can help
brain performance, popular among university students.
Suggestions of how it works include stimulating the brain to release a
hormone called histamine which makes us more wakeful or may affect brain
similarly to amphetamines and cocaine by increasing dopamine.
A study on modafinil gave 64 healthy volunteers modafinil or placebo and
asked them to complete language test. Showed it had slowed responses and
were no more accurate.
Common side effects of the drug include nausea, nervousness, anxiety and
insomnia.

Histamine Neurons which synthesize histamine are present in the tuberomammillary

nucleus (part of the hypothalamus in brain). These neurons innervate (supply
with nerves) the cortex, pituitary, thalamic nuclei, amygdala, hippocampus,
spinal cord and cerebellum.

Novichok Class of nerve agents that are acetylcholinesterase inhibitors (primary effect is
to block normal breakdown of the neurotransmitter acetylcholine).
Nerve agents shortcircuit parts of nervous system leading to constant
stimulation of muscles and uncontrolled brain activity. Can cause difficulties
breathing as it paralyses the muscles needed to breathe.
Ach is one of the most important transmitters in autonomic and somatic
nervous systems. This means it affects the function of these systems which are
required for autonomic nervous functions.
The inhibition of the breakdown of Ach leads to higher concentration in
synapses. Leads to symptoms which are seen in Novichok poisoning. Result is
involuntary contraction of all muscles which may lead to cardiac arrest.

VISION

Light Light is electromagnetic radiation which is all kinds of rays however only
sunlight waves are visible. Ripples in an electric field. Travels at 300000000
m/s. Waves have different frequencies and frequency of visible light ranges
from 430 trillian Hz to 750 trillion Hz. It reflects off the object and the
reflection gives us information about location, shape and colour. This process
depends on the eyes to receive the information and the brain the process it.
Light is on a spectrum and this is what determines its colour. The black
 section is the visible light and is only a tiny proportion of the spectrum.
Higher frequency waves have shorter length and lower frequency have bigger
length.

The Eye Parts of the eye:

Cornea: membrane which covers surface of the eye and makes sure objects
don’t penetrate, function: refract light which comes into eye.
Lens: changes thickness, function: focus light.
Fovea: in control of most acute vision.
Blind spot: beginning of optic nerve, no vision.
Optic nerve: no vision.
Iris: gives eye colour.
Pupil: changes shape, function: let different amounts of light in.

Light coming from a light source is focused onto the retina by the cornea and
lens and the retina (located at back of eyeball) is adapted by ciliary muscles
which allow it to be more/less rounded. It is curved which causes the upside
down image. Looking at a distant object does not require as much refraction
of light whereas a closer object gives more divergent light rays hence lens has
to refract light more - this happens by the ciliary muscles tightening which
allows lens to be more rounded.

Eyes continuously scan visual scene with small and quick movements called
saccades and these snapchats are integrated by the brain. Saccades move in the
line of light/right direction and antisaccades move away from light source. In
schizophrenic patients, antisaccades are higher implying less control of
movement.

Transduction All sensory organs perform this process including the eye.
It is converting light information into electrical information. The signals which
light waves carry are converted into electrical impulses in neurons which
means they are translated to the language of the brain for communication.

Rods and Cones Visual sensory cells found around the retina - 100 million rods and 7 million
cones per retina.
Rods: nighttime vision, high sensitivity to light, more convergence than cones
which increases sensitivity but reduces acuity.
Cones: daytime vision. High acuity which is good for seeing details, found at
fovea.
They react/communicate to different types of cells and this is how message is
passed down optic nerve.
They contain photosensitive pigments and when light strikes them, a chemical
reaction occurs which generates electrical signals which are carried to the
brain by optic nerve. This happens during transduction.
There are three types of cones, each has different colour sensitive pigments
(red, green and blue). Amount of activation of these pigments depends on
type of colour being perceived. Perception of colour depends on relative
 activities in cones. Colour blindness is a deficit in red and green cones.

Ganglion Cells Optic nerve fibres which combine electrical outputs of rods and cones. Each
ganglion cell leads into a bipolar cell which either has a layer of rods or cones
leading into it.. The rod cells are in groups so convergence is high. Only one
cone cell so low convergence.
These ganglion cells combine the output of rods and cones and form receptive
fields. Some fields look at centre of image and some at surroundings. Each cell
responds to a different section of the image and the combination of lots of
cells responding to sections builds up the whole image.
These cells are sensitive to edges and the detection of edges influences build
up of whole image. They search for edges to create the image even thought
edges may not be present, such as blocks of colour together.

Neural Pathway Optic nerve carries information to thalamus which projects to the primary
visual cortex. Different neurons carry information about different played in
the image. These signals get to primary brain areas where the outer layer
receives input for sense so vision messages get sent straight to primary visual
cortex.
In this cortex, outputs from neurons in the eye are combines to produce
neurons that respond best to edges and bars. Analysis of edges and
orientations happens in this cortex.

Perception of Depth Position of the eyes required to focus the image onto fovea gives the brain a
cue about depth. If an object is further away the depth perception is not as
good. This is known as convergence.
The eyes get slightly different views of the world which provides another cue
to depth and one eye is usually dominant. Known as stereopsis.

Cortical Mechanisms The flow of visual information starts at primary visual cortex, into secondary
visual cortex and then to visual association cortex. A this flow happens,
receptive fields of neurons become larger and respond to more complex
stimuli.
There are two streams for this information. Dorsal stream specialises in spatial
perception and ventral stream specialises in pattern recognition.

Prosopagnosia A selective visual agnosia - inability to interpret sensations. Characterized by

the inability to recognize the identity of faces including family members and
friends. May cope by using strategies like hairstyle or voice recognition.
Other cognitive abilities - such as recognising objects - remains the same.
There are acquired forms (happen from brain damage) and developmental
forms (can be born without ever acquiring these functions of recognition).
The core face network consists of the fusiform face area, occipital face area
and posterior temporal sulcus. Functional abnormalities in FFA or
abnormalities in extended face area may cause it. Degree of altered white
matter also shows to contribute.

Hemispatial Neglect Majority of right hemisphere stroke survivors suffer acute neglect/loss of
 awareness of left (Buxbaum et al, 2004). This means the left side of the body
still has motor sensation and function but cannot be perceived or used.
Endogenous plasticity - ability to adapt due to learning - drives recovery of
this during first 3 months after stroke however recovery halts in the chronic
stage (after 3 months) (Ramsey et al, 2016).
In vision, this can lead to only drawing one half of an object from memory,
such as a clock, in studies. Also leads to walking into objects on left side and
may only apply makeup or shave on half of face. Could suggest even though
vision is still there on left side, cannot process the information normally.

Recovery: Patients wear glasses containing prisms which bend light as this
makes objects appear to be on the right. This results in mismatch between
where they see object and where they must move hand to touch it. With
training, patients learn to adapt to the prism by shifting their hand-eye
coordination leftwards. However, benefit only lasts 24 hours after training.
Results of this training (O’Shea et al, 2016) showed disinhibition of left
motor cortex during prism adaptation can enhance consolidation of after
effects (lasts longer).

Cross Modal Adaptive reorganization of neurons to integrate function of two or more

Plasticity sensory systems. It is a type of neuroplasticity and occurs after sensory
deprivation due to disease or brain damage.
There are two categories for this:
1. Cross modal recruitment: primary sensory cortex of the deprived
sense such as vision, is recruited by the remaining senses
2. Compensatory plasticity: primary sensory cortices of the working
senses reorganize to allow for better processing despite deprived
sense.
This links to how primary sensory cortices do not work in isolation but are
influenced by other senses.
Usually, visual cortex processes visual stimuli and responds to visual training,
as with tactile cortex and so on. When this doesn’t happen it is the result of
large-scale reorganization which s induced by sensory loss or injury.

In a study on this, participants taught to read braille for 9 months and brain
scans taken before and after training. Activation to tactile braille reading
relative to the tactile control condition peaked within the visual word form
area and activation was specific to tactile condition. To test the role of VWFA
in braille reading, rTMS (repetitive transcranial magnetic stimulation,
inducing currents in neuron networks) was applied to it alongside two control
sites whilst subjects performed lexical decision task. This caused accuracy to
decrease during comprehension but only when applied to VWFA not the
control sites, showing VWFA is necessary for reading tactile braille words.

Paul Bach-y-Rita, Developed a vibro-chair in which patients who were blind from birth could
1969 distinguish between straight and curved lines and identify basic objects (coffee
mug, telephone). Used the skin’s spatial resolution (smallest feature it can
 detect) and how it varies widely. On the back of the patient, stimuli had to be
quite far apart. Hand would’ve given good results however would have caused
movement ease issues. Instead used the tongue as the moisture makes it a
good transmitter of electrical energy and is as sensitive to discrimination
between the objects as a fingertip.
Works as the tongue is very sensitive so the user feels the image rather than
sees it which leads to the brain learning to see the object detected on the
tongue.

BrainPort V100 Used touch as a substitute for sight and is a more recent variation of Rita’s
work. General idea comes from Rita’s original work.

Polymodal Brain The idea we have a polymodal brain comes from the way the primary visual
cortex can be activated by other sensory inputs after loss of primary inputs.
Shown in rats as removing the eye reduces activity in this cortex but activity
gradually increases to normal levels as a result of whisker stimuli.
Could possibly mean the synaptic plasticity in this cortex may allow
strengthening of inputs by carrying other sensory information to the cortex to
reactivate it.

HEARING

Sound Produced by vibrating objects and composed of pressure vibrations in some

medium (solid, liquid or gas).
Travels relatively slowly: 330 m/s in the air.
Waves have different frequencies and frequency of audible sound in humans is
20 to 20000 Hz.

The higher the frequency of vibration, the higher the frequency of sound
waves. Complex sounds are composed of multiple types of waves such as sine
waves and can be produced by adding together sinusoidal sound waves.
Amplitude and frequency of these components determines spectrum of the
sound.
Amplitude corresponds to loudness, frequency to pitch and complexity to
timbre.

The Auditory System Peripheral auditory system: parts of hearing system which are outside the
brainstem and auditory cortex - outer ear, middle ear, inner ear and auditory
nerve which carries information into the brain.

Sound waves enter ear canal and cause eardrum to vibrate. Vibrations carried
by the three tiny bones in middle ear (malleus, incus and stapes) to the
cochlea. In the cochlea (thin fluid filled tube curled into a spiral) , acoustic
vibrations are transduced into electrical neural impulses by the hair cells. Hair
cells are organized along the membrane in one row of inner (3500) and three
rows of outer (12000). Transduction is where the inner hair cells depolarise
 and release neurotransmitter but this only occurs when stereocilia are bent in
one direction - phase locking.

The cochlea has a membrane which runs its length known as the basilar
membrane. Each place on this membrane is tuned to a particular frequency of
sound and hence separates out the different frequency components of a
complex sound. Auditory nerve fibres connect to each place on the membrane
and different fibres are sensitive to different frequencies which determines
where the activity is produced. Known as place coding and continues up to
the auditory cortex. In auditory nerve, frequency components are represented
by place of activity (higher frequency sounds excite neurons close to base of
cochlea) and timing of activity (higher frequency produced higher rate of
synchronised firing). This information is then used by the brain to identify
sounds and separate out ones that occur together.

Auditory Cortex In the temporal lobe and its core region includes primary cortex and belt
region surrounds the core region. Secondary cortex which is outside the belt
region is referred to as parabelt areas.

Hearing Loss Hearing can be measured by an audiogram which involves being played tones
at different frequencies and patient responds until they can no longer hear it.
Maximum we can hear is 20000 Hz but test typically stays under 8000.
Hearing loss can be mild, moderate or severe or profound.
Mild: hearing level in decibels between 20 and 30
Moderate: 50 and 60
Profound: 90 and 100.
The range of hearing loss shows how it can occur for different reasons such
as infection. Age related hearing loss shows losses at high frequencies and this
is permanent.

Hearing loss was studied using an audiometry which was undertaken before
and within half an hour following a heavy metal concert. Unprotected ears
showed a temporary threshold shift and there was some evidence that early
noise damage has occured meaning hearing needs to be protected from loud
noise.

Hearing loss an have an effect on speech perception but the effect is not clear
cut as hearing impairment varies greatly and speech perception involves a
combination of sensory and cognitive processes. This means there are multiple
factors which can affect it - even sensory aspects of speech perception not the
result of auditory processing alone. Hearing loss impacts ability to distinguish
sounds at normal levels, some sounds become harder to hear than others. In
speech, frequency and intensity varies depending on speech sound meaning
that hearing loss of the higher frequencies leads to missing the speech sounds
in this area. Example: in ‘spoon’ the ‘sp’ is high frequency so would only hear
‘oon’. The brain can fill in the blanks when this happens such as knowing
which names are likely to be mentioned in a conversation helps process them.
 Sensory substitution can be used for hearing loss. Individual wears vibrating
vest under clothes and sound through a microphone is converted into
vibration patterns on the vest. Individual learns to read vibrational mapping of
sound.

Extra Hearing Auditory verbal hallucinations (AVH): sensory experience of hearing a voice
in the absence of a corresponding external source. Patients often report the
experience of someone speaking to them often with negative comments and
the voice is typically emotionally negative. Differs from non-clinical
individuals hearing voices who more often report positively.

AVH are one of the key symptoms of schizophrenia and psychosis. They can
severely handicap patients if they engage in recurrent conversation with the
voices. Contributes to impaired reality orientation. CBT treatment aims to
stop obsession over internal voice and encourages attention to be turned to
outside world. Can also be symptoms of bipolar, PTSD, OCD, drug abuse etc.
Also symptoms of neurological diseases such as Parkinson’s and dementia.

AVH implicate speech perception areas in left temporal lobe which impairs
perception and attention to external sounds. Brain responds to actual sounds
in similar way to inner voices. It’s possible the amygdala is implicated in
assigning emotion to these voices and that frontal language areas are involved.
No difference in clinical and non clinical subjects can be seen in neurobiology
or involvement of brain areas.

Most prominent theory on AVH proposes they occur due to a failure to

recognize self-generated inner speech and left hemisphere language
production and perception areas play a crucial role in causing them. Subjects
may not realise these voices are their own inner voice. During AVH,
activation of left frontal and temporal regions observed.

Receptive Aphasia Carl Wernicke, 1874. Described patient who lost ability to comprehend
speech after stroke and produced meaningless speech but actual ability to
produce it was unimpaired. Area which causes this located in posterior
superior temporal gyrus. Lesion in this area leads to difficulty in
comprehending and interpreting speech e.g trouble interpreting meaning of
questions. This form is known as “Wernicke’s aphasia”.

Expressive Aphasia Paul Broca, 1861. Described patient who lost ability to speak after a stroke
and was limited to articulating one specific syllable but could comprehend
speech fine. Area which causes this located in inferior frontal gyrus. Problem
in production but not in comprehension or muscle motor control.
Understanding question but not able to speech to answer it. Known as
‘Broca’s aphasia’.

Lesion Studies Issues: no single connection between lesion location and size and type of
symptoms so not possible to predict site and size of lesion from symptoms.
 No single connection between receptive and expressive types as there is
usually a problem in language production and nearly all have anomia.
Diagnosis not always straightforward .
Patient groups not homogenous (the same) so have to look at patients case by
case.
Unlikely the rest of the brain would function normally after the accident
anyway so not representative for neurotypical functioning.

However, studies still used. Casual links can be assumed such as removal of
cortical area causing loss of a behavior then this area presumed to be
responsible for behaviour.

Types of lesion studies include: behavioural/neuropsychology, neuroanatomy

(such as MRI), function MRI/EEG,MEG,PET and TMS.

Measuring Ability to Speech processing is one measurement of hearing as it is a stream of acoustic

Hear elements consisting of rich spectral and temporal information, and the ability
to decode these elements involves multiple stages of neural processing. Models
of speech processing focus on cerebral cortex (Hickok & Poeppel, 2007).
Before it is perceived, relevant acoustic cues must be delivered to the auditory
cortex, hence showing hearing.

Also measure auditory brainstem function used an EEG and is measured by

the transmission of electric or magnetic fields from an electric primary
current source through biological tissue towards measurement sensors.
Auditory brainstem responses can be recorded and played back to see what
the brain heard.

Long term experience with music shows enhancement in processing in

brainstem and cortical regions. Musicians have enhanced processing of native
speech sounds and emotionally salient vocal sounds.

Bilingual speakers’ processing at the brainstem is less affected by background

noise. Also demonstrate enhanced attentional control and more consistent
brainstem responses (Krizman et al, 2014).

MOVEMENT

Movement Signals for movement move through multiple levels before causing a change in
muscle function and have to flow in certain direction.
Start in association cortex, into frontal brain areas then to secondary motor
cortex and finally to primary motor cortex from where signals leave and go
into spinal cord.

Pathway of Posterior parietal association cortex (PPAC) receives integrated (body part
Information location and external objects) visual, auditory and somatosensory information
 which it outputs to motor cortex and dorsolateral prefrontal cortex.
Dorsolateral prefrontal association cortex is where the needed response is
decided and outputs the information to the secondary motor cortex which
outputs to primary motor cortex and frontal eye field. This frontal eye field is
responsible for saccadic eye movements. Primary motor cortex is main point of
convergence of sensorimotor signals and is where they depart before reaching
body parts.
The primary motor cortex controls complex actions such as eating. Each region
in this cortex controls a specific body part and the area of each depends on
complexity of movements (more parts used for complex actions). For example,
fingers must be very precise in movements so more cortex is dedicated to
fingers compared to parts such as the hip.

Mirror Neurons These neurons do not just react to start movement but also when observing it.
Shown through monkeys as neurons in ventral premotor area and parietal
cortex responded when performing and observing an action. Has also been
shown through fMRI in humans.
Could possible be how we understand movement of others, helping to imitate
these actions.

Motor Pathways Signals sent from the primary motor cortex travel down pathways until they
reach the medullary pyramid and reach spinal cord. There are two types:
1. Dorsolateral tracts: corticospinal (contralateral so left controls right etc
and is in control of wrists, hands, fingers and toes) and
corticorubrospinal (contralateral and controls muscles in face, distal
muscles of arms and legs).
2. Ventromedial tracts: corticospinal (ipsilateral so right controls right etc
and controls trunk and proximal limb muscles) and
cortico-brainstem-spinal (interacts with brainstem structures and
controls trunk and proximal limb muscles). Proximal limb muscles are
those close to the midline such as in the abdomen.

Spinal Circuits Complex motor circuits which can do some functions independently without
the brain such s reflexes and allow us to generate movement with it.

Monosynaptic Movement that happens without brains involvement where muscle spindle
Stretch Reflex fibres stretch in response. Sends signals through dorsal root ganglion where
they synapse with alpha motor neurons in spinal cord. Signals then go back to
muscle to create reflex. For example, instinctively reaching out to catch a falling
object.

Cerebellum and Interact and communicate with different levels of sensorimotor hierarchy. They
Basal Ganglia coordinate and modulate movement.
The cerebellum receives information from primary motor cortex and from
motor tracts via brainstem motor areas. Helps to correct and coordinate
movements and is involved in controlling rapid sequences of movements.
‘Feedback’ which it obtains allows correctment of movement such as walking
 around and stumbling - feedback is change in balance which it will then
communicate to hierarchy to return to normal circumstance.
The basal ganglia is a set of subcortical structures involved in movement of
muscles and body which receives signals and cortical input. Projects signals
back to the cortex. Involved in modulation of movement.

Parkinson’s Disease Characterised by damage to dopamine receptors and dopaminergic neurons.

His reduced input to motor cortex leading to slowness of movement, difficulties
initiating habitual movements and a tremor at rest. This slowness is caused by
less information being fed back to the cortex.
Deep brain stimulation is used to treat symptoms - not a cure but helps control
problems. Works best to lessen motor symptoms such as slowness and tremor.
Process where electrodes are implanted into brain (into subthalamic nucleus or
globus pallidus) and connected to extensions which are put under the skin
behind the ear and down neck. Extensions connected to pulse generator which
is places around chest or stomach and this resets the rhythm and changes
electrical signals in the brain such as changing neuron firing rate which
prevents the symptoms.

Learning Learning a new skill requires lots of activity in: cerebellum, posterior parietal
motor, primary, secondary and dorsolateral prefrontal association cortices. Also
highly involves sensorimotor hierarchy. As movement are practised, this
involvement from association areas and cerebellum reduces but still active.
Eventually lots of activity in primary and somatosensory cortex and reduced in
premotor. Eventually no activity in dorsolateral prefrontal. Movements
eventually become automatic. Deliberate conscious control becomes
unconscious smooth sequences adjusted by sensory feedback.

Paralysis Paralysis occurs during a stroke or transient ischaemic attack (TIA): sudden
weakness on one side of the face with arm weakness. TIA occurs from small
blood clot and has many symptoms of stroke.
Bell’s palsy: sudden weakness on one side of the face with ear or face pain.
Sleep paralysis: temporary paralysis when waking up or falling asleep.
Multiple sclerosis: weakness in face, arms or legs that comes and goes.

Paralysis is common following a stroke.

Hemiparesis: weakness on one side of the body and causes issue with everyday
tasks. Can be treated by brain stimulation therapy:
Transcranial magnetic stimulation (TMS): applies magnetic fields to the head
via a coil. Leads to change in neuron potential and electron communication,
can modulate neural activity. Can have beneficial or disruptive effect. Shown to
improve clinical outcome in early stroke patients after 10 consecutive days of
the therapy - found comparing treatment patients to placebo patients.

Spinal cord injury can cause paralysis. A case study (2018) showed a patient
injured spinal cord and was diagnosed with complete loss of function below the
injury. Participated in 22 weeks of physical therapy and then had electrode
 implanted in epidural space just below injured area. When stimulator turned on
implant, man was able to move with a walker. Made 113 visits to rehabilitation
in over a year and managed to walk 102 metres in total, 331 steps and 16
minutes of walking time. Shows networks of neurons below an injury can still
function after paralysis (Kendall Lee, 2018).

Epidural Electrical Stimulation (EES) works by implanting a device that

delivers electrical signals into the spinal cord. Injury interrupts the connection
between spinal cord and brain and prevents signals reaching below the site of
injury so EES can help bridge this gap by providing electric signals to spinal
cord below injury. Researchers looked at motor neuron maps of healthy people
to see where electrodes go to stimulate certain areas and replicated this in
paralysed people. Fed information about maps into a computer which created
maps for paralysed people.

Prosthetic Limbs Designed with usability and function as a central purpose. Body powered
prosthetic limbs are controlled by cables connecting them to elsewhere on the
body such as an arm being controlled with a strap to the opposite shoulder.
More advanced way is using muscle signals from remaining muscles. Works
because muscles generate small electrical signals when they contract so
electroduced placed on the surface of the skin can measure muscle movements.
The electrical contractions are detected by the electrodes and then used to
control the prosthetic limb. Known as myoelectric.
It is possible this mechanism means we could control another person’s
movement which was studied by Greg Gage and colleagues.

SLEEPING & DREAMING

Sleep Sleep appears to have a significant biological function supported by how
much time we spend sleeping. For most people this is over 175000 hours in
lifetime.
Can be measure in multiple ways: through an electroencephalogram (EEG),
electrooculogram (EOG) or electromyogram (EMG).
Has multiple stages.

Measures EEG measure electrical activity of neurons and shows majority of time high
voltage and slow waves with periods of low voltage and fast waves within.
Low voltage period is when REM sleep occurs. Major changes occur in EEG
overnight.
EOG measures eye movements during REM sleep.
EMG measure activity of neck muscles.

Stages Before sleep: ‘alert wakefulness’. Alpha waves occur in bursts of 8 to 12 Hz

(shown on EEG). Eyes closed in preparation to sleep.

Stage 1: Sudden transition from wakefulness with similar EEG to being

awake, but waves are slower. Low voltage and high frequency waves.
 Stage 2: Gradual increase in voltage, decrease in frequency when progressing
into this stage. Characterised by ‘K complexes’ (one large negative wave
followed by large positive wave) and ‘sleep spindles’ (bursts of 12-14 Hz
waves) waveforms. Alternates between the two types.

Stage 3 and 4: known as slow wave sleep. Mostly delta waves which are
largest and slowest EEG waves. Progresses back through the other stages
ager this but now with addition of REM.

Cycle Stage 1 begins as person falls asleep, firstly stage one is NREM, progresses
through stages to 3 then back to 1. Following stages of 1 are different this
time and have addition of REM.
Each cycle around 90 minutes long.
More time in stage 1 as time progresses and less time in stage 3.

REM REM (rapid eye movement) sleep involves core-muscle tone loss and high
frequency EEGs alongside cerebral activity such as oxygen consumption and
neural firing is at waking levels. The waves are rapid compared to slow wave
sleep. Eye movements are rapid compared to slow/absent eye movements in
slow wave. Dreams occur in this stage.
Cortical activity is low during REM sleep in prefrontal and striate cortex and
high in extrastriate cortex. Low activity in prefrontal reflects lack of
organization and planning that occur in dreams as prefrontal cortex involved
in planning. High activity in extrastriate reflects visual hallucinations and
dreaming. Low activity in striate is due to lack of visual input.
Purpose of REM: some argue it is to process explicit memories but argued
against by the way antidepressant drugs which block REM do not affect
memory. May be to prepare for wakefulness and is one of two states in
NREM (wakefulness/REM) as REM difficult to stay in. Evidence for this
idea is in the fact REM blocking drugs cause periods of wakefulness (cannot
stay in NREM).

Neural Control Wakefulness depends on function of reticular formation. Shown when a cat
brain was severed between superior and inferior colliculi as there was
constant slow-wave sleep. Also showed normal sleep-wake cycle when
severed caudal to colliculi.
Lesions at mid collicular level which damaged the core of reticular formation
produced cortical EEG which indicated slow wave sleep. Electrical
stimulation of pontine reticular formation awakened sleeping cats.
Overall suggests wakefulness producing area is in reticular formation.

Noradrenaline and Hormone released by medulla as a neurotransmitter. Project throughout the

Sleep brain originating from locus coeruleus. Activity in these noradrenergic
neurons produces an increase in attentiveness.
Noradrenaline levels shown to be highest in waking stage when the neurons
are activated and lowest in REM sleep. The function of noradrenaline is to
 mobilize the brain and body for action, hence why it’s highest when waking.

Acetylcholine Neurons which release this hormone as a neurotransmitter are involved in

cortical arousal, REM sleep and learning/memory. The release of this is
highest in REM sleep and it is associated with cortical arousal which is an
increase in wave frequency. Therefore it explains why it is at highest level in
REM as REM is characterised by higher frequency waves.
When acetylcholine is released from nerve cells as a transmitter, it is known
as cholinergic activity. This activity is low in NREM sleep and highest in
waking stage in the cortex and in REM sleep in the hippocampus.

Function of Sleep Sleep functions are theorised in two main ways:

1. Recuperation theories: idea that wakefulness interrupts homeostasis
and sleep is needed to restore it, common theories include function
is to restore energy and to clear toxins.
Evidence against: no clear relation between species’ sleep time and activity
level.
Evidence for: all mammals and birds sleep so must have important function
and different animals sleep for different periods of time as all have different
requirements.
2. Adaptation theories: idea that sleep has evolved to protect us from
dangers of night and to conserve energy. Supported by how humans
have internal 24-hour timing system that programs us to sleep at
night. We are programmed to sleep but may not necessarily require
it.
Evidence against: all mammals and birds sleep - not all evolved same way.
Evidence for: different species vary in amount of sleep (could depend on
how they evolve) and some animals more vulnerable to predation sleep less
(evolved to sleep depending on risks).

Sleep Deprivation Effects of stressors which cause lack of sleep and effects of sleep loss hard to
differentiate between. Means even if the sleep was not lost these effects could
still be present.
By recuperation theories: sleep deprivation will cause long periods of
wakefulness resulting in disturbances which get worse as deprivation
continues and missed sleep will eventually be regained. Predicts little effect
on logical and critical thinking but large effects on executive function.
Just 4 hours of sleep can eliminate effects of 64 hours of sleep loss.
REM deprivation: as deprivation increases, proceed into REM quicker and
more time spent in REM after deprivation period ends which suggests it
serves a special function.

Dreaming 80% of REM awakenings have reports of story like dreams suggesting this is
when dreaming occurs.
External stimuli may be incorporated in them and they run in real time.
Sleep talking/walking less likely during dreaming.
Freud argued dreams are triggered by unacceptable repressed wishes and that
 they contain manifest content (what you remember experiencing in the
dream) and latent content (the underlying meaning). However there is no
evidence to support this and in fact many dreams contain unpleasant
experiences.

LEARNING

Memory There are two types of memory: short and long term. The main distinction is
between declarative long term and non declarative.
Declarative: can be consciously recalled, store of facts and events etc,
separated into two main forms episodic and semantic.
Episodic: related to personal experiences or specific events at specific time.
Semantic: general knowledge about the word, concepts, language etc.
Non declarative: unconscious, sensory and motor skills, classical conditioning,
operant conditioning and priming.

Classical Pavlov (1903) measured the salivation of a dog, an unconditioned response,

Conditioning when food was placed in its mouth, an unconditioned stimulus. Then linked
the delivery of food with sound of a bell. After 5/6 pairings, dog would
salivate, which was now a conditioned response, in response to the bell alone,
where the bell was the conditioned stimulus. Shows dog had learned an
association. This is an example of classical conditioning.
Classical conditioning occurs due to a strengthening of the synapse in the
neuron by conditioned stimulus and unconditioned stimulus pairing.
Cravings and drug dependency are a result of this, such as the link between
the sight of a cigarette (conditioned stimulus) and the craving in a smoker
(conditioned response).

Emotional Learning Classical conditioning can be generalised to complex situations.

This includes hearing a particular piece of music during an event that
produces an emotional response (e.g a funeral) and then feeling the same
way whenever the music is played. Conditioned emotional responses happen
in the hypothalamus, midbrain, pons and medulla.

Operant Conditioning In operant conditioning, animal learns to repeat a behaviour which produces
reinforcement in response to the stimulus. An example is a rat quickly
learning to press a level to receive food (Skinner). Reinforcement can be
positive (rewarding) or negative (avoiding aversive stimulus such as a shock
when a behaviour is performed). Negative reinforcement may lead to
learning to not perform a certain behaviour.

Dopamine and Several brain areas act as a reward when stimulated electrically and the
Reinforcement receive dopaminergic input from the central tegmental area. This system is
called the mesolimbic dopamine system. Dopamine is released during
reinforcement which means it is involved in operant conditioning.
Addictive drugs are rewarding as they activate the brain’s reward circuits, in
 particular the dopaminergic pathway (directly affected by cocaine).
Reinforced the pathway from stimulus to response causing behaviour to be
repeated.

Classical vs Operant The main difference is the point where stimulus is linked to response. In
classical, the stimulus and association occur together which produced the
response. In operant, the stimulus leads to the response which then produced
the reward. In classical, the response is a result of the association whereas in
operant the response gains the reward.

Synaptic Plasticity Learning in the brain occurs due to modification of transmission across
synapses.
The Hebb Rule was introduced by Donald Hebb, 1949. It states if the
postsynaptic membrane is active at the same time as the presynaptic
membrane then the synapse will be strengthened. This is called long-term
potentiation and is the basis of learning and memory.
In classical conditioning, the synapse is only strengthened when both the
stimulus and the association are present.

Glutamate Receptor If a molecule of glutamate binds with the NMDA receptor, calcium channel
cannot open because magnesium ion blocks the channel. This leads to
depolarization of the membrane which evicts the magnesium ion and
unblocks the channel. Now glutamate is able to open the ion channel and
calcium ions can enter. This process has to happen to enable NMDA receptor
to be activated by binding with glutamate as inhibitory magnesium ions stop
this happening. This happens before classical conditioning.

Hippocampus in Short term memory involves persistent electrical activity in neurons rather
Memory than changes to synapses. Electrical stimulation of the parietal cortex can
erase visual short term memory in humans and information may then get
encoded into long term memory -which happens due to changes in synapses.
The hippocampus is involved in this transfer from short to long term
memory. It receives information from sensory and motor association cortex
and also send information to it. Does this for subcortical structures such as
basal ganglia too. Damage to the hippocampus impairs ability to consolidate
declarative memories.

Anterograde Amnesia A case study of a patient with anterograde amnesia showed he was unable to
form new LT declarative memories after an epilepsy surgery which involved
removal of medial temporal lobes, showing how they are involved in LTM..
However, he could remember events leading up to the surgery and ST
memory was unimpaired. Could still form classical conditioning associations.
Could not remember where he lived or who cared for him, did not recognise
old photograph of himself. Found it difficult to form coherent plans through
sentences - language issues.
This research helped understanding of long term memory as it indicated
there is more than one type and revealed important distinction between long
 and short term memory as one was still intact whereas other was impaired.

Alzheimer’s Disease First lesions appear in poorly myelinated neurons in areas related to memory
and learning such as hippocampus. Low myelination increases overall energy
expenditure of neurons. Left hippocampal grey matter volume significantly
links with performance in memory tasks. AD causes this volume to decrease.
Decline happens slowly but up to ten times more of the volume of brain
vanishes compared to healthy people per year.
Memory loss is one of first reported symptoms of disease. STM and LTM
declarative affected early (cannot remember dates/names etc). At later stages,
non declarative can also be affected, such as everyday tasks like getting
dressed.

Stress and Memory Acute stress has been shown to impair working memory performance. This is
because working memory is maintained by neural activity in the dorsolateral
prefrontal cortex (DLPFC) which is disrupted by stress-induced release of
neurotransmitters:
Noradrenergic neurons originate from the locus coeruleus and terminate
throughout cortex. Optimal performance in the DLPFC is associated with
noradrenaline levels that bind adrenoceptors. Elevated levels (caused by
stress) of noradrenaline can suppress DLPFC neural spiking, hence impairing
working memory.