Psyc

Front 1

WHAT IS COGNTIIVE NEUROSCIENCE?

Back 1

study of the neural (brain)basis of behaviour and thought

Concerned with what happens in the brain when weperform cognitive functions

Front 2

FACTS ABOUT NEURONS?

Back 2

· Neurons connected to each otherby synapses

Each Neuron connected tothousands of other neurons

Allows for incredibly largenumber of possible circuits in brain

Front 3

GREY MATTER?

Back 3

cortex (outer layer) of brain

Neuron cell bodies found here

Front 4

WHITE MATTER?

Back 4

No (lol)

inner layer of brain undercortex

all “wiring” found here

contains axons of all neurons here, connecting to spinal cord andother areas of cortex

Front 5

WHAT ARE THE TWO PARTS OF THE NERVOUS SYSTEM?

Back 5

Central Nervous System – brain andspinal chord

Peripheral nervous system – nervesthroughout body

Front 6

WHAT ARE NERVES?

Back 6

extendedbundle of axons of the neurons

Front 7

WHAT IS THE SOMATIC NERVOUS SYSTEM?

Back 7

voluntary,motor, sensory

Front 8

WHAT IS THE AUTONOMIC NERVOUS SYSTEM?

Back 8

involuntary

Front 9

SYMPATHETIC?

Back 9

increase HR, increase respiration,sweating, stress, arousal, “fight-or-flight”

Front 10

PARASYMPATHETIC?

Back 10

“opposes” sympathetic nervoussystem

“rest & digest’, lower HR, lower respiration, digest

Front 11

3 MAJOR PARTS OF THE BRAIN?

Back 11

1. Cerebrum // forebrain// cerebral hemispheres

2. Cerebellum // hind brain

3. Brainstem

Front 12

CEREBRUM?

Back 12

o Consists of two hemispheres§

Divided by longitudinal fissure

Front 13

CORPUS CALLOSUM?

Back 13

connects hemispheres

Front 14

CORTEX?

Back 14

outer layer

– white matter

–neuron cell bodies found here

Highly folded to maximise surface area

Front 15

FRONTAL LOBE?

Back 15

· Anterior to central sulcus

Executive functions: reasoning, working memory, etc

Emotion

Motor functions

Premotor cortex (planning)

Primary motor cortex(execution)· Speech (broca’s area)

Front 16

PARIETAL LOBE?

Back 16

· Posterior to central sulcus

Primary (somato)sensory cortex

Touch, pain

Spatial attention

Linking vision to action

Front 17

OCCIPITAL LOBE?

Back 17

Posterior part of brain, underparietal lobe Important for vision

Primary visual cortex (allvisual perception) Higher visual areas (processshape, colour motion, etc)

Damage to certain areas causes prosopagnosia– inability to recognise faces

Front 18

TEMPORAL LOBE?

Back 18

· Area under all lobes

Auditory cortex – soundperception Limbic system amygdala

– fear & arousal

hippocampus – memory (formingnew episodic memories)

Note on Central Sulcus:

Anterior side – primary motor cortex· Posterior side – primary sensory cortex

Front 19

WHAT IS THE CEREBELLUM FOR?

Back 19

o Balance

o Coordination of complex movement

Front 20

WHAT IS THE BRAINSTEM MADE UP OF?

Back 20

1. MENDULLA

Controls the autonomic nervous system

Basic survival control - HR, respiration, body temp etc

2. PONS

Relay between cortex and cerebellum, relay between cortex and spinal chord.

Front 21

2 DISORDERS OF CONSCIOUSNESS?

Back 21

1. Persistent vegetative state – massive damage to upperbrain causes no conscious awareness, brainstem undamaged so respiration, HR,eye tracking maintained

2. Locked in syndrome – intact cerebrum andbrainstem, but disconnected from spinal cord – patients conscious & awarebut totally unresponsive

Front 22

WHAT DOES THE PRIMARY MOTOR CORTEX DO?

Back 22

Motor Programs – movements planned and“programmed” into brain before initiation

Brain creates programs just before movement

Brain can also retrieve program for learned skilled actions (e.g.signature)

Feedback & Control – planned actionscompared with feedback from actual actions performed, brain computes differenceand makes adjustments. Learned for future

Learning of a motor skill results in the minimisation of prediction error

Sense of Agency – when feedback matches predictions from planned actions

Sense that my action caused thatevent· E.g. in the tickling machine,if the hand action matches the tickling action, we will have a sense that wecaused this to happen. But if there is a delay between my action and themachine, we won’t have that sense and we will feel tickle.

Front 23

PHRENOLOGY? (IN RE HISTORY OF BRAIN MAPPING)

Back 23

Proposed that brain composed of different faculties

By touching bunds on skull we can find different areas that affectdifferent faculties

Total BS, but introduced notion of localisation of brain function

Front 24

WHERE DID THE FIRST REAL TECHNIQUE OF LOCALISING COME FROM?

Back 24

o First real technique of localising brain function came from studiesof brain damage

Front 25

PHINEAS GAGE- WHAT WAS UP W HIM?

Back 25

Frontal lobe damaged

Changed manner & temperament

changed into man who was“no longer Gage”·

indicates prefrontalcortex involved in executive control of behaviour

Front 26

WHAT IS BROCA'S AREA? WHAT IS IT IMPORTANT FOR?

Back 26

Important for speech production

Left frontal lobe damage makes patientunable to speak properly ( called Broca’s aphasia ) Speech slow//Difficulty finding appropriatewords (particularly joining words)// speechstill carries meaning//comprehension (listening) unaffected

Front 27

WHAT IS WERNIKE'S AREA? WHAT IS IT IMPORTANT FOR?

Back 27

Important for speech comprehension

Left posterior temporal lobe damagecauses deficit in language comprehension

Called Wernicke’s Aphasia//unable to understand language//speech fluent, but has no meaning

Front 28

WILDER PENFIELD?

Back 28

Stimulated brain with electrical probes while patients consciousduring surgery for epilepsy

Recorded patient behaviour

Published maps of motor and sensory cortex Size of area on cortex determines sensitivity / fine motor control

E.g. hands over represented in terms of brain SA relative to handflesh SA

Front 29

THINGS ABOUT NEURONS?

Back 29

Neuron singles are all or nothing –neuron either fires, passing a single, or does not

All action potentials are of a fixed and identical size

either afull action potential is fired or none at all

Strength of neuronal singledepends on rate of action potentials, E.g. actions potentials sequentially fire at high frequency forstrong single

Neurons integrate inputs from many other neurons to determine whether theysend on their action potential (fire)

Front 30

WHAT DOES A NEURON CONSIST OF?

Back 30

Cell body (Soma) contains normal cellcomponents (e.g. Nucleus containing DNA)

Dendrites - Receives signals (inputzone)

Many per neuron, receives input from many other neurons

Axon – sends signals/ One per neuron/ Wrapped in myelin sheath– acts as an insulator, critical for efficient neural communication

Prevents leakage ofdepolarisation wave· Boosts conduction speed 100x

Axon Terminal // Terminal Boutons

Forms synapses with thedendrites of another neuron

Sends information to thatneuron· Secretes neurotransmitter whenaction potential reaches them

Front 31

3 KINDS OF GALIAL CELLS?

Back 31

1. Oligondendrocytes – produce myelinsheath that wraps around axons

2. Astrocytes – supply nutrients from bloodto neurons, maintain “blood-brain barrier”

3. Microglia – brains immune system,removes foreign or toxic substances

Front 32

SYNAPSES?

Back 32

join axon terminals of oneneuron to dendrites of another neuron for single transmission Signals go one way

from cell body to axon terminal, to dendrite, to cell body

Front 33

WHATS IN/OUTSIDE OF CELLS?

Back 33

· Cell membrane – separatesintra- and extra- cellular fluid

Cell is surrounded by water,and contains water

Extra-cellular fluid – outsidecellIntra-cellular fluid – inside cell

Front 34

WHAT ARE POSITIVELY CHARGED IONS? (2)

Back 34

· Sodium (Na+) and Potassium (K+)are positively charged ions

o Different concentrationsoutside vs inside cellHence there is an electrical potential acrosscell membrane

Front 35

WHAT IS MEMBRANE POTENTIAL?

Back 35

· change difference betweeninside and outside of cell (across cell membrane)

o More positive ions outside cellthan inside = negative membrane potential

Front 36

WHAT IS A RESTING POTENTIAL?

Back 36

electrical potential acrosscell membrane when neuron at rest (no action potential)

o -70mV (hence, at rest, more positive chargesoutside cell than positive charges inside)

Front 37

WHAT IS ACTION POTENTIAL? WHAT IS THE PROCESS?

Back 37

· transmission of electricalsignal along axon

o Input from other neuronsincreases membrane potential

o If voltage exceeds threshold, triggers action potential

o Depolarisation: membrane potential becomesless negative – closer to zero

o Repolarisation: membrane potential backto -70mV resting potential

o Depolarisation &repolarisation very fast - <0.002 seconds

o Depolarisation “overshoots” –becomes more positive than 0

o Repolarisation “undershoots” –becomes more negative than resting for a short period – causes refectory period – harder for anotheraction potential to occur

Front 38

Ion Channels in Cell Membrane

Back 38

open and close to pass orblock movement of ions across cell membrane

Three important types of ionchannel:

sodium potassium pump, voltage-dependent ion channels, ligand-gatedion channels

Front 39

SODIUM POTASSIUM PUMP?

Back 39

Works to make charge insidecell less positive (i.e. maintain negative resting membrane potential)

Front 40

VOLTAGE-DEPENDENT ION CHANNELS?

Back 40

· Na+

o Closed at resting potential

o Open when membrane exceeds threshold voltage

o Na+ flows into cell – lessnegative potentialo Causes depolarisation of cell(voltage less negative = closer to zero)

o Closed after depolarisation

o Na+ in = depolarisation

K+

o Closed at resting potential

o Open after depolarisation

o K+ flows out of cell

o More negative potentia

lo Repolarisation

o K+ out = repolarisation

Front 41

LIGAND-GATED ION CHANNEL?

Back 41

· Neurotransmitter opens theseion channels when neurotransmitter binds

Different neurotransmitterscause different ion channels to open, hence changing membrane potential indifferent ways

Receptor binding

o Can cause depolarisation (lessnegative – e.g. Na+ flows in)

o Can cause hyperpolarisation(more negative, e.g. K+ flows out, Cl- flows in)

Front 42

TELL ME ABOUT ACITON POTENTIAL CONDUCTION ALONG AXON?

Back 42

o Starts at axon hillock

Membrane at axon hillock has lowest threshold to trigger actionpotential

Depolarisation spreads from site of action potential to neighbouringregion of cell membrane

Repolarisation

undershoot (refectory period) prevent actionpotential going backward (i.e. traveling back along axon in wrong direction)

Front 43

WHERE DOES DEPOLARISATION JUMP BETWEEN?

Back 43

Depolarisation jumps between

Nodes of Ranvier (gaps in myelin sheath)

Front 44

2 KINDS OF NEURON SIGNALS

Back 44

o Electrical: within neuron – fromaxon hillock, along axon, to pre-synaptic axon terminal

o Chemical: between neurons –neurotransmitter signal across synapse

Front 45

NEUROTRANSMITTERS (SYNAPSES)

Back 45

Chemical messenger

Released from pre-synapticterminal

Acts on post-synapticreceptors

Wide range of neurotransmitters, all withdifferent effects

Front 46

SYNAPTIC VESICLES?

Back 46

Stores neurotransmitter in pre-synapticterminal

Joins cell membrane to release neurotransmitter into synaptic cleft

Reused – neurotransmitters are taken back up and repackaged intovesicles

Front 47

NEUROTRANSMITTER RECEPTORS?

Back 47

Gates on post-synaptic side (dendrite side)

Neurotransmitter joints with receptor· Activates receptor to open ion channels on post synapticneuron·

Hence change membrane potentialon dendrite, causing transmission of signal

Each receptor only accepts a specific neurotransmitter for binding

Lock & key

Drugs can act on specificreceptors to cause specific effects

Front 48

RE-UPTAKE PUMP?

Back 48

Clearssynaptic cleft, pumping neurotransmitter back into pre-synaptic terminal

Front 49

ENZYMES?

Back 49

Break down neurotransmitter in synaptic cleft

o Re-uptake pump + enzymes workto stop neurotransmitter signalling when appropriate, hence allowing thepost-synaptic neurons ion channels to close

o Anti-depressants – work to keepserotonin in cleft for longer time to increase signalling

Front 50

SSRIs – SelectiveSerotonin re-uptake Inhibitors

Back 50

· Inhibit action of re-uptakepump

Front 51

MAOIs – Monoamine OxidaseInhibitors

Back 51

· Inhibit enzymes that breakdownserotonin

Front 52

SENDING SIGNALS?

Back 52

o Depolarisation of axon terminal(action potential) triggers neurotransmitter release

Neurotransmitter acts on receptor onpost-synaptic neuron to open ion channels and pass signal

Front 53

2 EFFECTS OF RECEPTOR BINDING?

Back 53

o Depolarisation – makes cellmore positive, sodium ions flow in

o Hyperpolarisation – makes cellmore negative, potassium ions flow out while chlorine ions flow in

Front 54

2 EFFECTS NEUROTRANSMITTERS CAN CONFER?

Back 54

o Excitatory

Brings cell to EPSP: excitatory post-synaptic potential

receptor opens channels causing depolarisation

closer to threshold - more likely to fire

o Inhibitory

Bring cell to IPSP: inhibitory post-synaptic potential

receptor opens channels that cause hyperpolarisation

further from threshold – less likely to fire

Front 55

TELL ME ABOUT GRADED POTENTIALS

Back 55

o Excitatory and inhibitoryinputs sim together, hence changing membrane potential at axon hillock

o Strength of graded potential ataxon hillock depends on: Strength of synapse connection on dendrite

Strong connection = largechange in membrane potential//Weak connection = small changein membrane potential

Timing on inputs If enough excitatory inputsoccur simultaneously, membrane potential will exceed threshold level for actionpotential

o If membrane potential exceedsthreshold level at axon hillock§ Triggersaction potential Neuron fires (sends signal along its axon)