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55 Cards in this Set
- Front
- Back
WHAT IS COGNTIIVE NEUROSCIENCE? |
study of the neural (brain)basis of behaviour and thought Concerned with what happens in the brain when weperform cognitive functions |
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FACTS ABOUT NEURONS? |
· Neurons connected to each otherby synapses Each Neuron connected tothousands of other neurons Allows for incredibly largenumber of possible circuits in brain |
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GREY MATTER? |
cortex (outer layer) of brain Neuron cell bodies found here |
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WHITE MATTER? |
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 |
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WHAT ARE THE TWO PARTS OF THE NERVOUS SYSTEM? |
Central Nervous System – brain andspinal chord Peripheral nervous system – nervesthroughout body |
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WHAT ARE NERVES? |
extendedbundle of axons of the neurons |
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WHAT IS THE SOMATIC NERVOUS SYSTEM? |
voluntary,motor, sensory |
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WHAT IS THE AUTONOMIC NERVOUS SYSTEM? |
involuntary |
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SYMPATHETIC? |
increase HR, increase respiration,sweating, stress, arousal, “fight-or-flight” |
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PARASYMPATHETIC? |
“opposes” sympathetic nervoussystem “rest & digest’, lower HR, lower respiration, digest |
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3 MAJOR PARTS OF THE BRAIN? |
1. Cerebrum // forebrain// cerebral hemispheres 2. Cerebellum // hind brain 3. Brainstem |
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CEREBRUM? |
o Consists of two hemispheres§ Divided by longitudinal fissure |
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CORPUS CALLOSUM? |
connects hemispheres |
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CORTEX? |
outer layer – white matter –neuron cell bodies found here Highly folded to maximise surface area |
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FRONTAL LOBE? |
· Anterior to central sulcus Executive functions: reasoning, working memory, etc Emotion Motor functions Premotor cortex (planning) Primary motor cortex(execution)· Speech (broca’s area) |
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PARIETAL LOBE? |
· Posterior to central sulcus Primary (somato)sensory cortex Touch, pain Spatial attention Linking vision to action |
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OCCIPITAL LOBE? |
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 |
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TEMPORAL LOBE? |
· 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 |
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WHAT IS THE CEREBELLUM FOR? |
o Balance o Coordination of complex movement |
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WHAT IS THE BRAINSTEM MADE UP OF? |
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. |
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2 DISORDERS OF CONSCIOUSNESS? |
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 |
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WHAT DOES THE PRIMARY MOTOR CORTEX DO? |
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. |
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PHRENOLOGY? (IN RE HISTORY OF BRAIN MAPPING) |
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 |
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WHERE DID THE FIRST REAL TECHNIQUE OF LOCALISING COME FROM? |
o First real technique of localising brain function came from studiesof brain damage |
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PHINEAS GAGE- WHAT WAS UP W HIM? |
Frontal lobe damaged Changed manner & temperament changed into man who was“no longer Gage”· indicates prefrontalcortex involved in executive control of behaviour |
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WHAT IS BROCA'S AREA? WHAT IS IT IMPORTANT FOR? |
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 |
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WHAT IS WERNIKE'S AREA? WHAT IS IT IMPORTANT FOR?
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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 |
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WILDER PENFIELD? |
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 |
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THINGS ABOUT NEURONS? |
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) |
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WHAT DOES A NEURON CONSIST OF? |
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 |
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3 KINDS OF GALIAL CELLS? |
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 |
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SYNAPSES? |
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 |
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WHATS IN/OUTSIDE OF CELLS? |
· Cell membrane – separatesintra- and extra- cellular fluid Cell is surrounded by water,and contains water Extra-cellular fluid – outsidecellIntra-cellular fluid – inside cell |
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WHAT ARE POSITIVELY CHARGED IONS? (2) |
· Sodium (Na+) and Potassium (K+)are positively charged ions o Different concentrationsoutside vs inside cellHence there is an electrical potential acrosscell membrane |
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WHAT IS MEMBRANE POTENTIAL? |
· change difference betweeninside and outside of cell (across cell membrane) o More positive ions outside cellthan inside = negative membrane potential |
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WHAT IS A RESTING POTENTIAL? |
electrical potential acrosscell membrane when neuron at rest (no action potential) o -70mV (hence, at rest, more positive chargesoutside cell than positive charges inside) |
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WHAT IS ACTION POTENTIAL? WHAT IS THE PROCESS? |
· 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 |
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Ion Channels in Cell Membrane |
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 |
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SODIUM POTASSIUM PUMP? |
Works to make charge insidecell less positive (i.e. maintain negative resting membrane potential) |
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VOLTAGE-DEPENDENT ION CHANNELS? |
· 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 |
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LIGAND-GATED ION CHANNEL? |
· 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) |
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TELL ME ABOUT ACITON POTENTIAL CONDUCTION ALONG AXON? |
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) |
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WHERE DOES DEPOLARISATION JUMP BETWEEN? |
Depolarisation jumps between Nodes of Ranvier (gaps in myelin sheath) |
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2 KINDS OF NEURON SIGNALS |
o Electrical: within neuron – fromaxon hillock, along axon, to pre-synaptic axon terminal o Chemical: between neurons –neurotransmitter signal across synapse |
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NEUROTRANSMITTERS (SYNAPSES) |
Chemical messenger Released from pre-synapticterminal Acts on post-synapticreceptors Wide range of neurotransmitters, all withdifferent effects |
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SYNAPTIC VESICLES? |
Stores neurotransmitter in pre-synapticterminal Joins cell membrane to release neurotransmitter into synaptic cleft Reused – neurotransmitters are taken back up and repackaged intovesicles |
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NEUROTRANSMITTER RECEPTORS? |
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 |
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RE-UPTAKE PUMP? |
Clearssynaptic cleft, pumping neurotransmitter back into pre-synaptic terminal |
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ENZYMES? |
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 |
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SSRIs – SelectiveSerotonin re-uptake Inhibitors |
· Inhibit action of re-uptakepump |
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MAOIs – Monoamine OxidaseInhibitors |
· Inhibit enzymes that breakdownserotonin |
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SENDING SIGNALS? |
o Depolarisation of axon terminal(action potential) triggers neurotransmitter release Neurotransmitter acts on receptor onpost-synaptic neuron to open ion channels and pass signal |
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2 EFFECTS OF RECEPTOR BINDING? |
o Depolarisation – makes cellmore positive, sodium ions flow in o Hyperpolarisation – makes cellmore negative, potassium ions flow out while chlorine ions flow in |
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2 EFFECTS NEUROTRANSMITTERS CAN CONFER? |
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 |
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TELL ME ABOUT GRADED POTENTIALS |
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) |