l2- neurons n cortex Flashcards

1
Q

Electrochemical Neuronal Signalling

electrical signals

A
  • within a neuron
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2
Q

Electrochemical Neuronal Signalling

chemical signals

A
  • between neurons at synapses
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3
Q

neuronal signalling

A
  • process of transmitting info in the nervous system
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4
Q

information

A
  • =signal= any change in:
  • membrane potential (diff in electrical charges inside/outside neuron)- postsynaptic (input) and action (output) potentials
  • neurotransmitter quantity (chemical signal between neurons)
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5
Q

Electrical neuronal signalling within a neuron

neuron mebrane

A
  • seperates inside (intercellular) from outside (extracellular)
  • has 3 types of transmembrane proteins: Na+/k+ ion pump, Na+ and K+ voltage-gated ion channels
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6
Q

electrical neuronal signalling within a neuron

ion pump (Na+/K+ pump)

A
  • continously moves Na+ out n K+ in- keeps a voltage difference
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7
Q

electrical neuronal signalling within a neuron

volateg gated ion channels

A
  • open/close based on membrane voltage
  • only let specific ions (Na+ or K+) through
  • closed at rest, open during signalling
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8
Q

Resting Membrane Potential

Resting Potential

A
  • the normal voltage across the membrane at rest (~ -70 mV)
  • Created by the Na+/K+ pump (3 Na+ out, 2 K+ in = more positive outside).
  • voltage gated channels stay closed below -55mV
  • input from other neurons can change this voltage
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9
Q

post synaptic potentials

A
  • small voltage changes due to input from other neurons
  • PSPs can add up:
  • if enough EPSPs- reach -55mV= trigger action potential.
  • IPSPs make it harder to reach threshold
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10
Q

PSPs

excitatory psp

A
  • makes membrane less negative then -70mV
  • depolarisation
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11
Q

psps

inhibitory

A
  • makes membrane more negative
  • hyperolarisation
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12
Q

action potential

A
  • triggers at -55mV: all or nothing event
  • phases:
    1. depolarisation- Na+ channels open → Na+ enters → inside becomes positive (up to +40 mV).
    2. Repolarisation: K+ channels open → K+ exits → voltage drops. (from +40 mV to -70 mV)
    3. Hyperpolarisation: Becomes more negative than resting (~ -80 mV).
  • Na+/K+ pump restores original state.
  • Takes ~2 ms.
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13
Q

actional potential propagation

A
  • ap starts at axon hillock
  • depolarisation spreads- triggers AP in next part of axon- continues forward
  • refractory period: after firing, a section of the axon cant fire again immediately- ensures one way travel
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14
Q

APP

refactory period

A
  • after firing, a section of the axon cant immediately fire again- esures one way travel
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15
Q

myelination

A
  • speeds up AP transmission
  • aps only occurs at gaps between myelin= nodes of ranvier
  • ap ‘jumps’ between nodes- saltatory conduction
  • myelin= found in white matter
  • w/out myelin, signals would be too slow
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16
Q

myelination

myelin sheath

A
  • fatty insulation speeds up AP transmission
  • theyre protrusions from oligodendrocytes, a type of glial cell
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17
Q

properties of action potentials

all or nothing

A
  • once an ap is triggered, same ap process always ensues
  • fully happens or nothing at all
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18
Q

properties of action potentials

self-propagation

A
  • once triggered keeps going
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19
Q

properties of action potentials

unidirectional

A
  • moves one way thanks to refactory period
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20
Q

properties of action potentials

does not dissipate

A
  • ap keeps the same strength (+40 mV) as it travels along the axon
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21
Q

Chemical communication between neurons at the synapse

chemical signalling between neurons

A
  • happens at snypases
  • ap arrives at axon terminal- causes neurotransmitter release
  • NT crosses synaptic cleft- binds to receptos on next neuron
  • triggers PSP
22
Q

Chemical communication between neurons at the synapse

signal conversion at synpase

A
  1. electrical (AP) arrives
  2. triggers chemical release (NT)
  3. causes electrical response in next neuron (PSP)
23
Q

Post-synaptic potential (PSP)

neurotransmitter action at synpase

A
  • NT receptors r linked to ion channels
  • bindning opens channels, which either:
    1. hyperpolarises membrane potential=IPSP
    2. depolarises membrane potential= EPSP
24
Q

properties of PSP

A
  • local (near post synpatic dendrite)
  • dissipate (weaken as travel)
  • graded (not AoN)
  • smaller in amplitude than aps (up to 5mv)
25
PSPs to action potentials
- sum at axon hillock - if total= -55mv-triggers ap - if too many IPSPs- ap=blocked - this= neuronal intergration
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neuronal coding
- the represenation of stimulus intensity by the rate of AP firing\ - NTs-more input- more released (graded) - PSPs: stronger input - stronger psp (graded) - APs: - always same size - stronger input- more aps fired-higher firing rate
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# neuronal coding firing rate
- number of APs fired per second, increases w stronger stimulation
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# neurotransmitters amino acid NTs: glutamate
- main excitatory NT- leads to ESPS (20% of CNS synpases) - too much causes excito-toxicity- neurons overexcite n die - involved in epilepsy: reduced firing threshold leads to overactivation
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# neurotransmitters amino acid NTs: GABA
- main inhibitory NT- leads to IPSPS (40% of CNS synpases) - prevents excessive excitation - key for fine tuning of activation patterns - alcohol enhances GABA receptor sensitivity- sedative + anxiolytic effects
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# neurotransmitter system NTs (specific brain circuits)
- **acetylcholine**- cholinergic system - **serotonin**- serotonergic system - **noradrenaline**- noradrenergic system - **dopamine**- dopaminergic system
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the cerebal cortez
- divided through: lesion studies, neuroimaging/stimulation, animal electrophysiology - 3 types: sensory, motor, association
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# sensory n motor cortex primary sensory cortex
- recieves input from sensory organs
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# sensory n motor cortex secondary sensory cortex
- processes inputs from cortex not direct sensory organs- higher level processing
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# sensory n motor cortex primary motor cortex
- sends commands to mucles
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# sensory n motor cortex premotor cortex
- plans motor actions
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# sensory n motor cortex brodmann areas (BA)
- BA17 = visual (V1) BA22 = auditory BA1,2,3 = somatosensory BA4 = motor
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cortical maps
- cortex contains maps of body/senses: - somatosensory+motor: body parts- disorted based on sensitivty/dexeterity - visual:maps of visual field - aduitory: maps of sound frequencies - olfactory+gustary: unclear - Contralateral representation: left hemisphere = right body/field and vice versa.
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motor and somatosensory cortical maps
- diff parts of MC control diff muscles - diff parts of SSC recieve tactile info from skin (pain/pressure etc) - more dexterous/sensitive parts=maginified -maps=contralateral - homunculus man
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visual cortical maps
- diff locs in primary VC correpsond to diff locs in visual field - vsiual fields= contralateral - centre=magnified -secondary visual cortex=more maps
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auditory cortical maps
- cochlea in inner ear breaks down sound into frequencies - PAC= maps - ear sends info bilaterally to auditory cortex
41
association cortex
- handles non-sensory n non-motor processing (so everything else): - intergrates multisensory info - supports compex cogniton (recogintion, memory etc) - in frontal, partial n temporal lobes
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frontal lobe
- prefrontal cortex: lateral, orbital n medial parts - functions: - executive control (planning, prediction) - working memory - language - decision making + error monitoring - emotional processing
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parietal lobe
- specialised in: - spatial awareness n attention - multisensory integration (perception n memory action) - object localisation n spatial relationships - spatial-motor translation - reading+writing
44
temporal lobe
1. medial side: - memory (hippocampus) - emotion (amygdala) 2. lateral side - visual object recogntion (ventral temporal) - auditory object recognition (superior temporal)
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localisation vs distributed networks
- localisationsim: brain regions have specific functions - BUT functions= distributed across networks - connections r as important as regions themselves
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white matter tracts
- connect cortical regions - **tracts**= bundles of axons (white matter highways) - major egs; - corpus callosum: connects hemispheres - superior longtudinal fasciculus: connects frontal to parietal/occipital (attention, exec. control) - arcuate fasciculus : connects frontal to temporal (language)
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NT systems
- brain circuits driven by specific NTs - theyre made in subcortical/brainstem nuclei, projected widely - each system supports multiple behaviours
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cholinergic system
- NT:acetylcholine - made in basal forebrain nucleus - projects to most cortex - *functions*: cortical arousal/excitability, selective attention, memory (via hippocampus projections from pons/midbrain)
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noradrenergic system
- NT: noradrenaline - made in locus coeruleus (pons), medulla - projects to: thalamus, hypothalamus, cortex (esp PFC) - functions: sleep+arousal, attention+vigialnce, emotional memory
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serotoninergic system
- NT: serotonin - made in raphe nuclei (brainstem) - projects to hypothalamus, hippocampus, amygdala, cerebellum, thalamus - functions: homeostasis behaviours (sleep, sex, appetite), mood regulation, long term memory - low serotonin- linked to depression - SSRIs (eg antidepressants) affects sleep, sex, appetite - MDMA damages serotengic neurons- LT memory deficits
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dopaminergic system
- NT: dopamine - made in substantia nigra, ventral tegmental area, nucleus accumbens 3 subsystems: 1. ***nigrostriatal***: substantia nigra → basal ganglia → movement initiation & stopping 2. ***Mesolimbic***: VTA → limbic system → reward & reinforcement 3. ***Mesocortical***: VTA → prefrontal cortex → planning, working memory, problem solving - dopamine in nucleus accumbens increases w: natural rewards (food), drugs, abstract rewards (money)
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