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Summary PYC1501 Study Notes 2021
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Summary of 46 pages for the course PYC1501 - Basic Psychology at Unisa (PYC1501 Study Notes)
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Study Notes:PYC1501 - Basic Psychology
Human Nervous System
Impulse Conduction in the Neuron
Neurons → Neural networks → Nervous system
All human behaviour
Stimuli → sensory organs → electrochemical energy → Neurons → impulse conduction → Neurons
External stimuli → sensory organs → internal stimuli → brain
2 Main processes of impulse conduction:
1) Electrical - impulse 1st segment of axon → terminals ∵ electrical events at cell membrane
2) Chemical - passage of impulse neuron to next ∵ chemical process in synaptic cleft
1) Neuron is electrically charged
Potential difference - difference between positive and negative charge
Ions - positive, negative parts
Neural membrane - Barrier splits charge - barrier bridged charge forms neutral particles
Fluid inside, outside of neuron - chemical particles eclectically charged
Neuron electrically charged ∵ potential difference inside, out
2) Resting membrane potential
Impulse conducted - charge across neural membrane changes.
Resting membrane potential - inactive readiness before impulse conduction - (-) inside = (+) outside
Ions move - high concentration to low + opposite charges attract, similar repel
Mechanisms maintain potential difference - selective ion permeability of membrane
Sodium (+) ions - high concentration on outside ∴ (+) outside
Potassium (+) ions, (-) protein, (-) nucleic acid molecules ∴ (-) inside
3) Action potential
Neuron → Neuron
High concentration → low concentration
Info → Synaptic connections soma - changing potential across soma membrane → propagate axon hillock,
summed - total potential = threshold level → action potential triggered in axon
Axon must have resting membrane potential for action potential to trigger
Summed potential in axon hillock - threshold > resting potential
Resting membrane potential, Polarised - difference in potential ∵ (+) outside, (-) inside
Action potential triggered → membrane permeable to (+) sodium influx ∴ less (-) on inside → charges even out -
membrane depolarised, no potential difference → (+) sodium - influx stops ∵ inside slightly more (+) vs outside →
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,membrane permeable to (+) potassium outflow ∴ outside (+) again ∵ gain, inside (-) ∵ loss → membrane repolarised
→ continues till outside potassium > inside sodium ∴ membrane hyperpolarised shortly → resting membrane
potential again, refectory period
Refectory period - sodium, potassium ions back to original states ∵ membrane pumps sodium back outside,
potassium inside
Absolute refectory period - neuron not respond to stimulus, cannot conduct impulse
Relative refectory period - towards end refectory period - very intense stimulus can trigger impulse
4) Characteristics of impulse conduction
Impulse initiated axon hillock → conducted down axon, propagated down each segment at a time ∵ changing
membrane potentials → terminals
After axon segment impulse conducted → refectory period follows per segment ∴ impulse only one direction
Refectory period prevents overstimulation in nervous system
Intense stimuli ≠ bigger changes in potential, bigger impulses, faster impulses ∵ always same magnitude, speed
Intense stimuli = more frequent impulses ∵ intense potential differences, axon hillock threshold reached faster
Impulse conduction - all-or-nothing
Aspects of impulse conduction:
Strength, speed of impulse constant in a particular neuron
Strength, speed vary different thicknesses of nerve fibres
◦ thicker = stronger, faster impulse ~ 100 mps
◦ thinner = slower impulse ~ 100 cmps
Speed of impulse ∝ if neuron myelinated
◦ myelinated axon = faster impulse jumping node to node
2 kinds of impulse conduction:
1) Salutatory conduction - myelinated axon impulse jumping node to node
2) Action potential conduction - un-myelinated axon impulse propagates smoothly
Impulse Conduction in the Synapse
Electric - conduction of nerve impulses in a neuron
Chemical - communication between different neurons
1) The synapse
Synapse = synaptic cleft + presynaptic membrane + postsynaptic membrane
Presynaptic membrane - axon terminals
Postsynaptic membrane - dendrites, soma
Action potential reaches terminals → chemical neurotransmitters release into synaptic cleft
Neurotransmitters can alter activity in neurons
Vesicles release neurotransmitters - mix with flued outside cells, combine with receptors
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, Different neurons = different neurotransmitters
Each neuron = same neurotransmitters from all terminals
2) Postsynaptic potentials
Postsynaptic potential - excitatory neurotransmitter increases likeliness of action potential in next neuron
◦ inhibitory neurotransmitter attempts to prohibit action potential in next neuron
◦ not all-or-nothing, graded potential
After release in synaptic cleft neurotransmitter:
◦ Re-uptake - neurotransmitter in synaptic cleft reabsorbed by axon that released it
◦ Diffuse away, broken up by enzymes
◦ Bounce around then return to postsynaptic receptor
Longer time neurotransmitter in synaptic cleft = greater chance of affect
Many dendrites connect to many axon terminals
Spatial summation - postsynaptic potentials reinforced by action potentials of terminals of many axons ~ same
time → action potential reinforced ∵ more neurotransmitter accumulates in cleft
Temporal summation - same axon discharges repeatedly ∴ more neurotransmitter accumulates in cleft
Spatial, temporal summation increase, decrease impulse firing ∵ excitatory, inhibitory postsynaptic potentials
3) Nature of neurotransmitters
Neurotransmitter = excitatory, inhibitory, both
Excitatory, Inhibitory effect depends on:
◦ Nature of the neurotransmitter
◦ Place where it acts
◦ Quality of neurotransmitter ∝ enzyme that destroys it
◦ Amount of inhibitory neurotransmitter ∝ excitatory neurotransmitter
Neurotransmitter identifying characteristics:
◦ Chemicals present in or synthesised by neurons
◦ Active neuron release chemical, produces response in target cell
◦ Mechanism for removing neurotransmitter from cleft once done
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, Classic neurotransmitters:
Acetylcholine (Ach)
◦ Brain, spinal chord, parasympathetic nerves
◦ Effects vary
◦ Causes skeletal muscles to contract
◦ Curare poisoned arrowheads - prevent Ach reaching receptors ∴ muscle paralysis, suffocation
◦ Related to memory, supports normal wakeful behaviour, mental alertness
◦ Insufficiency in brain areas ∝ Alzheimer's, decline cognitive function
Adrenalin / Epinephrine
◦ Released by sympathetic nerves, adrenal glands.
◦ Increases heart rate, contraction of blood vessels, skeletal muscles, heart muscles
◦ Speeds up metabolism, release of glucose into blood
Noradrenalin (NA) / Norepinephrine (NE)
◦ Released by brain cells, sympathetic nerves, adrenal glands
◦ Excitatory effect
◦ Lack - depression
◦ Excess - mania
Dopamine (DA)
◦ Good mental health, motor behaviour
◦ Excess - schizophrenia - loss of contact with reality
◦ Lack - muscle rigidity, tremor, Parkinson's, dementia
Serotonin
◦ In brain, digestive tract, blood
◦ Helps regulate sleep-wake cycle, temperature
◦ SAD - seasonal depression
◦ Antidepressants affect modulation of serotonin at synapses
Gamma-aminobutyric acid (GABA)
◦ Excitatory in developing brain
◦ Inhibitory in adult brain
◦ Regulates excitability nervous system
◦ Controls muscle tone, manages aggression, appetite
Endorphin
◦ Experience of pleasure
◦ Suppression of pain
◦ Produced during feel good activity - laughter, love, exercise
4) Effect of drugs on synaptic processes
Drugs work by affecting synaptic processes
2 Main Classes:
1) Agonists - similar effect to neurotransmitters - morphine, codeine painkillers
2) Antagonists - block actions of neurotransmitters - barbiturates sedatives
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