Psychology 1000 Chapter Notes - Chapter 3: Agnosia, Sensory Cortex, Lobotomy

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Chapter 3
Note: Look at All Textbook Charts and **Figures**
Neural Bases of Behaviour
Neurons
-Neurons:
-basic building blocks of nervous system
-linked in circuits
-vary in size/shape
-3 main parts:
1) cell body (soma) contains biochemical structures for neuron survival, nucleus has its genetic
info determining function and development
2) dendrites: fibres, receiving units of impulses
3) axon: conducts impulses away from cell body to other neurons, muscles, glands
-branches out into axon terminals: connects to numerous neurons’ dendrites to
communicate one neuron can talk with 50000 others
-Glial cells: support neuron function by:
-surround them, hold them in place
-manufacture nutrient chemical neurons need
-form myelin sheath
-absorb toxins and wastes
-long fibres guide new neurons to targeted area of brain
-modulate neuron-neuron communication
-protect brain from toxins: blood-brain barrier prevents toxins & other from entering brain
-brain blood vessels have smaller gaps & covered in special glial cells
Electrical Activity of Neurons
Neurons: 1) release chemicals to communicate with muscles, glands, neurons
2) generate electrical nerve impulses
Nerve activation:
1) At resting potential (-70mV) the neuron has an electrical potential due to high [Na+] ions outside
and neg. protein anions inside (some Cl- outside but not a lot, K+ inside but not as much Na+ as
outside) polarized (inside more neg. than outside)
a. sodium-potassium pump maintain charges by moving 3Na+ out for every 2K+ coming in
b. sodium and potassium channels are closed
2) When stimulus passes all-or-none law,
a. all-or-none law: action potential occur at uniform & maximum intensity or not at all
b. occurs by passing the action potential threshold of -50mV caused by stimulus making
enough Na+ flow into axon to change internal voltage differential of resting potential
c. changes in negative resting potential that don’t reach threshold (not enough stimulus):
graded potentials PROPORTIONAL to stimulus, some situations can build up in a
neuron to finally fire it off
3) sodium channel open for instant, Na+ flows into axon attracted to ve charged proteins, reverse
electric potential from -70 to +40mV
-this reversal is a nerve impulse and hits action potential at +40mV
-depolarization: shift from neg. to pos. voltage across membrane (outside more now)
4) to attempt to restore balance, within instant, sodium channels close, K+ channels open and they flow
out by repulsion
a. restores negative voltage resting potential
b. this neuron is absolute refractory period: not excitable for a certain time
-causes rate of 300 impulses per second max for humans
5) restoration of ions, Na+ goes back out, K+ comes back : repolarization
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a. this neuron still in refractory as it returns to resting potential
b. adjacent sodium channels open... process continues along and keeps moving to axon
terminals
Hodgkin and Huxley: action-potential
-mild electrical stimulus to axon, interior voltage differential shifts from -70mV to +40mV
-forced axon to generate a nerve impulse, or action potential
-found that relies of sodium potassium channels
-some anaesthetics stop flow of Na+ ions, meaning no pain impulses sent by neurons
Myelin sheath:
-fatty, whitish insulation and protective layer derived from glial cells
-covers many axons in brain and spinal cord
-speeds up nerve impulses to 300km/h by jumping gaps:
-nodes of Ranvier: regular intervals of extremely thin or absent myelin
-MS: immune system attacks myelin sheath
-damaged myelin disrupts delicate timing of impulses, resulting in jerky movement, and paralysis
How Neurons Communicate: Synaptic Transmission
-at synapses: functional (but not physical) connection between a neurons (don’t actually touch)
-synaptic cleft: tiny gap between axon terminal of one neuron and dendrite of next neuron
-Otto Loewi: chemical neurotransmission: neurons release chemicals that carry messages to other cells
Neurotransmitters
-neurons produce neurotransmitters: chemicals that carry messages across synapse to excite or inhibit firing of
other neurons...............steps of chemical communication: (therefore impulses carried btwn by chemicals)
-synthesis: chemicals formed inside neuron
-storage: in chambers, synaptic vesicles within axon terminals
-release: when action potential comes down axon, vesicles move to surface of axon terminal and are
released into fluid space between presynaptic (sending) neuron and postsynaptic (receiving) neuron
-binding: molecules cross space and attach to receptor sites, fitting like lock-and-key
-large protein molecules embedded in postsynaptic neuron’s membrane
-deactivation by reuptake or breakdown
o Binding of neurotransmitters to receptor site causes two possible effects:
Excitation depolarizes the postsynaptic cell membrane by stimulating flow of Na+ (excitatory
transmitters)
Alone (temporal) or combo (spatial) with other activity at excitatory synapses on
dendrites or cell body can exceed threshold and cause postsynaptic to fire
Inhibition hyperpolarizes the postsynaptic cell membrane by stimulating ion channels that allow
K+ to flow out of the neuron, or negatively charged ions to flow in (changes potential from 70
mV to 72 mV) (inhibitory transmitters)
Makes it more difficult for excitatory transmitters at other receptor site to depolarize the
neuron to the threshold, even if excitatory stimuli from many other neurons at one time
o Neurotransmitters continue to do their excitatory or inhibitory function until deactivation by:
Some deactivated by other chemicals in synaptic space that break them down
Reuptake transmitters reabsorbed into presynaptic axon terminal
o Most only effect specific receptors with receptors for them, but neuromodulators have widespread
influence by modulating (inc. Or dec.) sensitivity of 10000s of neurons to their specific transmitters:
related sleep, eating, and stress
o Examples of neurotransmitters: (pg. 76 for disorders associated**)
Acetylcholine (Ach) excitatory (related to memory storage, muscle activity & movement,
behavioural inhibition) lack: Alzheimers too much: muscle contractions, convulsions
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Ex. black widow venom has lots of ACHviolent seizures, death
Glutamate (Glutamic Acid)
found in CNS, therefore related to all behaviour basically
Excitatory
Learning & Memory
Too much causes seizures
--------------------
Norepinephrine (NE) functions in excitatory and inhibitory systems (related to arousal, eating)
Neural circuits controlling memory, learning, wakefulness, eating
Lack: depression too much: panic and stress
Dopamine (DA) inhibitory or excitatory
Parkinsons and depression (lack) or schizophrenia (too much)
Emotional arousal, voluntary movement, learning, motivation, pleasure
------------------------
Seratonin (5-HT) mostly inhibitory
sleep, mood, eating, sexual behaviour (arousal), pleasure & pain
Lack: depression, eating, sleeping disorders
Endorphins: inhibits transmission of pain impulses, causes feeling of well-being
too much: cant feel pain too little: immune issues and hypersensitivity to pain
Gamma Aminobutynic Acid (GABA)
functions in inhibitory systems (related to motor control and anxiety control)
ex. drugs to treat anxiety often raise GABA, alcohol raises brain sensitivity to it
Found in CNS, therefore related to all behaviours basically
Lack: tremors, loss of motor control, also personality changes
o Drugs function by affecting neurotransmitters
Increase (agonist) or decreases (antagonist) action of neurotransmitter:
stimulates or blocks receptor sites
Enhance or reduce neuron ability to synthesize, store or release transmitters
Make difficult to deactivate transmitter, ex. inhibiting uptake (agonist only)
Examples:
Amphetamines: stimulants that boost arousal and mood by increasing dopamine and
norepinephrine activity:
o 1) cause neurons release more transmitters
o 2) inhibit reuptake
Cocaine increases activity of dopamine and norepinephrine
o 1) inhibits reuptake only
Alcohol agonist and antagonist:
o stimulates GABA: depressing neural activity (agonist)
o reduces activity of glutamate
o inhibits clear thinking, emotional control and motor
Curare blocks receptor sites for ACh, causes complete paralysis
Black widow venom stimulates release of ACh
Botulism toxin Blocks release of Ach
Rohypnol and GHB: date rape drugs increasing GABA action, reduce memory
Nicotine “duplicating” effects of Ach by fitting in its receptor sites
o Agonist for Ach and dopamine neurons, increasing neural excitation
Caffeine increases neuron and cellular activity
o Antagonist for adenosine transmitter: blocks adenosine receptor sites which
inhibits release of excitatory transmitters
o Disinhibition inhibition of inhibitory neurons to bring system back to normal state
The Nervous System
Three major types of neurons the carry out functions:
o Sensory neurons carry input messages from the sense organ to the spinal cord and brain
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Document Summary

Note: look at all textbook charts and **figures** Branches out into axon terminals: connects to numerous neurons" dendrites to communicate one neuron can talk with 50000 others. Long fibres guide new neurons to targeted area of brain. Protect brain from toxins: blood-brain barrier prevents toxins & other from entering brain. Neurons: 1) release chemicals to communicate with muscles, glands, neurons. Brain blood vessels have smaller gaps & covered in special glial cells. This reversal is a nerve impulse and hits action potential at +40mv. Mild electrical stimulus to axon, interior voltage differential shifts from -70mv to +40mv. Forced axon to generate a nerve impulse, or action potential. Some anaesthetics stop flow of na+ ions, meaning no pain impulses sent by neurons. Fatty, whitish insulation and protective layer derived from glial cells. Covers many axons in brain and spinal cord. Speeds up nerve impulses to 300km/h by jumping gaps: Nodes of ranvier: regular intervals of extremely thin or absent myelin.

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