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Psych year 1 semester 2 > Brain and Behaviour > Flashcards

Brain and Behaviour Flashcards

1
Q

What is cognition? Give 4 examples

A

Higher mental processes e.g., thinking, speaking, acting, planning

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2
Q

What is behavioural neuroscience?

A

Scientific study of how brain activity influences behaviour

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3
Q

What is cognitive neuroscience?

A

Study of neural basis of behaviour

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4
Q

What can understanding the neural basis of a mental process help distinguish between?

A

Different theories relating to how that process is performed

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5
Q

What are mental representations?

A

The sense in which properties of the outside world (e.g., colours, objects) are copied by cognition

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6
Q

What are neural representations?

A

The way in which properties of the outside world manifest themselves in the neural signal (e.g., different spiking rates for different stimuli)

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7
Q

What word is associated with mental representations?

A

Simulation

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8
Q

What word is associated with neural representations?

A

Implementation

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9
Q

Where did Aristotle and Plato think mental experiences came from? (Historical perspectives)

A

Aristotle - heart

Plato - mind

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10
Q

What is the mind-body problem? (Historical perspectives)

A

How can a physical substance (brain/body) give rise to mental experiences?

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11
Q

Who had the theory of dualism and what was the basic idea? (Historical perspectives)

A

Descartes

Mind (eternal) and body (mortal) are separate substances

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12
Q

What did Descartes believe about the soul (Dualism - Historical perspectives)

A

It controls the movement of muscles through influence on the pineal body

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13
Q

How did Descartes believe our muscles moved? (Dualism - Historical perspectives)

A

The eye send visual info to the brain
The soul examines this info and decided to act
The soul tilts the pineal body
This diverts pressurised fluid through nerves to appropriate muscles

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14
Q

Who proved Descartes wrong and how? (Historical perspectives)

A

Galvani
electrical stimulation of decapitated frog nerves’ caused contraction of attached muscle
Muscles contracting was its own characteristic
Brain didn’t inflate muscles with directed pressurised air

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15
Q

What is dual aspect theory?

A

Mind and body are 2 levels of explanation of the same thing

e.g. like photons with wave-particle duality

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16
Q

What is reductionism?

A

Mind will eventually be explained solely in terms of physical/biological theory

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17
Q

True or false?

Dual-aspect theory and reductionism are issues still relevant to modern cognitive neuroscience

A

True

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18
Q

What do psychologists often deal in terms of?

A

Generalisation e.g., behaviours as general laws

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19
Q

What do physiologists often deal in terms of?

A

Reduction e.g., complex behaviour explained in simpler terms

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20
Q

What is the modern history of behavioural neuroscience?

A

combined experimental methods of psychology and physiology and applied them to issues that concern all psychologists
e.g., recent interest in studying physiology of pathological conditions such as addiction and MH disorders

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21
Q

What surgery have split brain patients had and why?

A

Splitting of corpus callosum to cure severe epilepsy

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22
Q

What is the corpus callosum?

A

A bundle of nerve fibres connecting the left and right brain hemispheres

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23
Q

Who studied split brain patients?

A

Sperry and Gazzinga

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24
Q

What did Sperry and Gazzinga find about split brain patients?

A

Left hemisphere = language (and right side motor control)

Right hemisphere = motor control of left side

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25
Q

What is used to insure that stimuli are only presented to one hemisphere in split brain patients?

A

Tachistoscope presentation

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26
Q

How quickly do stimuli need to be presented for in a Tachistoscope presentation and why?

A

150ms or less

Eye movements cause loss of lateralisation and 150ms is faster than the eye can move from central fixation to stimuli

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27
Q

What were the results of Sperry and Gazzinga’s experiments on Split brain patients?

A

object presented to RVF, ppt verbally names object

object presented to LVF, ppt “sees nothing” but can use left hand to pick out correct object

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28
Q

What side of brain is smelling processed on?

A

Same side hemisphere

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29
Q

What is smelling like in split brain patients?

A

Smelling on left is process by LH and can name smell

Smelling on right is processed by RH and can choose corresponding scent with left hand

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30
Q

What does lateral mean?

A

Towards side

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31
Q

What does medial mean?

A

Towards middle

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32
Q

What does dorsal mean?

A

Top

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33
Q

What does ventral mean?

A

bottom

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34
Q

What does rostral (anterior) mean?

A

Front

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35
Q

What does caudal (posterior) mean?

A

Back

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36
Q

What is the neuraxis?

A

Imaginary line from head to toe

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37
Q

What does ipsilateral mean?

A

same side

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38
Q

What does contralateral mean?

A

opposite side

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39
Q

What are the 3 ways of slicing the brain?

A

Transverse section - right angle to neuraxis
Sagittal section - parallel to neuraxis and perpendicular to ground
Horizontal section - parallel to ground

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40
Q

What is the CNS made up of?

A

Brain and spinal cord

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41
Q

What is the peripheral NS made up of?

A

Cranial and spinal nerves

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42
Q

What is the texture of the brain?

A

Soft and jelly like

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43
Q

How much does the brain weigh?

A

Approximately 1400g

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44
Q

How much body weight does the brain account for?

A

2%

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45
Q

What is the brain protected by?

A

Skull and CSF

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46
Q

True or false?

Different areas of the brain support different functions?

A

True

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47
Q

How much blood and oxygen does the brain use?

A

20% of blood supply

15-20% of oxygen

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48
Q

How long are the blood vessels in the brain?

A

400 miles

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49
Q

What is the Foramen Magnum? Where is it located?

A

Large hole for passage of spinal cord in the skull

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50
Q

What are the 3 Meninges

A

Dura Mater - tough, flexible, outermost meninx
Arachnoid - middle layer, like cellophane draped around brain, doesn’t dip into valleys of brain contour
Pia Mater - last layer, adheres to surface of brain

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51
Q

What is the subarachnoid space?

A

The space between the arachnoid and pia meninges

It is filled with CSF

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52
Q

What are ventricles?

A

A set of hollow chambers within the brain filled with CSF

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53
Q

What are the 4 ventricles?

A

Lateral ventricles
Third ventricles
Cerebral aqueduct
Fourth ventricle

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54
Q

What is cerebrospinal fluid (CSF) like?

A

similar to blood plasma composition

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55
Q

How is CSF formed?

A

By the choroid plexus

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56
Q

What is the purpose of CSF

A

To form a watery cushion to protect the brain

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57
Q

Where is CSF circulated?

A

Arachnoid space
ventricles
central canal of spinal cord

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58
Q

What is the total volume of CSF?

How many times does it turn over a day?

A

125-150 ml

3-4 times a day

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59
Q

Where is CSF secreted and what does it do constantly?

A

Secreted by brain

Constantly made, circulated and reabsorbed into bloodstream

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60
Q

What is Hydrocephalus in infants? What happens?

A

Happens when CSF is not reabsorbed
doesn’t circulate around the brain or leave properly instead it sits in ventricles
leads to expansion of the head

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61
Q

Which ventricle(s) are in the forebrain?

A

Lateral and Third

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62
Q

Which ventricle(s) are in the midbrain?

A

Central aqueduct

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63
Q

Which ventricle(s) are in the hindbrain?

A

Fourth

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64
Q

What are the 3 major divisions of the brain?

A

Forebrain
Midbrain
Hindbrain

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65
Q

Which is the largest major division of the brain?

A

The forebrain

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66
Q

What are the 2 subdivisions of the forebrain?

A

Telencephalon and Diencephalon

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67
Q

What are the principle structure of telencephalon?

A

Cerebral cortex
Basal ganglia
Limbic system

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68
Q

What does the cerebral cortex look like?

A

The outermost layer of the brain
Thin wrinkled layer of tissue consisting of 2 hemispheres that are connected via the corpus callosum
Crumpled up to fit into skull (area = 2500cm^2)

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69
Q

What are the 5 key structures of the cerebral cortex?

A
  • sulcus = grove
  • fissure = deep sulci
  • gyrus = bulge
  • grey matter = made up of cell bodies of neurons
  • white matter = made up of axons and dendrites
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70
Q

What are the 4 lobes of the cerebral cortex?

A

Frontal
Parietal
Occipital (FPOT)
Temporal

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71
Q

What is the function of the frontal lobe?

A

primary motor cortex

controls different areas of body

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72
Q

What is the function of the parietal lobe?

A

primary somatosensory cortex

receives external information about the senses

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73
Q

What is the function of the temporal lobe?

A

primary auditory cortex

processes auditory information

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74
Q

what is the function of the occipital lobe?

A

primary visual cortex

processes visual information

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75
Q

What divides the 4 lobes?

A

Fissures

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76
Q

Which fissure divides the frontal and temporal lobes?

A

Sylvian fissure

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77
Q

Which fissure divides the frontal and parietal lobes?

A

Central fissure

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78
Q

Which fissure divides the parietal and occipital lobes?

A

occipital fissure

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79
Q

Which fissure divides the temporal and occipital lobes?

A

Extra occipital fissure

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80
Q

What type of organisation does the motor cortex have? What does this mean?

A

Somatotopic organisation = body parts that are used more (e.g., hands, tongue) have more dedicated areas of motor cortex than those used less frequently

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81
Q

What are Brodmann areas?

A

different regions of the cerebral cortex that are defined based on their structure and organisation of cells

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82
Q

What is cytoarchitectonics?

A

the study of the cellular composition of the central nervous system’s tissues under the microscope

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83
Q

How many Brodmann areas are there?

A

47

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84
Q

Why are Brodmann areas useful?

A

They have been closely correlated to different cortical functions
e.g., areas 1, 2, and 3 = primary somatosensory cortex
e.g., area 17 = primary visual cortex
This allows people to describe exact parts of the brain for things like damage

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85
Q

What is the Limbic system?

A

A set of structure involved in learning, memory and emotion

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86
Q

What 5 structures are a part of the limbic system?

A

Limbic cortex
Hippocampus - memory and memory recognition
Amygdala - processing emotions (especially negative emotions)
Fornix
Mammillary bodies (part of hypothalamus)

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87
Q

What is the Basal Ganglia?

A

A set of structures involved in movement

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88
Q

What are the 3 structures of the Basal Ganglia?

A

Caudate nucleus
Putamen
Globus Pallidus

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89
Q

What are the principle structures of Diencephalon?

A

Thalamus

Hypothalamus

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90
Q

What is nuclei?

A

Group of neurons of similar shape

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91
Q

What is the Thalamus?

A

Main sensory relay for all senses (except smell) and the cortex
Is subdivided into different parts for processing information from the different senses

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92
Q

What is the hypothalamus?

A
  • set of nuclei involved in regulating the autonomic NS and controlling the pituitary gland
  • much of endocrine system is controlled by hormones produced in hypothalamus
  • concerned with body and regulation e.g., fighting, feeing, fleeing and mating
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93
Q

What is the subdivision of the midbrain?

A

Mesencephalon

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94
Q

What are the principle structures of mesencephalon?

A

Tectum

Tegmentum

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95
Q

What are the 2 structure of the Tectum

A

superior colliculi

inferior colliculi

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96
Q

What is the superior colliculi?

A

the subcortical sensory pathway involved in fast eye movements (vision)

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97
Q

What is the inferior colliculi?

A

Part of the auditory pathway

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98
Q

What is the role of the Tegmentum?

A

Role in motor movement

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99
Q

What are the 3 structures of the Tegmentum?

A

Reticular formation
red nucleus
substantia nigra

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100
Q

What is the subdivisions of the the hindbrain?

A

Metencephalon and myelencephalon

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101
Q

What are the principle structures of metencephalon?

A

Cerebellum

Pons

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102
Q

What is the cerebellum?

A

mini brain

involved in motor coordination and smooth execution of movement

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103
Q

What is Pons?

A

Part of the reticular formation
Involved in sleep and arousal
It is the link between the cerebellum and cerebrum

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104
Q

What is the principle structure of myelencephalon?

A

Medulla oblongata

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105
Q

What is the medulla oblongata function?

A

Involved in basic life functions

e.g., breathing, swallowing, vomiting, coughing, sneezing, heart rate, wake-sleep cycles

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106
Q

What is the structure of the spinal cord?

A

Grey matter in middle, surrounded by white matter

Butterfly like structure with wings facing towards body

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107
Q

What is the function of the spinal cord?

A

Communicates with sense organs and muscles below head level

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108
Q

What are the primary components of the spinal cord?

A

Dorsal roots and ventral roots

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109
Q

What are dorsal roots?

A

Carry sensory information to CNS = afferent

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110
Q

What are ventral roots?

A

Carry motor information to muscles and glands away from CNS = efferent

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111
Q

What is the peripheral NS?

A

Located outside skull and spine
Bring information into CNS and carries signals out of CNS
contains somatic NS and autonomic NS

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112
Q

What is the somatic NS?

A

Control movement of skeletal muscles

transmits somatosensory information to CNS

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113
Q

What is somatic NS made of?

A

cranial nerves and spinal nerves

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114
Q

What are afferent nerves?

A

Carry information towards CNS

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115
Q

What are Efferent nerves?

A

Carry motor information to muscles and glands and away from CNS

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116
Q

How many cranial nerves are there?

A

12

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117
Q

What are cranial nerves?

A

Attached to ventral surface of brain
control sensory and motor functions of head and neck
some are efferent and some are afferent

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118
Q

What are spinal nerves?

A

Peripheral nerves attached to spinal cord

Are efferent and afferent and travel to muscles and sensory receptors

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119
Q

What is the autonomic NS?

A

Controls body’s vegetative functions e.g., heart
regulation of smooth muscles, cardiac muscles and glands
all nerves are efferent

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120
Q

What is the autonomic NS made up of?

A

Sympathetic NS and Parasympathetic NS

These divisions have opposite effects

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121
Q

What is the sympathetic NS?

A

Fight or flight
arousal and preparing body for expenditure of energy
e.g., increased: heart rate, breathing and gland secretion

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122
Q

What is the parasympathetic NS?

A

Rest and restore
relaxing body
opposite effect of sympathetic NS

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123
Q

What type of cell makes up the NS?

A

The neuron

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124
Q

What does the neuron do?

A

Support cognitive functioning

Transmits and processes information

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125
Q

What are the key structure of a neuron

A 
Dendrites
Axons
Soma (cell body)
Myelin sheath
Terminal buttons
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126
Q

What are the 3 types of function of neurons

A

Sensory - detect changes in external and internal environment
Motor - control muscle contraction and gland secretion
Interneurons - lie within CNS and are involved in cognition

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127
Q

What are the 2 types of interneurons?

A

Local and projection

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128
Q

What are the different types of structures of neurons?

A

Multipolar neuron - 1 axon, many dendrites attached to soma
Bipolar neuron - 1 axon, 1 dendrite attached to soma
Unipolar neuron - 1 axon attached to soma, axon divides with one branch receiving sensory information and another sending sensory information to CNS

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129
Q

How did early anatomists discover neurons

A

Golgi staining technique

Cajal used this to find pyramidal cells

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130
Q

How many types of multipolar cells are there? What are they?

A

3

Motor neuron, pyramid cell, Purkinje cell

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131
Q

What are Glial cells? Where are they found?

A

Supporting cells that glue the NS together

Found in CNS

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132
Q

What are the 4 types of glial cells?

A

Oligodendrocytes
Astrocytes
Microglia (modified immune cells)
Ependymal

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133
Q

What do oligodendrocytes form?

A

Myelin sheath

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134
Q

What do astrocytes form, help form, secrete and take up?

A

form support for CNS
help form blood-brain barrier
secrete neurotropic factors
take up K+ neurotransmitters

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135
Q

What does microglia act as?

A

Scavengers

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136
Q

What does ependymal cells create? What are they?

A

Create barriers between compartments

are sources of neural stem cells

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137
Q

What does the microglia do?

A

Control immune response of the brain

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138
Q

What do oligodendrocytes do?

A

support axons and produce myelin sheath which provides insulation and is made of lipids

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139
Q

What are the nodes of Ranvier?

A

Bare part of axon

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140
Q

How many Schwann cells wrap round axon in CNS and PNS?

A 
CNS = many
PNS = one
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141
Q

What do astrocytes do?

A

“star cells”
provide physical support to neurons
provide nourishment by taking glucose from bloodstream and breaking it down for neurons
clean up debris and form scar tissue when neurons die
control chemical composition of fluid surrounding neurons

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142
Q

What is the blood-brain barrier?

A

A semipermeable barrier between CNS and circulatory system which helps to regulate flow of nutrient rich fluid into the brain

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143
Q

Are all areas of blood-brain barrier equally permeable? Give an example

A

No
Area Postrema - region of medulla where blood-brain barrier is weak. Allows toxins in the blood to stimulate this area - initiates vomiting so poison is expelled from body

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144
Q

Give an example of a useful behaviour that only involves neurons, How does it work?

A

Reflexes e.g., withdrawal reflex
sensory –> interneuron –> motor
happens in Spinal cord

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145
Q

What is a membrane potential?

A

electrical charge across cell membrane
the difference in electrical potential in and out of cell
stored up source of electrical energy

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146
Q

What is resting potential?

A

Membrane potential of neuron when it isn’t being altered by excitatory/inhibitory postsynaptic potentials
about 70mV

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147
Q

What is depolarisation?

A

Reduction of the negative charge (toward 0) of membrane potential when we stimulate neuron

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148
Q

What is action potential?

A

brief electrical impulse that provides the basis for conduction of information along an axon
results from movement of ions through membrane

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149
Q

What is the threshold of excitation?

A

The value of the membrane potential that must be reached to produce an action potential

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150
Q

What is hyperpolarisation?

A

increase in the membrane potential of a cell

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151
Q

What are the 2 forces that membrane potentials go through to remain balanced?

A

Diffusion and electrostatic pressure

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152
Q

What is intercellular and extracellular fluids?

A 
Intercellular = fluid within cells
Extracellular = fluids outside cells
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153
Q

Draw the process on diffusion and electrostatic pressure across a cell membrane
Involve Na+, K+, Cl- and A- ions

A

drawing on Wk 3 Lecture 3 notes

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154
Q

How can Na+ be found outside of cell when both diffusion and electrostatic pressure push it inside?

A

Sodium-potassium pump

a protein that is an active transporter - pumps 3 sodium ions out and 2 potassium ions in

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155
Q

What type of ion channel allows ions to move through membrane? How does it work?

A

Voltage dependent (gated) ion channels - a protein that allows flow of specific ions, opens and closes depending on charge that arrives to it

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156
Q

What 6 stages explain how voltage dependent ion channels work for Na+ and K+ ions

A
  1. depolarisation starts, threshold of excitation is reached, Na channel opens, changes membrane potential from -70 to +40 mV
  2. K channels open after slight delay
  3. Na channels become blocked when AP reaches peak (40mV) - no more can enter
  4. K+ ions move out of cell, bring membrane potential back to resting potential
  5. K channel closes, Na channel resets
  6. membrane potential overshoots its resting -70mV and hyperpolarisation occurs as a result of extra K+ ions outside of axon. These diffuse away and resting membrane potential is restored
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157
Q

What is the all or none law?

A

once AP begins, it proceeds without decrement to terminal buttons (either occurs or doesn’t)

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158
Q

What is rate law?

A

variations in the intensity of a stimulus are represented by variations in the rate at which that axon fires
rate of firing causes stronger muscles contraction

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159
Q

Is the all or none law supplemented by rate law?

A

Yes

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160
Q

What is saltatory conduction?

A

conduction of APs by myelinated axons

AP appears to jump from one node of Ranvier to next

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161
Q

What are the 2 advantages of saltatory conduction?

A

economy - less energy used by the Na-K pump (located only at nodes of Ranvier)
speed - conduction much faster in myelinated axon

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162
Q

What is the synapse?

A

junction between 2 neurons

primary means of communication between 2 cells

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163
Q

What is the synaptic cleft?

A

Narrow gap (20nm) between neurons

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164
Q

can action potential cross the synaptic cleft?

A

No - are carried by neurotransmitters (chemical components)

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165
Q

What is the pre-synaptic neuron?

A

neuron sending impulse

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166
Q

What is the post-synaptic neuron

A

neuron receiving impulse

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167
Q

Where are neurotransmitter made and stored?

A

made in pre-synaptic neuron

stored in synaptic vesicles at end of axon

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168
Q

What are neuroreceptors?

A

chemical gated ion chemicals on the membrane of the post-synaptic neuron

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169
Q

Do neuroreceptors have specific binding sites for neurotransmitters?

A

yes

neurotransmitters fit binding sites with lock and key mechanism

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170
Q

What are the 2 ways that transmitter-dependent ion channels can be opened?

A

direct - inotropic receptor - opening from outside

indirect = metabotropic receptor - opening from inside (like ringing a bell to get attention)

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171
Q

Is the exposure of a neurotransmitter to a receptor prolonged or brief?

A

brief

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172
Q

How are molecules of neurotransmitters destroyed?

A

Enzymes

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173
Q

What is an excitatory postsynaptic potential (EPSP)?

A

excitatory depolarisation of postsynaptic membrane

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174
Q

What is inhibitory postsynaptic potentials (IPSP)?

A

inhibitory hyperpolarisation of postsynaptic membrane

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175
Q

How is the nature of a postsynaptic potential determined?

A

determined by postsynaptic receptors

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176
Q

What are the 3 major types of ion channels and do they exhibit EPSP or IPSP?

A 
Na+ = EPSP
K+ = IPSP
Cl- = IPSP
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177
Q

What is neural integration?

A

process by which inhibitory and excitatory postsynaptic potentials summate and control the rate of firing of a neuron

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178
Q

What type of effect do most neurotransmitters have?

A

Both excitatory and inhibitory

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179
Q

Which 2 neurotransmitters get most of the synaptic communication done?

A 
glutamate = excitatory effects
GABA = inhibitory effects
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180
Q

Which neurotransmitter mainly does synaptic communication in the spinal cord? What is its effect?

A

Glycine = inhibitory effect

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181
Q

What are most neurotransmitters responsible for?

A

Having modulating effects

Tend to activate/ inhibit entire circuits of neurons that are involved in particular brain functions

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182
Q

What is psychopharmacology?

A

Study of effects of drugs on NS and behaviour

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183
Q

What are drug effects?

A

The changes a drug produces in an animal’s physiological processes and behaviour

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184
Q

What do most drugs affect in the NS?

A

Synaptic transmission

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185
Q

What is an antagonist?

A

drug that inhibits effects of neurotransmitter on postsynaptic cell

186
Q

What is an agonist?

A

Drug that facilitates effects of neurotransmitter on postsynaptic cell

187
Q

Where is Acetylcholine secreted?

A

secreted by efferent axons on CNS

188
Q

What roles does Acetylcholine have?

A

All muscular movement achieved by its release
Involved in regulating REM sleep
Facilitating effects

189
Q

Where is Acetylcholine found?

A

Found at the target of parasympathetic branch of ANS

190
Q

Is Acetylcholine an antagonist or agonist?

A

Antagonist - prevents release by terminal buttons

191
Q

What does Acetylcholine bind to?

A

Nicotinic and muscarinic receptors

192
Q

What are nicotinic receptors?

A

An ionotropic acetylcholine receptor stimulated by nicotine

193
Q

What are nicotinic receptors blocked by?

A

Curare

acts at the junction between nerve cells and muscles causing paralysis

194
Q

What are muscarinic receptors?

A

Metabotropic acetylcholine receptors that produce parasympathetic nerve effects in the heart, smooth muscles and glands

195
Q

What are muscarinic receptors blocked by?

A

Atropine
acts by preventing ACh from depolarising the postsynaptic membrane in the parasympathetic branch
used in treatment of low heart rate

196
Q

What neurotransmitters are the Monoamines made up of? Why is this?

A

Dopamine, norepinephrine, epinephrine and serotonin

Have similar molecular structure so some drugs affect the activity in all of them to a degree

197
Q

What do the Monoamines regulate?

A

Mood

198
Q

How does Tyrosine become norepinephrine through an enzyme?

A

Tyrosine –> L-DOPA –> Dopamine –> Norepinephrine

199
Q

What does dopamine regulate?

A

Reward processing, energy, addiction pathways

200
Q

Describe study on rats and reward pathway

A

If reward pathway was directly stimulated by drugs (e.g., cocaine, heroin), rats would self-administer these drugs more compared to when there drugs were injected in the body’s periphery

201
Q

What are natural rewards in the reward pathway?

A

Food, sex, water, nurturing

202
Q

What is addiction?

A

A state in which an organism engages in compulsive behaviour, behaviour is reinforcing, loss of control for intake
This starts in the midbrain

203
Q

What is tolerance?

A

A state in which organism no longer responds to a drug –> higher dosage required to get same effect

204
Q

What is dependence?

A

A state in which organism functions normally only in presence of a drug –> manifested as physical disturbance when drug is withdrawn

205
Q

Are dependence and addiction intertwined?

A

Normally happen together but not always as they follow different circuits in the brain
e.g., a patient may be dependent on morphine but not addicted to it

206
Q

How does cocaine increase activation on the reward system?

A

cocaine binds to cocaine binding sites
dopaminergic synapse in nucleus accumbens
effect of cocaine = inhibition of dopamine reuptake
increased activation of reward system

207
Q

What do PET scans show about cocaine usage?

A

Glucose reduction in metabolic activity

208
Q

Does dopamine also regulate movement and control attention?

A

YES

209
Q

What is the nigrostriatal system?

A

starts in substantia nigra and ends in basal ganglia - plays a role in controlling movement

210
Q

What disease comes as a result of the degeneration of the nigrostriatal system? How is it treated?

A

Parkinson’s disease

Treated with L-DOPA

211
Q

What does serotonin (5-HT) regulate?

A

mood, eating, sleeping, dreaming, arousal
pain
memory and learning, temperature regulation, behaviour, cardiovascular function, muscle contraction, endocrine regulation and depression

212
Q

Where does serotonin start and what pathway does it take?

A

Starts in Raphe nuclei

The goes to spine or through midbrain

213
Q

What are low levels of serotonin associated with?

A

Depression

214
Q

How can serotonin treat depression?

A

SSRIs increase serotonin levels at the synapse by blocking the reuptake of serotonin into the presynaptic cell

215
Q

What effects does LSD have on the body?

A

Stimulates sympathetic NS in midbrain

pupillary dilation, increased body temp, raised blood sugar levels

216
Q

What effects does MDMA have on the body?

A

Serotonergic agonist = excitatory and hallucinogenic effects

217
Q

What effects does MDMA have on serotonin transporters in the short term and long term?

A 
ST = prevents reuptake, brings more serotonin to synapse - feeling warm, empathetic, energetic, low appetite
LT = lack of serotonin in pre-frontal cortex (animal studies), impairments of verbal and visual memory
218
Q

Is norepinephrine (NE)/ noradrenaline a hormone and neurotransmitter?

A

YES

219
Q

How does norepinephrine (NE)/ noradrenaline work as a hormone?

A

Secreted by adrenal gland, works with epinephrine/adrenaline to give body energy when stressed (fight/flight response)

220
Q

Can norepinephrine (NE)/ noradrenaline be an effective treatment for depression?

A

Yes if the mediation inhibits the reuptake of it

221
Q

What does elevated levels on norepinephrine (NE)/ noradrenaline indicate?

A

Mania

222
Q

What is epinephrine/ adrenaline?

A

hormone secrete by adrenal medulla

It is a neurotransmitter in the brain

223
Q

What is the name given to the most common neurotransmitters in the CNS
What is this group made up of

A

Amino acids

Glutamate, GABA, Glycine

224
Q

Where is glycine found?

A

In the spinal cord

225
Q

What is glutamate? What does it bind to?

A

Most important excitatory neurotransmitter in brain

Bind to NMDA receptor = specialised ionotropic glutamate receptor

226
Q

What is GABA?

A

Most important inhibitory neurotransmitter in brain
critical to how we think and act = fine-tune our moods, thoughts and actions
Its inhibitory effect is needed to block out excessive brain activity (like car brakes)

227
Q

What can imbalances of GABA lead to?

A

BD, Sz, anxiety disorder

228
Q

What is an indirect agonist for GABA A receptor?

A

Benzodiazepines –> anxiolytic drug which has a tranquilising effect

229
Q

Where does dopamine start?

A

ventral tegmental area

230
Q

What is a stressor?

A

a situation that causes stress to a system e.g., aversive events

231
Q

What is stress reactivity?

A

the way we respond to a stressor

232
Q

How does our body change when stressed?

A

changes in breathing –> increased risk of asthma attack, hyperventilation leading to increased risk of panic attack
exacerbates existing MH conditions
changes in eating behaviour
diarrhoea/constipation (changes in digestion)

233
Q

What are some symptoms of chronic stress?

A

muscles tense up = constant state of guardedness
tension-type headaches and migraines
long term heart/blood problems e.g., hypertension, heart attack

234
Q

What did a longitudinal study into chronic stress find?

A

chronic stress measured at baseline increased likelihood of stroke over the follow-up period

235
Q

Who founded the fight/flight response? How did it come about?

A

Cannon - work with rats saw peristalsis would stop when they were stressed

236
Q

What is peristalsis?

A

rhythmic wave of movement that pushes food through oesophagus and intestine

237
Q

What is an example of an acute and chronic physical cause of stress?

A 
acute = injury
chronic = hunger, cancer
238
Q

What is an example of an acute and chronic psychological cause of stress?

A 
acute = deadline
chronic  = chronic work pressure
239
Q

What is an example of an acute and chronic social cause of stress?

A 
acute = humiliation
chronic = chronic isolation
240
Q

True or false? Stress via cortisol can directly suppress activity of the immune system?

A

True

241
Q

Give 3 examples of studies that show the effects of cortisol on the immune system

A
  1. ) when adrenal gland is removed from rats there is no change to immune system when shocked however there is a change when adrenal gland is intact
  2. ) wounds take longer to heal in caregivers compared to a CG
  3. ) immune systems response is weakened for med students during exam period compared to 1 month prior
242
Q

What are the 3 components of the HPA Axis?

A

hypothalamus
pituitary gland
adrenal gland

243
Q

How does the HPA axis work?

A

hypothalamus releases CRH into bloodstream
pituitary gland detects circulation of CRH and releases ACTH into bloodstream
adrenal gland detects circulation of ACTH and releases cortisol into bloodstream

244
Q

What are the functions of cortisol?

A

anti-inflammatory
helps regulate BP and blood sugar
manages body’s use of carbohydrates, fats and proteins
acts on hypothalamus to deregulate release of CRH and ACTH to prevent a continuous cycle
has a slowed effect on body (peaks around 10-30 mins after relsease)

245
Q

What is Selye’s General Adaptation Syndrome?

A

Chronic exposure to stressor leads to 3 stages:
Alarm
Resistance
Exhaustion

246
Q

What happens in the alarm stage of Selye’s General Adaptation Syndrome?

A

arousal of ANS –> happens during first encounter with stressor
potential for shock
SNS is activated
Adrenaline and cortisol released

247
Q

What happens in the resistance stage of Selye’s General Adaptation Syndrome?

A

continued exposure to stressor
PNS returns physiological functions to normal
over time resistance to stressor increases
adaption to environmental stressors

248
Q

What happens in the exhaustion stage of Selye’s General Adaptation Syndrome?

A

stressor continues beyond body’s capacity
stressor depletes available resources
loss of ability to adapt to situations
susceptible to illness and death

249
Q

What are 3 examples of studies that show the effects of prenatal stress?

A

WW2 pregnant Dutch women had children (foetus) who learned that food was scare and so their metabolism shifted to store consumed food
Finnish study on BW found that lower BW = higher basal cortisol levels in adults
Prenatally stressed rats showed greater evidence of anxiety and their amygdala’s’ showed greater glucocorticoid receptors

250
Q

What did a study on postnatal stress find? (rats)

A

rats showed greater glucocorticoid response to stress

stress in infancy reduced growth hormones leading to lower adult height

251
Q

What did a study on Romanian orphanages and stress find?

A

the longer children remained in orphanages (>8 months) the higher their levels of cortisol

252
Q

Where is noradrenaline released from? Can it enhance the function and retrieval of memory?

A

Released from Locus Coeruleus

Yes

253
Q

Can chronic stress change your brain structure?

A

Yes

Neurons in the hippocampus of rats have a reduced structure as a result of stress

254
Q

What was the result of brain activity when people with snake phobias chose to move the snake closer to them?

A

reduced amygdala activity

255
Q

What was the result on the amygdala when ppts incidentally viewed fearful faces?

A

more active

256
Q

What is the medial prefrontal cortex? When does its activity increase?

A

the midline of the brain, in front of the motor cortex

increased activity when trying to regulate stress

257
Q

How is emotion regulation like a balancing act?

A

bottom-up signalling from amygdala indicates threats in environment
top-down regulation from the medial pre-frontal cortex prevents this from triggering constant stress responses

258
Q

Is information that is encoded during a stressful event well remembered?

A

Yes, particularly if the information is relevant to the stressor
Normally adaptive but dysregulation could result in psychological trauma

259
Q

Give an example of results of a stress at encoding study

A

during stress there is lower activity in hippocampus at encoding leading to a better memory

260
Q

Give an example of results of a stress at consolidation study

A

stress enhances consolidation of emotional pictures but not neutral pictures

261
Q

Give an example of results of a stress at retrieval study

A

memory retrieval during stress is impaired

262
Q

What is cognitive appraisal theory?

A
  1. ) primary appraisal –> is the situation relevant to someone’s needs?
  2. ) secondary appraisal –> whether a person has the resources to cope with the event
263
Q

What are the 3 patterns of conflict within the individual?

A
  1. ) approach - approach conflicts = least stressful, choosing between pleasant options
  2. ) avoidance - avoidance conflicts = choosing between equally negative options
  3. ) approach - avoidance = equally challenging, need to decide to do something that could have either positive or negative effects
264
Q

What is eustress?

A

seeking out stressful experiences e.g., riding a rollercoaster

265
Q

How is dopamine involved in stress?

A

involved in motivation to seek out a reward

Greatest release in the anticipation of the event

266
Q

What are the 3 components of emotional response?

A
  1. ) behavioural
  2. ) autonomic
  3. ) hormonal
267
Q

What integrates the behavioural, autonomic and hormonal emotional responses?

A

the amygdala

268
Q

does the amygdala have a role in physiological and behavioural reaction to objects and situations with biological consequences?

A

yes

269
Q

what role does the lateral nucleus have in emotions?

A

receives sensory information from hippocampus

projects to different brain areas

270
Q

what role does the central nucleus have in emotions?

A

receives signals from lateral nucleus
sends signals to hypothalamus, midbrain, pons, medulla
when threatening stimuli is perceived, neurons in central nucleus become activated

271
Q

What evidence shows that the central nucleus becomes activated when threatened?

A
  1. ) damage to central nucleus –> monkeys show less fear, are more tame, have lower stress levels
  2. ) stimulation to central nucleus –> demonstrates fear response and can lead to stress related illnesses if exposure is prolonged
272
Q

What are the 2 types of fear responses?

A
  1. ) Automatic fear responses –> automatic activation of central nucleus e.g., loud noises, heights
  2. ) Conditioned emotional responses –> learned danger e.g., CC
273
Q

What does CER do to the brain?

A

physical changes responsible for establishing a CER occur in lateral nucleus
lateral nucleus communicates with central nucleus = behavioural, autonomic and hormonal responses

274
Q

Does excitation = forgetting? (CER)

A

no
instead learns that the association is no longer there –> conditioned response inhibited
vmPFC plays a role in inhibiting these responses

275
Q

What evidence shows the vmPFC plays a role in inhibiting conditioned responses?

A

stimulation to vmPFC inhibits CER
excitation training activates vmPFC
lesions to vmPFC impair excitation

276
Q

What are CERs like in humans?

A
  1. ) little albert –> conditioned fear of white rats
  2. ) amygdala stimulation –> humans reported being more afraid
  3. ) activity of vmPFC correlates with extinction
277
Q

How are CERs acquired in humans?

A
  1. ) socially

2. ) through instruction

278
Q

What did a case study about a woman with localised damage to the amygdala show?

A

fear conditioning was severely impaired
showed approach rather than avoidance behaviours
led to her being victim of many crimes and ultimately dying

279
Q

What are the 2 main reasons for anger?

A

reproduction

self defence

280
Q

What are the 3 parts of the neural control for aggressive behaviours?

A

hierarchal system

  1. ) sensory system –> perceives threat, relays information to hypothalamus and amygdala
  2. ) hypothalamus and amygdala –> control activity of circuits in brain stem
  3. ) neural circuits in the brain stem –> control the particular movements that an animal makes when attacking/ defending
281
Q

What is the role of serotonin in aggressive behaviour?

A

high levels = aggression inhibition

low levels = aggressive attacks

282
Q

How are serotonin levels measured?

A

serotonin breaks down into 5-HIAA which ends up in CSF and can be measured
high levels of 5-HIAA in CSF = high levels of serotonin

283
Q

What studies show the link between serotonin and risk-taking behaviour?

A

1.) monkeys with low levels of 5-HIAA had increased risk taking behaviour and were more likely to die than those with high levels

284
Q

What studies show the link between serotonin and aggression?

A
  1. ) selective breeding lead to animals with high levels of 5-HIAA being tamer and friendlier
  2. ) in humans low 5-HIAA is associated with antisocial behaviour
  3. ) role of heredity –> higher concordance between MZ twins than DZ twins on measures of antisocial behaviour
285
Q

What is Prozac an example of?

A

a serotonin agonist –> reduces irritability and aggressiveness

286
Q

What is the role of vmPFC in aggression?

A

controls emotion regulation and inhibition of emotional responses
impulsive violence is thought to be the consequence of faulty emotional regulation

287
Q

What is inputted and outputted to vmPFC?

A

input to vmPFC –> information about environment, what plans are being made by the rest of the frontal lobes

output of vmPFC –> affect a variety of behaviours and physiological responses including emotional responses organised by the amygdala

288
Q

What 2 case studies show the role of vmPFC in emotion regulation?

A

1.) Phineas Gage –> damage to prefrontal region (including vmPFC) led to a personality change where he was more aggressive
resulted in problems with planning, moral judgments and emotional control
2.) EVR –> removal of vmPFC led to bankruptcy, being unable to keep a job, disorganised and late, marriage broke down despite seeming initially fine after surgery
was unable to distinguish between trivial and important decisions
had intact cognitive abilities but poor utilisation of these abilities in real life contexts

289
Q

What did a study following the findings of EVR show?

A

informant rating of emotional dysfunction and real-world difficulties significantly correlated for patients with damage to vmPFC but their cognitive abilities were intact

290
Q

What studies show that vmPFC is involved in moral decision making?

A

neuroimaging evidence –> moral problems activate vmPFC, non-emotional decisions don’t
vmPFC damage evidence –> vmPFC patients chose logical decisions in personal moral dilemmas

291
Q

True or False?
vmPFC is the interface between brain mechanisms involved in autonomic emotion response and those involved in the control of complex behaviour
What evidence shows this?

A

true
evidence –> decreased prefrontal activity and increased subcortical activity (including amygdala) in impulsive and emotional murderers but cold-blooded and calculating murderers had prefrontal cortex levels closer to normal

292
Q

What is link between the prefrontal cortex volume and serotonin activity?

A

PFC receives projection of serotonergic axons

serotonergic input to PFC activates this region

293
Q

What is the James-Lange theory of emotion?

A

emotion producing situations elicit:

  1. ) physiological responses e.g., trembling
  2. ) certain behaviours e.g., running away
  3. ) feedback from the organs and muscles involved in those responses constitute how we feel emotion –> emotional feeling based on what we find ourselves doing
294
Q

What is a limitation of the James-Lange theory of emotion?

A

it is hard to test because it refer to feelings which are private events

295
Q

What evidence is there for the James-Lange theory of emotion?

A
  1. ) fear and anger greatly reduced in those with higher levels of paralysis (critiques - experimenter bias, measurements lack validity and reliability, sample was unique so unrepresentative, no control group)
  2. ) simulated emotions alter activity of ANS –> different facial expressions produce different patterns of activity
  3. ) ppts who received Botox showed less negative mood compares to others
  4. ) holding pen between teeth = smile, between lips = frown, smiles found a cartoon funnier (lacks replicability)
  5. ) recalling emotions activates somatosensory cortex and upper brain stem nuclei which are areas involved in the control of internal organs and detection of sensations received from them
296
Q

What is the Cannon-Bard theory of emotion?

A

thalamus sends simultaneous signals to cortex and ANS so autonomic arousal and conscious emotion happen at the same time

297
Q

What evidence is there for the Cannon-Bard theory of emotion?

A

cats with severed nerves in ANS can’t experience somatic signals but could still demonstrate emotions such as fear, anger and pleasure

298
Q

What did Darwin believe about emotional expressions and how did he conclude this?

A

believed emotional expressions were innate and biologically determined
concluded this through observations of his own children and corresponding with people in isolated cultures around the world

299
Q

Give 2 examples of cross cultural studies of emotion and what conclusions can be made from these?

A
  1. ) people in the New Guinea tribe could recognise western emotional expressions
  2. ) tribesmen produced facial expressions based on stories which westerners could then identify correctly

conclusions –> expression of emotions are unlearned as they are the same in cultures that haven’t been exposed to each other

300
Q

What does research with visually impaired people suggest about emotion? Give 2 examples and conclusion

A
  1. ) facial expressions of children who are blind are very similar to those of sighted children
  2. ) few differences in emotional expressions of congenitally blind, noncongenitally blind and sighted athletes in 2004 Paralympics

Conclusion –> emotion expression is innate - doesn’t require learning by imitation

301
Q

What study shows that vocal emotion is cross cultural? What did this study conclude?

A

English and Himba speaking people listened to vocalisations of the others culture and matched these to the story given
Both could correctly identify vocalisations of the others culture on an above average level

Conclusions –> can universally recognise emotional content of vocalisations

302
Q

What study shows that emotions are more pronounced in groups than when alone?

A

e.g., when bowling:
small sign of happiness when alone
much more likely to smile if ppt were interacting socially with others

infants, as young as 10 mn, smile more when in presence of an audience

Conclusions –> emotions depend on social context

303
Q

What study demonstrated recognition of facial expression?

A

ppts can accurately recognise the emotion of facial expressions even if only presented briefly
when given more time there was little improvement to the classification of the emotions

conclusion –> recognise facial expressions automatically, rapidly and accurately

304
Q

What study demonstrated recognition of body language?

A

ppts are faster and more accurate at identifying emotion when face and body language were congruent rather than incongruent

Conclusion –> perception of emotion in others is based on multiple cues

305
Q

Is there laterality of emotion recognition? What evidence is there?

A

RH plays more important role than LH in emotion comprehension:

  • meaning of words = bilateral activation of PFC
  • tone of voice = right lateralised activation of PFC

Conclusion –> meaning of words and tone of voice are independent functions

306
Q

What case study provides evidence for the idea that comprehension of meanings of words and tone of voice are independent?

A

pure word deafness (auditory verbal agnosia) = impaired speech comprehension
all other abilities were intact
shows meaning and tone recognition are separate –> here can understand tone but not meaning

307
Q

What role does the amygdala play in facial emotion recognition?

A

plays role in emotional responses and recognition

particularly fear recognition

308
Q

What evidence shows that the amygdala is important for fear recognition?

A
  1. ) large increase in activity when viewing fearful faces and body posture, only small increase for happy faces
  2. ) speed of activity quicker than conscious visual processing
  3. ) amygdala lesion = problems recognising facial expression –> fear recognition particularly impaired
309
Q

Is the amygdala important in vocal emotion recognition? What evidence is there?

A

may not be as critical as it is for facial expressions
case studies:
1.) SM –> localised bilateral damage - could recognise emotion in voice despite being unable to recognise emotion in face –> amygdala doesn’t play role in vocal recognition
2.) RH –> bilateral amygdala damage and damage to surrounding structures - normal prosody perception on most but not all measures –> surrounding areas partly important for vocal emotion recognition

310
Q

What is the simulationist hypothesis? What evidence is there?

A

= emotion recognition involves simulation of emotion that we are viewing

  1. ) neuroimaging studies –> brain regions that are activated in response to observing emotion are similar to the regions activated when making emotional expressions
  2. ) TMS study –> disruption in either visual or somatosensory (stops feedback from own face) areas impaired peoples ability to recognise facial expression of emotion
311
Q

What study shows that imitation is important in emotion recognition?

A

ppts who were poorest at facial emotion recognition had damage to right somatosensory cortex
ppts with somatosensory impairments also had impairments in emotion recognition

Conclusions –> we see facial expression of emotion and then unconsciously imagine ourselves making that expression

312
Q

Where are mirror neurons located?

A

in the ventral premotor cortex of frontal lobe

313
Q

When are mirror neurons activated?

A

when an animal performs a particular behaviour (important role in control of movement)
When an animal sees another animal performing that behaviour

314
Q

What is the role of mirror neurons?

A
  • helps us to understand what another person is trying to accomplish
  • activation when observing facial movements of others helps us understand how other people feel
315
Q

What evidence is there for mirror neurons?

A

Mobius Syndrome –> facial paralysis caused by defective development of nerves in facial muscles

  • cannot express emotion and have difficulty recognising emotion in others
  • possible that inability to produce facial emotions –> hard to imitate expressions of others –> lack of internal feedback from motor system to somatosensory cortex –> recognition is hard
316
Q

Is the expression of emotions automatic?

A

Kind of

not easy to produce a realistic facial expression of emotion if we don’t really feel that way

317
Q

What are Duchenne smiles?

A

fake smiles involve contraction of mouth muscles only

real smile also involve muscles near eyes

318
Q

What does method acting do to expression of emotion?

A

imaging a situation that produced a genuine desired emotion allows actors to convincingly portray facial emotions

319
Q

What evidence is there for the automaticity of facial expression?

A
  1. ) volitional facial paresis –> difficulty in moving facial muscles voluntarily but no difficulty expressing genuine emotion with those muscles
    - damage = face region of the primary motor cortex or its subcortical connections
  2. ) emotional facial paresis –> lack of movement of facial muscles in response to genuine emotions but no difficulty in moving facial muscles voluntarily
    - damage = insular PFC, subcortical white matter of frontal lobe or parts of thalamus

= different areas of brain responsible for voluntary and genuine movements

320
Q

What is the laterality of emotion expression?

A

RH has role in recognition of facial expression, vocal emotion and expression of emotions

321
Q

What is the laterality of emotion expression?

A

RH has role in recognition of facial expression, vocal emotion and expression of emotions

322
Q

What evidence is there for RH having a role in recognition of facial expression?

A
  1. ) left halves of faces are more expressive than right halves
  2. ) observation - people tend to make stronger expressions on left side than right
  3. ) Lit review - 48 other studies support above findings
323
Q

What evidence is there for RH having a role in vocal emotion?

A
  1. ) RH lesions impair both facial and vocal expansion of emotions
  2. ) LH lesions usually don’t impair expression of vocal emotion
    - exception = Wernicke’s aphasia –> speech is meaningless but modulate voice according to mood
324
Q

What evidence is there for RH having a role in expression of emotions?

A

amygdala only involved in recognition of facial emotions, not expression
case study –> bilateral amygdala damage
1.) facial affect recognition task –> great impairment in fear recognition in faces
2.) lexical affect recognition task –> normal on all emotions
3.) facial affect generation tasks –> normal/ above normal for all expression types

Conclusion –> impairment to recognition not expression

325
Q

What is measured in sleep research?

A

EEG - brain activity
EMG - muscle activity
EOG - eye movements
HR, respiration, skin conduction

326
Q

What are the 2 basic patterns of brain activity in wakefulness?

A

Beta (13 - 30 Hz) –> alert, attentive, active thinking, many neural circuits processing info
Alpha (8 - 12 Hz) –> resting, not engaged in mental activity, usually eyes closed

327
Q

What are the stages of sleep?

A

Stage 1 and 2 REM sleep (theta, 3.5 - 7Hz)

Stage 3 and 4 (Delta <3.5 Hz)

328
Q

What is stage 1 sleep?

A 
theta
firing of neurons in neocortex = more synchronised 
transition between sleep and wakefulness
drowsy
approx 10 minutes
329
Q

What is stage 2 sleep

A

theta
approx 15 mins
if woken during this they will say they haven’t been asleep

330
Q

What are sleep spindles?

A

short bursts of waves 12-14HZ
occur 2 - 5 times a minute during sleep
high numbers of these have been associated with higher intelligence

331
Q

What are k complexes?

A

sudden sharp wave forms in stage 2
associated with consolidation of memories
forerunner of delta waves

332
Q

What is stage 3 and 4 sleep (SW sleep)?

A

delta
stages 3 and 4 are split by level of delta activity (20-50% vs 50+%)
loud noises wake people up and they will be confused and grogy
slow wave oscillations

333
Q

What are slow wave oscillations?

A 
< 1 Hz
Down state (off) --> neurons rest
Up state (on) --> neurons briefly fire at high rate
334
Q

What is REM sleep?

A 
theta
desynchrony --> rapid and irregular 
we dream
people react to meaningful stimuli e.g., their name
if woken = attentive and alert
335
Q

What physiological changes occur during REM sleep?

A

rapid eye movements
muscular paralysis
body temp regulation stops
brain is active –> increased blood flow and oxygen

336
Q

what is sleeping with one hemisphere like in humans?

A

usually in a novel env. and have trouble sleeping
LH is more vigilant than RH
Disappears by day 2

337
Q

Do animals sleep with 1 hemisphere?

A

Some do e.g., dolphins

338
Q

What are the functions of slow wave sleep?

A

allows brain to rest
metabolic rate and blood flow falls by 75%
people are unresponsive, confused if woken –> suggests cerebral cortex “shuts down”

339
Q

What happen if someone suffers from slow wave sleep deprivation?

A

affects their cognitive, especially attention, but not physical abilities

340
Q

What is the rebound phenomenon?

A

if deprived of REM one night, more REM will take place the next night

341
Q

Is it possible to function normally without REM sleep?

A

Yes and many people do such as those on antidepressants or those with brain damage that stops or reduces REM

342
Q

What are 2 possible functions of REM?

A

promotes learning –> important for memory consolidation
brain development –> REM facilitates changes in the brain, highest proportion of REM sleep occurs during brain development BUT adults still have REM and this cannot be explained by brain development

343
Q

Do REM and SW sleep play different roles in the consolidation of implicit and explicit memories?

A

yes

344
Q

What study showed that REM was important for implicit learning?

A

ppts perform implicit task during morning, some have SW and REM nap, some have SW nap and some don’t nap
repeat task in evening
SW and REM nap = improved performance

345
Q

What study showed that SW sleep is important for consolidation of explicit memories?

A

implicit and explicit tasks given, nap or SW nap

SW nap = improved explicit but not implicit tasks

346
Q

What case study suggests that REM is not essential for learning?

A

brain damaged patient had little REM sleep but could still learn
REM may not be vital for learning but can help facilitate it

347
Q

What 5 neurotransmitters are involved in arousal?

A 
acetylcholine
norepinephrine 
serotonin
histamine
orexin
348
Q

How is acetylcholine involved in arousal?

A

high levels with awake or in REM
low during SW
activating AcH neurons causes wakefulness
hippocampus and neocortex areas

349
Q

How is norepinephrine involved in arousal?

A 
increases during wakefulness
low during SW
0 during REM
relating to tasks requiring sustained attention 
noradrenergic locus coeruleus area
350
Q

How is serotonin involved in arousal?

A

found in raphe nuclei
if stimulated = arousal
blocking = reduced arousal
most active when awake, declines to almost 0 in REM then temporarily activates before decreasing again

351
Q

How is histamine involved in arousal?

A

located in hypothalamus
high during waking
low during SW and REM

352
Q

How is orexin involved in arousal?

A

located in lateral hypothalamus
excitatory effect in areas involved in arousal
fires fastest in active waking

353
Q

What are the 3 factors that control sleep?

A

1.) homeostatic –> presence/ absence of adenosine
builds up when awake and destroyed by SW
2.) allostatic control –> mediated by hormonal and neural responses to stress
3.) circadian –> restricts sleep to particular part of day-night cycle

354
Q

Does the inhibition of arousal = sleep?

A

yes - can only have one or the other

355
Q

What are the sleep promoting neurons?

A

GABAnergenic neurons located in the hypothalamus

their activity suppresses the arousal system

356
Q

What is the sleep/ waking flip-flop?

A

sleep promoting neurons and arousal neurons can’t be active at the same time
flip-flop on = awake –> sleep promoting neurons inhibited and arousal neurons active
flip-flop off = asleep –> sleep promoting neurons active and arousal inhibited

357
Q

What do orexinergic neurons do?

A

help stabilise SW flip-flop

motivation to stay awake/ events that disturb sleep lead to activation of orexinergic neurons

358
Q

What factors control the activity of orexinergic neurons?

A
  • receive inhibitory input from vlPOA because of build up of adenosine
  • hunger related signal = activates
  • satiety related signals = inhibits
  • biological clock
359
Q

What is the REM sleep flip-flop?

A

REM flip-flop on neurons = in pons
REM flip-flop off neurons = in midbrain
(mutual inhibition of the 2)

REM off region receives excitatory input from orexinergic neurons and this activation tips the REM flip-flop into off state
REM region on = REM sleep begins

360
Q

What is paralysis during REM?

A

specific neurons control muscular paralysis during REM
REM flip flip on = motor neurons in spinal chord are inhibited
damage to paralysis neurons removes inhibition so people act out their dreams

361
Q

What is insomnia?

A

difficulty sleeping that affects day time functioning

362
Q

What are the causes of insomnia?

A

age - more common in older people
stress
env. factors e.g., noise, light
physiology
circadian rhythms e.g., shift work patterns
medical conditions and medications e.g., some antidepressants, heart conditions

363
Q

What are treatments for insomnia?

A

treated with drugs

can be treated with mindfulness and CBT

364
Q

What is sleep apnea?

A

inability to sleep and breathe at the same time

build up of CO2 means you gasp for air multiple times a night which affect daytime functioning

365
Q

What are the causes and treatments for sleep apnoea?

A

caused by an obstruction

can be treated surgically or by wearing a mask that uses pressurised air

366
Q

What is narcolepsy and its symptoms?

A

sleeping at inappropriate times
symptoms:
1.) sleep attacks - urge to sleep
2.) cataplexy - muscular paralysis of REM while awake due to strong emotions or sudden physical effort
3.) sleep paralysis - REM paralysis just before sleep or upon waking
4.) hypnagogic hallucinations - dreaming while awake and paralysed

367
Q

What are the causes and treatments for narcolepsy?

A

causes - heredity element, env. factors involved but unknown
treatments - drugs e.g., stimulants for sleep attacks (Ritalin) and antidepressants for REM sleep phenomenon

368
Q

What is REM sleep behaviour disorder, causes and treatments?

A

failure to exhibit paralysis during REM, act out dream
genetic component
treated with clonazepam (benzodiazepine tranquiliser)

369
Q

What are slow wave sleep problems, causes and treatments?

A

occur during childhood and have hereditary element
sleepwalking and night terrors are usually grown out of
bedwetting

370
Q

What is fatal familial insomnia and its symptoms?

A 
damage to thalamus 
symptoms:
- insomnia and vivid dreams
- disappearance of SW, brief REM
- deficits in attention, memory, dreamlike state
- affects autonomic NS and coordination

psychiatric complications e.g., panic attacks and paranoia
leads to inability to voluntarily move/ speak, coma and death

371
Q

What is the prevalence of ASD?

A 
Approx 1% - used to be less
Prevalence has increased due to:
- heightened awareness 
- broadening of diagnostic criteria
- biological factors e.g., premature birth
372
Q

Why is ASD a spectrum condition?

A
  • affects people differently and to different degrees
  • DSM-5 combined previously different conditions into one creating ASD (e.g., Asperger’s, persuasive developmental disorder)
373
Q

What is the key criteria for ASD?

A
  • deficits in social comm. and interaction
  • restricted, repetitive behaviour, interests and activities

+

  • must be present in early dev. period
  • symptoms cause clinically sig. impairment in important areas of functioning
  • disturbances aren’t better explained by another disability
374
Q

What is social impairment in ASD?

A
  • first identified
  • infant doesn’t want to be held, may arch back
  • difficulty entering social relationships, predicting other’s behaviour and understanding motivations
375
Q

What is communication impairment in ASD?

A

Language is impaired or absent

  • used for instrumental rather than social purposes
  • its content = repetitive and egocentric
  • nonverbal comm. impairments e.g., understanding facial expressions and gestures
  • literal meaning vs. sarcasm
376
Q

What is restricted, repetitive behaviour, interests, activities in ASD?

A
  1. ) repetitive movement, use of objects, speech
  2. ) routines, ritualised patters of verbal/ nonverbal behaviour
  3. ) restricted, fixated interests that are abnormal in intensity or focus
  4. ) hyper/ hypo reactivity to sensory input/ unusual interests in sensory aspects of the env.
377
Q

What is Asperger’s syndrome?

A
  • considered part of ASD
  • no delay in language dev.
  • social interaction difficulties, repetitive behaviours, obsessional interest in narrow subjects
378
Q

What are 2 theories of ASD?

A
  • mind blindness theory

- The extreme male brain

379
Q

What is the mind blindness theory of ASD?

A

TOM –> Sally and Anne doll task (only 20% of children with ASD successfully completed this)

  • children with ASD are delayed in dev. of TOM, leaving them with degrees of mind blindness
    explaining sypmtoms:
  • without TOM, other’s behaviours can be confusing
  • understanding other’s mental states = basis for social interaction + comm.
  • repetitive behaviours + routines –> provide predictability
    BUT cannot explain all non-social characteristic in ASD
380
Q

What is the extreme male brain?

A
  • ASD more prevalent in males

extreme male brain = individuals with above average scores on systemising tests but low scores on empathy tests

381
Q

What are 2 possible causes of ASD?

A
  • Heritability

- Env. risk factors

382
Q

What evidence is there for heritability as a possible cause of ASD?

A
  • strong evidence

- Colvert - large twin study –> Mz concordance = 77-99%, Dz = 22-65%

383
Q

What are some examples of env. risk factors as a possible cause of ASD?

A
  • advanced parent age
  • pregnancy and birth complications
  • pregnancies spaced less than 1 year apart
  • infection during critical periods of early utero neurodevelopment e.g., rubella, tuberous sclerosis
384
Q

What 4 brain pathologies are associated with ASD?

A
  1. ) Differences in brain growth
  2. ) Brain bases of TOM
  3. ) Fusiform Gyrus
  4. ) Role of oxytocin
385
Q

What differences in brain growth are associated with ASD?

A
  • smaller brain at birth, grows abnormally quick during infancy
  • slows sig. by adolescence
  • causality issues –> which causes which
386
Q

How is the brain bases of TOM associated with ASD?

A

Castelli –> triangle animations, describe intentions:

  • ASD = could describe action but not intention
  • functional imaging results = different levels of blood flow in ASD for areas associated with intention
387
Q

How is the Fusiform Gyrus associated with ASD?

A
  • traditionally thought to be impaired in ASD
    Decreased activity in ASD:
  • Shultz –> when viewing pics of faces
  • ERP study (Apicella) –> effect not due to impaired FFG but dysfunction of neural mechanisms that integrate social info
  • might be a dev. consequence of early dysfunction of amygdala
388
Q

What is the role of oxytocin in ASD?

A
  • lower levels in ASD
    Administering oxytocin =
  • increased performance of emotion recog.
  • increased performance of adults with high-functioning ASD on a game requiring social interaction
  • increased amygdala activity in response to facial stimuli
389
Q

When is ADHD most commonly shown?

A

in childhood

390
Q

What is the prevalence of ADHD?

A
  • boys 10x more likely to receive diagnosis than girls

- in adulthood, distribution = 2:1 –> underlying diagnosis issues?

391
Q

ADHD diagnosis have increased over time and are more common in the west, is this true?

A
  • studies found that geolocation has no sig. variability

- high degree of variability between estimates

392
Q

What is ADHD often associated with?

A 
aggression
conduct disorder
learning disabilities 
anxiety
low self-esteem

can lead to it being underdiagnosed

393
Q

What is the DSM5 criteria for ADHD?

A

Persistent inattention and/or hyperactivity –> interferes with function or dev.

  • 6+ symptoms of these present for at least 6 mns
  • several symptoms before age 12
  • symptoms occur in 2+ settings
  • symptoms interfere with social, school, work, functioning
  • symptoms aren’t better explained by another MD
394
Q

What are the risk factors of ADHD?

A
  • premature birth
  • epilepsy
  • brain damage
395
Q

What are the 5 possible causes of ADHD?

A
  • heritability
  • Role of prefrontal cortex
  • role of other brain structures
  • corpus callosum
    dopaminergic transmission
396
Q

How is heritability a possible cause of ADHD?

A
  • 75-91% heritability
  • twin study = 88% (Larson) –> nearly 59,514 twins studied, shared env. was not sig.
  • genetic risk factors, cognition, neuroimaging can be associated with the start of ADHD symptoms in future
397
Q

How is the role of the prefrontal cortex a possible cause of ADHD?

A
  • PFC = guides thoughts, behaviours, regulates attention
  • symptoms of ADHD are similar to those that are produced by damage to PFC
    e. g., distractibility, forgetfulness, impulsivity, poor planning, hyperactivity
398
Q

How is the role of other brain structures a possible cause of ADHD?

A

Meta - analysis:

- ADHD = consistent abnormalities in brain areas related to inhibition and attention

399
Q

How is the corpus callosum a possible cause of ADHD?

A
  • responsible for sustained attention and motor control
    Consistent evidence that it is involved but not agreed upon how
  • some report smaller volume in ADHD
  • others suggest that the white matter integrity is compromised
400
Q

How is dopaminergic transmission a possible cause of ADHD?

A

Underactivity in ADHD

  • dopamine agonist alleviates symptoms (Ritalin)
  • dopamine system plays role in abnormal cognitive-task related processing in ADHD
  • genetic studies have implicated dopamine receptor genes in ADHD
  • low levels of dopamine receptor stimulation impairs functioning of PFC (attention)
401
Q

What is the treatment for ADHD?

A
  • drugs
  • Ritalin –> inhibits reuptake of dopamine
    Dosage = important:
  • too low = no effect
  • too high = increased activity levels disrupting attention and cognition (makes it worse)
402
Q

What is substance abuse disorder?

A
  • pattern of drug use

- chronic and excessive reliance –> not therapeutic

403
Q

Is drug abuse a step up from addition and dependence?

A

no

addiction or dependence refers to being physically dependent on a drug in addition to abusing it

404
Q

How can cocaine use pose a serious threat?

A
  • psychotic behaviour, brain damage, death
405
Q

How can designer drug use pose a serious threat?

A

untested, potentially contaminated

406
Q

How can intravenous drugs use pose a serious threat?

A
  • risk of contracting infectious diseases
  • OD and death
  • harm caused to individuals, loved ones and society
407
Q

How can alcohol use pose a serious threat?

A
  • cirrhosis (scarring) of liver
  • increased risk of heart disease
  • Korsakoff’s syndrome
408
Q

How can smoking pose a serious threat?

A
  • increase risk of ulcers, heart disease, stroke
409
Q

What makes drugs so attractive?

A
  • addictive

- can result in positive and negative reinforcement –> conditioned responses

410
Q

What is the positive reinforcement of drugs?

A
  • operant conditioning
  • reinforcing stimuli = more likely to repeat that behaviour
  • gaining a reward e.g., euphoria feeling
411
Q

How is timing important in the positive reinforcement of drug use?

A
  • reinforcing stimuli have a greater effect if it occurs immediately after the behaviour
    e. g., drug users prefer heroin to morphine as heroin has a more rapid effect –> more lipid soluble meaning it passes through the blood-brain barrier more easily
412
Q

How are neural mechanisms involved in substance abuse?

A
  • produces long term changes
  • starts in ventral tegmental area

Increased strength of excitatory synapses on dopaminergic neurons in VTA of mice after 1 administration of an addictive drug

  • single administration –> effects for 5 days
  • administration for 2 weeks –> persistent changes
413
Q

What do changes in the VTA lead to?

A

increased activation in a variety of regions that receive dopaminergic input from the ventral tegmental area

414
Q

Where does the process of addiction begin?

A
  • begins in the mesolimbic dopaminergic system (VTA - nucleus accumbens)
  • reinforcers trigger release of dopamine in nucleus accumbens (reward role)
  • different drugs stimulate this release in different ways
415
Q

True or false?
Synaptic changes that are responsible for the compulsive behaviour that characterise addiction occur before continued use

A

False

They only occur after continued use

416
Q

Where do important changes occur in the brain following substance abuse?

A

In the dorsal striatum (part of the basal ganglia)

- plays a critical role in OC

417
Q

Where does the mesolimbic pathway run from and too?

A

from ventral tegmental areas to nucleus accumbens

418
Q

What is the negative reinforcement of substance abuse?

A
  • operant conditioning
  • reward = removal of an unpleasant stimuli
    e. g., unpleasant feelings
419
Q

How can negative reinforcement explain the start of addiction?

A
  • drug reduces unpleasant feelings
  • taking drug to deal with stress
  • eliminating physical/ emotional pain = negative reinforcement
420
Q

How can negative reinforcement explain the maintenance of addiction?

A
  • drug produces unpleasant feeling

- e.g., withdrawal –> drug removes these = negative reinforcement

421
Q

What is tolerance in SA?

A
  • decreased sensitivity from continued use
  • muse take larger and larger amounts to get the same effect
  • body may have started to compensate for the disturbed homeostatic mechanisms
422
Q

What are withdrawal symptoms in SA?

A
  • when you stop taking drug

- generally has opposite effect of the drug itself

423
Q

When can craving and relapse occur?

A

Can occur after a long period of abstinence e.g., months/ years

  • potentially due to long-lasting brain changes
  • increases likelihood of relapse
424
Q

What can craving and relapse be elicited by?

A
  • drug related stimuli –> physiological and subjective
    e. g., going to the pub
  • stress
425
Q

What role does dopamine play in craving and relapse?

A

Attentional bias model (Franken)

  1. ) conditioned drug stimuli
  2. ) dopamine level increases in certain brain areas –> anticipation
  3. ) further draws attention to stimuli
  4. ) promotes craving and relapse
    - dorsal striatum involved –> implicated in habit learning and action initiation
426
Q

What role does the PFC play in craving and relapse?

A

Drug users show PFC impairments

  • function - activity
  • structural abnormalities
  • deficits on task e.g., attention/ inhibition tasks
  • amount of cocaine negatively correlated with PFC activity
  • causality issues
427
Q

What are opiates?

A
  • come from resin of opium poppy
  • heroin, morphine, methadone, codeine
  • pain killer effects
  • can be eaten, smoked or injected
428
Q

What is heroin?

A

Most abused opiate

  • Can gain tolerance –> becomes more expensive, can turn to crime
  • needle use –> disease
  • transmission to unborn child
  • uncertainty of strength and what it can be mixed with
429
Q

What do opiates do to the brain?

A

Stimulate opiate receptors

  1. ) Analgesia –> pain relief
  2. ) Hypothermia –> low body temp
  3. ) Sedation
  4. ) Reinforcement –> release of dopamine
430
Q

What is the positive and negative reinforcement of dopamine?

A

Positive:
- dopamine –> mesolimbic pathway

Negative:

  • painkiller
  • feeling of pleasure
  • withdrawal
431
Q

How do opiates lead to cravings?

A
  • opiate related stimuli trigger release of dopamine

- increase of 150-300% in dopamine levels in rats when they pressed a level that delivered heroin

432
Q

What are the stimulants cocaine and amphetamine?

A

Similar behavioural effects but sites of action are different
- dopamine agonists

Cocaine –> deactivates dopamine transporter proteins, blocking reuptake
Amphetamine –> inhibit dopamine reuptake but directly stimulate dopamine release from terminal buttons as well

433
Q

What is the positive reinforcement of cocaine and amphetamine?

A
  • mesolimbic system
  • potent and rapid effects –> most effective
    e. g., rats are 3x more likely to die from cocaine OD than heroin
434
Q

How can the reinforcing effects of cocaine and amphetamine be lost?

A

by blocking/ destroying dopamine receptors in the nucleus accumbens

435
Q

How do cravings occur due to cocaine or amphetamine?

A
  • related stimuli resulting in the release of dopamine
436
Q

Is smoking a habit or an addiction?

A
  • addiction
  • animals self-administer nicotine
  • people smoke regularly or not at all –> can’t just smoke a little
  • addictive e.g., people still smoke after a heart attacker, cancer etc.
437
Q

What is the positive reinforcement of nicotine?

A
  • mesolimbic pathway
  • stimulates nicotinic ACH receptors
  • associated with release of dopamine in nucleus accumbens –> reinforcing
438
Q

What is the negative reinforcement of nicotine?

A

When people quit:

  • appetite increases
  • overeating and weight gain

Try to remove these things = negative reinforcement

439
Q

How does nicotine lead to cravings?

A
  • associated stimuli = dopamine
  • nicotine stimulates orexin –> involved in drug-seeking behaviour (insula)
  • damage to insula disrupts smoking addiction –> high correlation
440
Q

What is the case study of Jimmie G?

A
  • age 49
  • described as “helpless, demented, confused and disorientated”
  • still thought he was 19 –> 25 year memory gap
  • distressed looking in mirror then forgets
  • had Korsakoff syndrome
441
Q

What is Korsakoff syndrome?

A
  • chronic memory disorder –> anterograde amnesia
  • can’t form new memories
  • explicit memories affected, implicit not
442
Q

What is Korsakoff syndrome caused by?

A
  • caused by lack of vitamin B-1
  • exacerbated by toxic effects of alcohol
  • damage to thalamus and mammillary bodies (important for memory and encoding)
443
Q

What are the societal costs of alcohol?

A
  • accidents
  • violence and aggression
  • chronic alcoholism
  • liver cirrhosis
  • foetal alcohol syndrome
444
Q

What are two theories for the actions caused by alcohol?

A
  • disinhibition theory

- alcohol myopia theory

445
Q

What is disinhibition theory?

A

-alcohol = selective depressant on cortex and activated subcortical structures

446
Q

What is alcohol myopia theory?

A
  • tendency for people to respond to near and immediate cues while ignoring more remote cues and potential consequences
447
Q

What is the positive reinforcement of alcohol?

A
  • mild euphoria
    Increased dopamine neurons –> mesolimbic system
  • indirect antagonist on NMDA receptors
  • indirect agonist at GABA receptors

Can trigger release of endogenous opioids
- blocking opiate receptors also decreased alcohol reinforcing effects

448
Q

What is the negative reinforcement of alcohol?

A
  • anxiolytic and sedative effects –> reduces anxiety

- disinhibition

449
Q

How does alcohol lead to cravings?

A

opiate receptors –> level increases with abstinence

- thought to be related to craving for alcohol

450
Q

What are the withdrawal effects from alcohol?

A
  • mild to serious
    Seizures:
  • increases sensitivity of NMDA receptors after suppressive effect of alcohol removed = seizures
  • drugs that block NMDA receptors prevent seizures
451
Q

What are the 2 natural components of cannabis?

A

THC:
- psychoactive component
- small dose = euphoria
larger dose = anxiety and psychotic like behaviour

CBD:

  • antianxiety and antipsychotic effects
  • could be a treatment for Sz, social anx., PTSD
452
Q

What is the positive reinforcement of cannabis?

A
  • THC stimulates dopaminergic neurons

- Cannabinoid Type 1 (CB1) receptors mediate most psychotropic effects of THC

453
Q

Do CB1 receptors also reinforce the effect of other drugs?

A

yes

  • blocking CB1 receptors = abolish reinforcing effects of cannabis, morphine + heroin, reduce effects in alcohol
  • Rimonabant (drug blocking CB1 receptors) decreases reinforcing effects of nicotine
454
Q

Why can some people use drugs and not become dependent?

A
  • genetic and env. factors –> influence the likelihood of taking in the first place and likelihood of becoming dependent
  • general and drug specific factors
455
Q

What did a twin study find about the heredity of drug abuse?

A
  • env. plays a stronger role in drug use

- genetics play stronger role in who becomes addicted

456
Q

What % of vulnerability to addiction can be attributed to genetic factors?

A
  • 40-60%
  • different for different drugs because they affect dopamine pathways differently
  • env. still plays a role e.g., availability, stress, socioeconomic status
457
Q

What is alcohol addition determined by?

A
  • variability in metabolism

- differences in brain chemistry –> sensitivity to reinforcing effects

458
Q

What therapies are there for opiate addiction?

A

Methadone –> replacement oral drug

  • can still be abused, tolerance
  • only administered in clinic

Buprenorphine (newer) –> blocks effects of opiates and produces only a weak opiate effect

  • can be administered by GP
  • sometimes given with naloxone
  • decreases craving
459
Q

What is immunotherapy>

A
  • vaccines specific to the SA

- prevents substance from getting to brain

460
Q

What is deep brain stimulation?

A
  • DBS of nucleus accumbens has had promising effects but is risky
  • invasive –> requires placing an electrode in brain
461
Q

What is TMS for SA?

A
  • less invasive
  • effective in reducing tobacco use but the effects on nicotine use decrease over time
  • 1 treatment is not enough
  • would need constant treatment

Psych year 1 semester 2 (4 decks)

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