Brain and Behaviour Flashcards
1
Q
What is cognition? Give 4 examples
A
Higher mental processes e.g., thinking, speaking, acting, planning
2
Q
What is behavioural neuroscience?
A
Scientific study of how brain activity influences behaviour
3
Q
What is cognitive neuroscience?
A
Study of neural basis of behaviour
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
5
Q
What are mental representations?
A
The sense in which properties of the outside world (e.g., colours, objects) are copied by cognition
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)
7
Q
What word is associated with mental representations?
A
Simulation
8
Q
What word is associated with neural representations?
A
Implementation
9
Q
Where did Aristotle and Plato think mental experiences came from? (Historical perspectives)
A
Aristotle - heart
Plato - mind
10
Q
What is the mind-body problem? (Historical perspectives)
A
How can a physical substance (brain/body) give rise to mental experiences?
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
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
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
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
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
16
Q
What is reductionism?
A
Mind will eventually be explained solely in terms of physical/biological theory
17
Q
True or false?
Dual-aspect theory and reductionism are issues still relevant to modern cognitive neuroscience
A
True
18
Q
What do psychologists often deal in terms of?
A
Generalisation e.g., behaviours as general laws
19
Q
What do physiologists often deal in terms of?
A
Reduction e.g., complex behaviour explained in simpler terms
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
21
Q
What surgery have split brain patients had and why?
A
Splitting of corpus callosum to cure severe epilepsy
22
Q
What is the corpus callosum?
A
A bundle of nerve fibres connecting the left and right brain hemispheres
23
Q
Who studied split brain patients?
A
Sperry and Gazzinga
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
25
What is used to insure that stimuli are only presented to one hemisphere in split brain patients?
Tachistoscope presentation
26
How quickly do stimuli need to be presented for in a Tachistoscope presentation and why?
150ms or less
| Eye movements cause loss of lateralisation and 150ms is faster than the eye can move from central fixation to stimuli
27
What were the results of Sperry and Gazzinga's experiments on Split brain patients?
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
28
What side of brain is smelling processed on?
Same side hemisphere
29
What is smelling like in split brain patients?
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
30
What does lateral mean?
Towards side
31
What does medial mean?
Towards middle
32
What does dorsal mean?
Top
33
What does ventral mean?
bottom
34
What does rostral (anterior) mean?
Front
35
What does caudal (posterior) mean?
Back
36
What is the neuraxis?
Imaginary line from head to toe
37
What does ipsilateral mean?
same side
38
What does contralateral mean?
opposite side
39
What are the 3 ways of slicing the brain?
Transverse section - right angle to neuraxis
Sagittal section - parallel to neuraxis and perpendicular to ground
Horizontal section - parallel to ground
40
What is the CNS made up of?
Brain and spinal cord
41
What is the peripheral NS made up of?
Cranial and spinal nerves
42
What is the texture of the brain?
Soft and jelly like
43
How much does the brain weigh?
Approximately 1400g
44
How much body weight does the brain account for?
2%
45
What is the brain protected by?
Skull and CSF
46
True or false?
| Different areas of the brain support different functions?
True
47
How much blood and oxygen does the brain use?
20% of blood supply
| 15-20% of oxygen
48
How long are the blood vessels in the brain?
400 miles
49
What is the Foramen Magnum? Where is it located?
Large hole for passage of spinal cord in the skull
50
What are the 3 Meninges
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
51
What is the subarachnoid space?
The space between the arachnoid and pia meninges
| It is filled with CSF
52
What are ventricles?
A set of hollow chambers within the brain filled with CSF
53
What are the 4 ventricles?
Lateral ventricles
Third ventricles
Cerebral aqueduct
Fourth ventricle
54
What is cerebrospinal fluid (CSF) like?
similar to blood plasma composition
55
How is CSF formed?
By the choroid plexus
56
What is the purpose of CSF
To form a watery cushion to protect the brain
57
Where is CSF circulated?
Arachnoid space
ventricles
central canal of spinal cord
58
What is the total volume of CSF?
| How many times does it turn over a day?
125-150 ml
| 3-4 times a day
59
Where is CSF secreted and what does it do constantly?
Secreted by brain
| Constantly made, circulated and reabsorbed into bloodstream
60
What is Hydrocephalus in infants? What happens?
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
61
Which ventricle(s) are in the forebrain?
Lateral and Third
62
Which ventricle(s) are in the midbrain?
Central aqueduct
63
Which ventricle(s) are in the hindbrain?
Fourth
64
What are the 3 major divisions of the brain?
Forebrain
Midbrain
Hindbrain
65
Which is the largest major division of the brain?
The forebrain
66
What are the 2 subdivisions of the forebrain?
Telencephalon and Diencephalon
67
What are the principle structure of telencephalon?
Cerebral cortex
Basal ganglia
Limbic system
68
What does the cerebral cortex look like?
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)
69
What are the 5 key structures of the cerebral cortex?
- sulcus = grove
- fissure = deep sulci
- gyrus = bulge
- grey matter = made up of cell bodies of neurons
- white matter = made up of axons and dendrites
70
What are the 4 lobes of the cerebral cortex?
Frontal
Parietal
Occipital (FPOT)
Temporal
71
What is the function of the frontal lobe?
primary motor cortex
| controls different areas of body
72
What is the function of the parietal lobe?
primary somatosensory cortex
| receives external information about the senses
73
What is the function of the temporal lobe?
primary auditory cortex
| processes auditory information
74
what is the function of the occipital lobe?
primary visual cortex
| processes visual information
75
What divides the 4 lobes?
Fissures
76
Which fissure divides the frontal and temporal lobes?
Sylvian fissure
77
Which fissure divides the frontal and parietal lobes?
Central fissure
78
Which fissure divides the parietal and occipital lobes?
occipital fissure
79
Which fissure divides the temporal and occipital lobes?
Extra occipital fissure
80
What type of organisation does the motor cortex have? What does this mean?
Somatotopic organisation = body parts that are used more (e.g., hands, tongue) have more dedicated areas of motor cortex than those used less frequently
81
What are Brodmann areas?
different regions of the cerebral cortex that are defined based on their structure and organisation of cells
82
What is cytoarchitectonics?
the study of the cellular composition of the central nervous system's tissues under the microscope
83
How many Brodmann areas are there?
47
84
Why are Brodmann areas useful?
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
85
What is the Limbic system?
A set of structure involved in learning, memory and emotion
86
What 5 structures are a part of the limbic system?
Limbic cortex
Hippocampus - memory and memory recognition
Amygdala - processing emotions (especially negative emotions)
Fornix
Mammillary bodies (part of hypothalamus)
87
What is the Basal Ganglia?
A set of structures involved in movement
88
What are the 3 structures of the Basal Ganglia?
Caudate nucleus
Putamen
Globus Pallidus
89
What are the principle structures of Diencephalon?
Thalamus
| Hypothalamus
90
What is nuclei?
Group of neurons of similar shape
91
What is the Thalamus?
Main sensory relay for all senses (except smell) and the cortex
Is subdivided into different parts for processing information from the different senses
92
What is the hypothalamus?
- 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
93
What is the subdivision of the midbrain?
Mesencephalon
94
What are the principle structures of mesencephalon?
Tectum
| Tegmentum
95
What are the 2 structure of the Tectum
superior colliculi
| inferior colliculi
96
What is the superior colliculi?
the subcortical sensory pathway involved in fast eye movements (vision)
97
What is the inferior colliculi?
Part of the auditory pathway
98
What is the role of the Tegmentum?
Role in motor movement
99
What are the 3 structures of the Tegmentum?
Reticular formation
red nucleus
substantia nigra
100
What is the subdivisions of the the hindbrain?
Metencephalon and myelencephalon
101
What are the principle structures of metencephalon?
Cerebellum
| Pons
102
What is the cerebellum?
mini brain
| involved in motor coordination and smooth execution of movement
103
What is Pons?
Part of the reticular formation
Involved in sleep and arousal
It is the link between the cerebellum and cerebrum
104
What is the principle structure of myelencephalon?
Medulla oblongata
105
What is the medulla oblongata function?
Involved in basic life functions
| e.g., breathing, swallowing, vomiting, coughing, sneezing, heart rate, wake-sleep cycles
106
What is the structure of the spinal cord?
Grey matter in middle, surrounded by white matter
| Butterfly like structure with wings facing towards body
107
What is the function of the spinal cord?
Communicates with sense organs and muscles below head level
108
What are the primary components of the spinal cord?
Dorsal roots and ventral roots
109
What are dorsal roots?
Carry sensory information to CNS = afferent
110
What are ventral roots?
Carry motor information to muscles and glands away from CNS = efferent
111
What is the peripheral NS?
Located outside skull and spine
Bring information into CNS and carries signals out of CNS
contains somatic NS and autonomic NS
112
What is the somatic NS?
Control movement of skeletal muscles
| transmits somatosensory information to CNS
113
What is somatic NS made of?
cranial nerves and spinal nerves
114
What are afferent nerves?
Carry information towards CNS
115
What are Efferent nerves?
Carry motor information to muscles and glands and away from CNS
116
How many cranial nerves are there?
12
117
What are cranial nerves?
Attached to ventral surface of brain
control sensory and motor functions of head and neck
some are efferent and some are afferent
118
What are spinal nerves?
Peripheral nerves attached to spinal cord
| Are efferent and afferent and travel to muscles and sensory receptors
119
What is the autonomic NS?
Controls body's vegetative functions e.g., heart
regulation of smooth muscles, cardiac muscles and glands
all nerves are efferent
120
What is the autonomic NS made up of?
Sympathetic NS and Parasympathetic NS
| These divisions have opposite effects
121
What is the sympathetic NS?
Fight or flight
arousal and preparing body for expenditure of energy
e.g., increased: heart rate, breathing and gland secretion
122
What is the parasympathetic NS?
Rest and restore
relaxing body
opposite effect of sympathetic NS
123
What type of cell makes up the NS?
The neuron
124
What does the neuron do?
Support cognitive functioning
| Transmits and processes information
125
What are the key structure of a neuron
```
Dendrites
Axons
Soma (cell body)
Myelin sheath
Terminal buttons
```
126
What are the 3 types of function of neurons
Sensory - detect changes in external and internal environment
Motor - control muscle contraction and gland secretion
Interneurons - lie within CNS and are involved in cognition
127
What are the 2 types of interneurons?
Local and projection
128
What are the different types of structures of neurons?
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
129
How did early anatomists discover neurons
Golgi staining technique
| Cajal used this to find pyramidal cells
130
How many types of multipolar cells are there? What are they?
3
| Motor neuron, pyramid cell, Purkinje cell
131
What are Glial cells? Where are they found?
Supporting cells that glue the NS together
| Found in CNS
132
What are the 4 types of glial cells?
Oligodendrocytes
Astrocytes
Microglia (modified immune cells)
Ependymal
133
What do oligodendrocytes form?
Myelin sheath
134
What do astrocytes form, help form, secrete and take up?
form support for CNS
help form blood-brain barrier
secrete neurotropic factors
take up K+ neurotransmitters
135
What does microglia act as?
Scavengers
136
What does ependymal cells create? What are they?
Create barriers between compartments
| are sources of neural stem cells
137
What does the microglia do?
Control immune response of the brain
138
What do oligodendrocytes do?
support axons and produce myelin sheath which provides insulation and is made of lipids
139
What are the nodes of Ranvier?
Bare part of axon
140
How many Schwann cells wrap round axon in CNS and PNS?
```
CNS = many
PNS = one
```
141
What do astrocytes do?
"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
142
What is the blood-brain barrier?
A semipermeable barrier between CNS and circulatory system which helps to regulate flow of nutrient rich fluid into the brain
143
Are all areas of blood-brain barrier equally permeable? Give an example
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
144
Give an example of a useful behaviour that only involves neurons, How does it work?
Reflexes e.g., withdrawal reflex
sensory --> interneuron --> motor
happens in Spinal cord
145
What is a membrane potential?
electrical charge across cell membrane
the difference in electrical potential in and out of cell
stored up source of electrical energy
146
What is resting potential?
Membrane potential of neuron when it isn't being altered by excitatory/inhibitory postsynaptic potentials
about 70mV
147
What is depolarisation?
Reduction of the negative charge (toward 0) of membrane potential when we stimulate neuron
148
What is action potential?
brief electrical impulse that provides the basis for conduction of information along an axon
results from movement of ions through membrane
149
What is the threshold of excitation?
The value of the membrane potential that must be reached to produce an action potential
150
What is hyperpolarisation?
increase in the membrane potential of a cell
151
What are the 2 forces that membrane potentials go through to remain balanced?
Diffusion and electrostatic pressure
152
What is intercellular and extracellular fluids?
```
Intercellular = fluid within cells
Extracellular = fluids outside cells
```
153
Draw the process on diffusion and electrostatic pressure across a cell membrane
Involve Na+, K+, Cl- and A- ions
drawing on Wk 3 Lecture 3 notes
154
How can Na+ be found outside of cell when both diffusion and electrostatic pressure push it inside?
Sodium-potassium pump
| a protein that is an active transporter - pumps 3 sodium ions out and 2 potassium ions in
155
What type of ion channel allows ions to move through membrane? How does it work?
Voltage dependent (gated) ion channels - a protein that allows flow of specific ions, opens and closes depending on charge that arrives to it
156
What 6 stages explain how voltage dependent ion channels work for Na+ and K+ ions
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
157
What is the all or none law?
once AP begins, it proceeds without decrement to terminal buttons (either occurs or doesn't)
158
What is rate law?
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
159
Is the all or none law supplemented by rate law?
Yes
160
What is saltatory conduction?
conduction of APs by myelinated axons
| AP appears to jump from one node of Ranvier to next
161
What are the 2 advantages of saltatory conduction?
economy - less energy used by the Na-K pump (located only at nodes of Ranvier)
speed - conduction much faster in myelinated axon
162
What is the synapse?
junction between 2 neurons
| primary means of communication between 2 cells
163
What is the synaptic cleft?
Narrow gap (20nm) between neurons
164
can action potential cross the synaptic cleft?
No - are carried by neurotransmitters (chemical components)
165
What is the pre-synaptic neuron?
neuron sending impulse
166
What is the post-synaptic neuron
neuron receiving impulse
167
Where are neurotransmitter made and stored?
made in pre-synaptic neuron
| stored in synaptic vesicles at end of axon
168
What are neuroreceptors?
chemical gated ion chemicals on the membrane of the post-synaptic neuron
169
Do neuroreceptors have specific binding sites for neurotransmitters?
yes
| neurotransmitters fit binding sites with lock and key mechanism
170
What are the 2 ways that transmitter-dependent ion channels can be opened?
direct - inotropic receptor - opening from outside
| indirect = metabotropic receptor - opening from inside (like ringing a bell to get attention)
171
Is the exposure of a neurotransmitter to a receptor prolonged or brief?
brief
172
How are molecules of neurotransmitters destroyed?
Enzymes
173
What is an excitatory postsynaptic potential (EPSP)?
excitatory depolarisation of postsynaptic membrane
174
What is inhibitory postsynaptic potentials (IPSP)?
inhibitory hyperpolarisation of postsynaptic membrane
175
How is the nature of a postsynaptic potential determined?
determined by postsynaptic receptors
176
What are the 3 major types of ion channels and do they exhibit EPSP or IPSP?
```
Na+ = EPSP
K+ = IPSP
Cl- = IPSP
```
177
What is neural integration?
process by which inhibitory and excitatory postsynaptic potentials summate and control the rate of firing of a neuron
178
What type of effect do most neurotransmitters have?
Both excitatory and inhibitory
179
Which 2 neurotransmitters get most of the synaptic communication done?
```
glutamate = excitatory effects
GABA = inhibitory effects
```
180
Which neurotransmitter mainly does synaptic communication in the spinal cord? What is its effect?
Glycine = inhibitory effect
181
What are most neurotransmitters responsible for?
Having modulating effects
| Tend to activate/ inhibit entire circuits of neurons that are involved in particular brain functions
182
What is psychopharmacology?
Study of effects of drugs on NS and behaviour
183
What are drug effects?
The changes a drug produces in an animal's physiological processes and behaviour
184
What do most drugs affect in the NS?
Synaptic transmission
185
What is an antagonist?
drug that inhibits effects of neurotransmitter on postsynaptic cell
186
What is an agonist?
Drug that facilitates effects of neurotransmitter on postsynaptic cell
187
Where is Acetylcholine secreted?
secreted by efferent axons on CNS
188
What roles does Acetylcholine have?
All muscular movement achieved by its release
Involved in regulating REM sleep
Facilitating effects
189
Where is Acetylcholine found?
Found at the target of parasympathetic branch of ANS
190
Is Acetylcholine an antagonist or agonist?
Antagonist - prevents release by terminal buttons
191
What does Acetylcholine bind to?
Nicotinic and muscarinic receptors
192
What are nicotinic receptors?
An ionotropic acetylcholine receptor stimulated by nicotine
193
What are nicotinic receptors blocked by?
Curare
| acts at the junction between nerve cells and muscles causing paralysis
194
What are muscarinic receptors?
Metabotropic acetylcholine receptors that produce parasympathetic nerve effects in the heart, smooth muscles and glands
195
What are muscarinic receptors blocked by?
Atropine
acts by preventing ACh from depolarising the postsynaptic membrane in the parasympathetic branch
used in treatment of low heart rate
196
What neurotransmitters are the Monoamines made up of? Why is this?
Dopamine, norepinephrine, epinephrine and serotonin
| Have similar molecular structure so some drugs affect the activity in all of them to a degree
197
What do the Monoamines regulate?
Mood
198
How does Tyrosine become norepinephrine through an enzyme?
Tyrosine --> L-DOPA --> Dopamine --> Norepinephrine
199
What does dopamine regulate?
Reward processing, energy, addiction pathways
200
Describe study on rats and reward pathway
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
What are natural rewards in the reward pathway?
Food, sex, water, nurturing
202
What is addiction?
A state in which an organism engages in compulsive behaviour, behaviour is reinforcing, loss of control for intake
This starts in the midbrain
203
What is tolerance?
A state in which organism no longer responds to a drug --> higher dosage required to get same effect
204
What is dependence?
A state in which organism functions normally only in presence of a drug --> manifested as physical disturbance when drug is withdrawn
205
Are dependence and addiction intertwined?
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
How does cocaine increase activation on the reward system?
cocaine binds to cocaine binding sites
dopaminergic synapse in nucleus accumbens
effect of cocaine = inhibition of dopamine reuptake
increased activation of reward system
207
What do PET scans show about cocaine usage?
Glucose reduction in metabolic activity
208
Does dopamine also regulate movement and control attention?
YES
209
What is the nigrostriatal system?
starts in substantia nigra and ends in basal ganglia - plays a role in controlling movement
210
What disease comes as a result of the degeneration of the nigrostriatal system? How is it treated?
Parkinson's disease
| Treated with L-DOPA
211
What does serotonin (5-HT) regulate?
mood, eating, sleeping, dreaming, arousal
pain
memory and learning, temperature regulation, behaviour, cardiovascular function, muscle contraction, endocrine regulation and depression
212
Where does serotonin start and what pathway does it take?
Starts in Raphe nuclei
| The goes to spine or through midbrain
213
What are low levels of serotonin associated with?
Depression
214
How can serotonin treat depression?
SSRIs increase serotonin levels at the synapse by blocking the reuptake of serotonin into the presynaptic cell
215
What effects does LSD have on the body?
Stimulates sympathetic NS in midbrain
| pupillary dilation, increased body temp, raised blood sugar levels
216
What effects does MDMA have on the body?
Serotonergic agonist = excitatory and hallucinogenic effects
217
What effects does MDMA have on serotonin transporters in the short term and long term?
```
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
Is norepinephrine (NE)/ noradrenaline a hormone and neurotransmitter?
YES
219
How does norepinephrine (NE)/ noradrenaline work as a hormone?
Secreted by adrenal gland, works with epinephrine/adrenaline to give body energy when stressed (fight/flight response)
220
Can norepinephrine (NE)/ noradrenaline be an effective treatment for depression?
Yes if the mediation inhibits the reuptake of it
221
What does elevated levels on norepinephrine (NE)/ noradrenaline indicate?
Mania
222
What is epinephrine/ adrenaline?
hormone secrete by adrenal medulla
| It is a neurotransmitter in the brain
223
What is the name given to the most common neurotransmitters in the CNS
What is this group made up of
Amino acids
| Glutamate, GABA, Glycine
224
Where is glycine found?
In the spinal cord
225
What is glutamate? What does it bind to?
Most important excitatory neurotransmitter in brain
| Bind to NMDA receptor = specialised ionotropic glutamate receptor
226
What is GABA?
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
What can imbalances of GABA lead to?
BD, Sz, anxiety disorder
228
What is an indirect agonist for GABA A receptor?
Benzodiazepines --> anxiolytic drug which has a tranquilising effect
229
Where does dopamine start?
ventral tegmental area
230
What is a stressor?
a situation that causes stress to a system e.g., aversive events
231
What is stress reactivity?
the way we respond to a stressor
232
How does our body change when stressed?
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
What are some symptoms of chronic stress?
muscles tense up = constant state of guardedness
tension-type headaches and migraines
long term heart/blood problems e.g., hypertension, heart attack
234
What did a longitudinal study into chronic stress find?
chronic stress measured at baseline increased likelihood of stroke over the follow-up period
235
Who founded the fight/flight response? How did it come about?
Cannon - work with rats saw peristalsis would stop when they were stressed
236
What is peristalsis?
rhythmic wave of movement that pushes food through oesophagus and intestine
237
What is an example of an acute and chronic physical cause of stress?
```
acute = injury
chronic = hunger, cancer
```
238
What is an example of an acute and chronic psychological cause of stress?
```
acute = deadline
chronic = chronic work pressure
```
239
What is an example of an acute and chronic social cause of stress?
```
acute = humiliation
chronic = chronic isolation
```
240
True or false? Stress via cortisol can directly suppress activity of the immune system?
True
241
Give 3 examples of studies that show the effects of cortisol on the immune system
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
What are the 3 components of the HPA Axis?
hypothalamus
pituitary gland
adrenal gland
243
How does the HPA axis work?
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
What are the functions of cortisol?
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
What is Selye's General Adaptation Syndrome?
Chronic exposure to stressor leads to 3 stages:
Alarm
Resistance
Exhaustion
246
What happens in the alarm stage of Selye's General Adaptation Syndrome?
arousal of ANS --> happens during first encounter with stressor
potential for shock
SNS is activated
Adrenaline and cortisol released
247
What happens in the resistance stage of Selye's General Adaptation Syndrome?
continued exposure to stressor
PNS returns physiological functions to normal
over time resistance to stressor increases
adaption to environmental stressors
248
What happens in the exhaustion stage of Selye's General Adaptation Syndrome?
stressor continues beyond body's capacity
stressor depletes available resources
loss of ability to adapt to situations
susceptible to illness and death
249
What are 3 examples of studies that show the effects of prenatal stress?
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
What did a study on postnatal stress find? (rats)
rats showed greater glucocorticoid response to stress
| stress in infancy reduced growth hormones leading to lower adult height
251
What did a study on Romanian orphanages and stress find?
the longer children remained in orphanages (>8 months) the higher their levels of cortisol
252
Where is noradrenaline released from? Can it enhance the function and retrieval of memory?
Released from Locus Coeruleus
| Yes
253
Can chronic stress change your brain structure?
Yes
| Neurons in the hippocampus of rats have a reduced structure as a result of stress
254
What was the result of brain activity when people with snake phobias chose to move the snake closer to them?
reduced amygdala activity
255
What was the result on the amygdala when ppts incidentally viewed fearful faces?
more active
256
What is the medial prefrontal cortex? When does its activity increase?
the midline of the brain, in front of the motor cortex
| increased activity when trying to regulate stress
257
How is emotion regulation like a balancing act?
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
Is information that is encoded during a stressful event well remembered?
Yes, particularly if the information is relevant to the stressor
Normally adaptive but dysregulation could result in psychological trauma
259
Give an example of results of a stress at encoding study
during stress there is lower activity in hippocampus at encoding leading to a better memory
260
Give an example of results of a stress at consolidation study
stress enhances consolidation of emotional pictures but not neutral pictures
261
Give an example of results of a stress at retrieval study
memory retrieval during stress is impaired
262
What is cognitive appraisal theory?
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
What are the 3 patterns of conflict within the individual?
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
What is eustress?
seeking out stressful experiences e.g., riding a rollercoaster
265
How is dopamine involved in stress?
involved in motivation to seek out a reward
| Greatest release in the anticipation of the event
266
What are the 3 components of emotional response?
1. ) behavioural
2. ) autonomic
3. ) hormonal
267
What integrates the behavioural, autonomic and hormonal emotional responses?
the amygdala
268
does the amygdala have a role in physiological and behavioural reaction to objects and situations with biological consequences?
yes
269
what role does the lateral nucleus have in emotions?
receives sensory information from hippocampus
| projects to different brain areas
270
what role does the central nucleus have in emotions?
receives signals from lateral nucleus
sends signals to hypothalamus, midbrain, pons, medulla
when threatening stimuli is perceived, neurons in central nucleus become activated
271
What evidence shows that the central nucleus becomes activated when threatened?
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
What are the 2 types of fear responses?
1. ) Automatic fear responses --> automatic activation of central nucleus e.g., loud noises, heights
2. ) Conditioned emotional responses --> learned danger e.g., CC
273
What does CER do to the brain?
physical changes responsible for establishing a CER occur in lateral nucleus
lateral nucleus communicates with central nucleus = behavioural, autonomic and hormonal responses
274
Does excitation = forgetting? (CER)
no
instead learns that the association is no longer there --> conditioned response inhibited
vmPFC plays a role in inhibiting these responses
275
What evidence shows the vmPFC plays a role in inhibiting conditioned responses?
stimulation to vmPFC inhibits CER
excitation training activates vmPFC
lesions to vmPFC impair excitation
276
What are CERs like in humans?
1. ) little albert --> conditioned fear of white rats
2. ) amygdala stimulation --> humans reported being more afraid
3. ) activity of vmPFC correlates with extinction
277
How are CERs acquired in humans?
1. ) socially
| 2. ) through instruction
278
What did a case study about a woman with localised damage to the amygdala show?
fear conditioning was severely impaired
showed approach rather than avoidance behaviours
led to her being victim of many crimes and ultimately dying
279
What are the 2 main reasons for anger?
reproduction
| self defence
280
What are the 3 parts of the neural control for aggressive behaviours?
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
What is the role of serotonin in aggressive behaviour?
high levels = aggression inhibition
| low levels = aggressive attacks
282
How are serotonin levels measured?
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
What studies show the link between serotonin and risk-taking behaviour?
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
What studies show the link between serotonin and aggression?
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
What is Prozac an example of?
a serotonin agonist --> reduces irritability and aggressiveness
286
What is the role of vmPFC in aggression?
controls emotion regulation and inhibition of emotional responses
impulsive violence is thought to be the consequence of faulty emotional regulation
287
What is inputted and outputted to vmPFC?
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
What 2 case studies show the role of vmPFC in emotion regulation?
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
What did a study following the findings of EVR show?
informant rating of emotional dysfunction and real-world difficulties significantly correlated for patients with damage to vmPFC but their cognitive abilities were intact
290
What studies show that vmPFC is involved in moral decision making?
neuroimaging evidence --> moral problems activate vmPFC, non-emotional decisions don't
vmPFC damage evidence --> vmPFC patients chose logical decisions in personal moral dilemmas
291
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?
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
What is link between the prefrontal cortex volume and serotonin activity?
PFC receives projection of serotonergic axons
| serotonergic input to PFC activates this region
293
What is the James-Lange theory of emotion?
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
What is a limitation of the James-Lange theory of emotion?
it is hard to test because it refer to feelings which are private events
295
What evidence is there for the James-Lange theory of emotion?
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
What is the Cannon-Bard theory of emotion?
thalamus sends simultaneous signals to cortex and ANS so autonomic arousal and conscious emotion happen at the same time
297
What evidence is there for the Cannon-Bard theory of emotion?
cats with severed nerves in ANS can't experience somatic signals but could still demonstrate emotions such as fear, anger and pleasure
298
What did Darwin believe about emotional expressions and how did he conclude this?
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
Give 2 examples of cross cultural studies of emotion and what conclusions can be made from these?
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
What does research with visually impaired people suggest about emotion? Give 2 examples and conclusion
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
What study shows that vocal emotion is cross cultural? What did this study conclude?
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
What study shows that emotions are more pronounced in groups than when alone?
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
What study demonstrated recognition of facial expression?
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
What study demonstrated recognition of body language?
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
Is there laterality of emotion recognition? What evidence is there?
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
What case study provides evidence for the idea that comprehension of meanings of words and tone of voice are independent?
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
What role does the amygdala play in facial emotion recognition?
plays role in emotional responses and recognition
| particularly fear recognition
308
What evidence shows that the amygdala is important for fear recognition?
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
Is the amygdala important in vocal emotion recognition? What evidence is there?
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
What is the simulationist hypothesis? What evidence is there?
= 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
What study shows that imitation is important in emotion recognition?
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
Where are mirror neurons located?
in the ventral premotor cortex of frontal lobe
313
When are mirror neurons activated?
when an animal performs a particular behaviour (important role in control of movement)
When an animal sees another animal performing that behaviour
314
What is the role of mirror neurons?
- 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
What evidence is there for mirror neurons?
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
Is the expression of emotions automatic?
Kind of
| not easy to produce a realistic facial expression of emotion if we don't really feel that way
317
What are Duchenne smiles?
fake smiles involve contraction of mouth muscles only
| real smile also involve muscles near eyes
318
What does method acting do to expression of emotion?
imaging a situation that produced a genuine desired emotion allows actors to convincingly portray facial emotions
319
What evidence is there for the automaticity of facial expression?
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
What is the laterality of emotion expression?
RH has role in recognition of facial expression, vocal emotion and expression of emotions
321
What is the laterality of emotion expression?
RH has role in recognition of facial expression, vocal emotion and expression of emotions
322
What evidence is there for RH having a role in recognition of facial expression?
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
What evidence is there for RH having a role in vocal emotion?
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
What evidence is there for RH having a role in expression of emotions?
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
What is measured in sleep research?
EEG - brain activity
EMG - muscle activity
EOG - eye movements
HR, respiration, skin conduction
326
What are the 2 basic patterns of brain activity in wakefulness?
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
What are the stages of sleep?
Stage 1 and 2 REM sleep (theta, 3.5 - 7Hz)
| Stage 3 and 4 (Delta <3.5 Hz)
328
What is stage 1 sleep?
```
theta
firing of neurons in neocortex = more synchronised
transition between sleep and wakefulness
drowsy
approx 10 minutes
```
329
What is stage 2 sleep
theta
approx 15 mins
if woken during this they will say they haven't been asleep
330
What are sleep spindles?
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
What are k complexes?
sudden sharp wave forms in stage 2
associated with consolidation of memories
forerunner of delta waves
332
What is stage 3 and 4 sleep (SW sleep)?
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
What are slow wave oscillations?
```
< 1 Hz
Down state (off) --> neurons rest
Up state (on) --> neurons briefly fire at high rate
```
334
What is REM sleep?
```
theta
desynchrony --> rapid and irregular
we dream
people react to meaningful stimuli e.g., their name
if woken = attentive and alert
```
335
What physiological changes occur during REM sleep?
rapid eye movements
muscular paralysis
body temp regulation stops
brain is active --> increased blood flow and oxygen
336
what is sleeping with one hemisphere like in humans?
usually in a novel env. and have trouble sleeping
LH is more vigilant than RH
Disappears by day 2
337
Do animals sleep with 1 hemisphere?
Some do e.g., dolphins
338
What are the functions of slow wave sleep?
allows brain to rest
metabolic rate and blood flow falls by 75%
people are unresponsive, confused if woken --> suggests cerebral cortex "shuts down"
339
What happen if someone suffers from slow wave sleep deprivation?
affects their cognitive, especially attention, but not physical abilities
340
What is the rebound phenomenon?
if deprived of REM one night, more REM will take place the next night
341
Is it possible to function normally without REM sleep?
Yes and many people do such as those on antidepressants or those with brain damage that stops or reduces REM
342
What are 2 possible functions of REM?
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
Do REM and SW sleep play different roles in the consolidation of implicit and explicit memories?
yes
344
What study showed that REM was important for implicit learning?
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
What study showed that SW sleep is important for consolidation of explicit memories?
implicit and explicit tasks given, nap or SW nap
| SW nap = improved explicit but not implicit tasks
346
What case study suggests that REM is not essential for learning?
brain damaged patient had little REM sleep but could still learn
REM may not be vital for learning but can help facilitate it
347
What 5 neurotransmitters are involved in arousal?
```
acetylcholine
norepinephrine
serotonin
histamine
orexin
```
348
How is acetylcholine involved in arousal?
high levels with awake or in REM
low during SW
activating AcH neurons causes wakefulness
hippocampus and neocortex areas
349
How is norepinephrine involved in arousal?
```
increases during wakefulness
low during SW
0 during REM
relating to tasks requiring sustained attention
noradrenergic locus coeruleus area
```
350
How is serotonin involved in arousal?
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
How is histamine involved in arousal?
located in hypothalamus
high during waking
low during SW and REM
352
How is orexin involved in arousal?
located in lateral hypothalamus
excitatory effect in areas involved in arousal
fires fastest in active waking
353
What are the 3 factors that control sleep?
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
Does the inhibition of arousal = sleep?
yes - can only have one or the other
355
What are the sleep promoting neurons?
GABAnergenic neurons located in the hypothalamus
| their activity suppresses the arousal system
356
What is the sleep/ waking flip-flop?
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
What do orexinergic neurons do?
help stabilise SW flip-flop
| motivation to stay awake/ events that disturb sleep lead to activation of orexinergic neurons
358
What factors control the activity of orexinergic neurons?
- receive inhibitory input from vlPOA because of build up of adenosine
- hunger related signal = activates
- satiety related signals = inhibits
- biological clock
359
What is the REM sleep flip-flop?
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
What is paralysis during REM?
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
What is insomnia?
difficulty sleeping that affects day time functioning
362
What are the causes of insomnia?
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
What are treatments for insomnia?
treated with drugs
| can be treated with mindfulness and CBT
364
What is sleep apnea?
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
What are the causes and treatments for sleep apnoea?
caused by an obstruction
| can be treated surgically or by wearing a mask that uses pressurised air
366
What is narcolepsy and its symptoms?
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
What are the causes and treatments for narcolepsy?
causes - heredity element, env. factors involved but unknown
treatments - drugs e.g., stimulants for sleep attacks (Ritalin) and antidepressants for REM sleep phenomenon
368
What is REM sleep behaviour disorder, causes and treatments?
failure to exhibit paralysis during REM, act out dream
genetic component
treated with clonazepam (benzodiazepine tranquiliser)
369
What are slow wave sleep problems, causes and treatments?
occur during childhood and have hereditary element
sleepwalking and night terrors are usually grown out of
bedwetting
370
What is fatal familial insomnia and its symptoms?
```
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
What is the prevalence of ASD?
```
Approx 1% - used to be less
Prevalence has increased due to:
- heightened awareness
- broadening of diagnostic criteria
- biological factors e.g., premature birth
```
372
Why is ASD a spectrum condition?
- 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
What is the key criteria for ASD?
- 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
What is social impairment in ASD?
- first identified
- infant doesn't want to be held, may arch back
- difficulty entering social relationships, predicting other's behaviour and understanding motivations
375
What is communication impairment in ASD?
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
What is restricted, repetitive behaviour, interests, activities in ASD?
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
What is Asperger's syndrome?
- considered part of ASD
- no delay in language dev.
- social interaction difficulties, repetitive behaviours, obsessional interest in narrow subjects
378
What are 2 theories of ASD?
- mind blindness theory
| - The extreme male brain
379
What is the mind blindness theory of ASD?
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
What is the extreme male brain?
- ASD more prevalent in males
| extreme male brain = individuals with above average scores on systemising tests but low scores on empathy tests
381
What are 2 possible causes of ASD?
- Heritability
| - Env. risk factors
382
What evidence is there for heritability as a possible cause of ASD?
- strong evidence
| - Colvert - large twin study --> Mz concordance = 77-99%, Dz = 22-65%
383
What are some examples of env. risk factors as a possible cause of ASD?
- 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
What 4 brain pathologies are associated with ASD?
1. ) Differences in brain growth
2. ) Brain bases of TOM
3. ) Fusiform Gyrus
4. ) Role of oxytocin
385
What differences in brain growth are associated with ASD?
- smaller brain at birth, grows abnormally quick during infancy
- slows sig. by adolescence
- causality issues --> which causes which
386
How is the brain bases of TOM associated with ASD?
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
How is the Fusiform Gyrus associated with ASD?
- 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
What is the role of oxytocin in ASD?
- 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
When is ADHD most commonly shown?
in childhood
390
What is the prevalence of ADHD?
- boys 10x more likely to receive diagnosis than girls
| - in adulthood, distribution = 2:1 --> underlying diagnosis issues?
391
ADHD diagnosis have increased over time and are more common in the west, is this true?
- studies found that geolocation has no sig. variability
| - high degree of variability between estimates
392
What is ADHD often associated with?
```
aggression
conduct disorder
learning disabilities
anxiety
low self-esteem
```
can lead to it being underdiagnosed
393
What is the DSM5 criteria for ADHD?
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
What are the risk factors of ADHD?
- premature birth
- epilepsy
- brain damage
395
What are the 5 possible causes of ADHD?
- heritability
- Role of prefrontal cortex
- role of other brain structures
- corpus callosum
dopaminergic transmission
396
How is heritability a possible cause of ADHD?
- 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
How is the role of the prefrontal cortex a possible cause of ADHD?
- 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
How is the role of other brain structures a possible cause of ADHD?
Meta - analysis:
| - ADHD = consistent abnormalities in brain areas related to inhibition and attention
399
How is the corpus callosum a possible cause of ADHD?
- 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
How is dopaminergic transmission a possible cause of ADHD?
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
What is the treatment for ADHD?
- 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
What is substance abuse disorder?
- pattern of drug use
| - chronic and excessive reliance --> not therapeutic
403
Is drug abuse a step up from addition and dependence?
no
| addiction or dependence refers to being physically dependent on a drug in addition to abusing it
404
How can cocaine use pose a serious threat?
- psychotic behaviour, brain damage, death
405
How can designer drug use pose a serious threat?
untested, potentially contaminated
406
How can intravenous drugs use pose a serious threat?
- risk of contracting infectious diseases
- OD and death
- harm caused to individuals, loved ones and society
407
How can alcohol use pose a serious threat?
- cirrhosis (scarring) of liver
- increased risk of heart disease
- Korsakoff's syndrome
408
How can smoking pose a serious threat?
- increase risk of ulcers, heart disease, stroke
409
What makes drugs so attractive?
- addictive
| - can result in positive and negative reinforcement --> conditioned responses
410
What is the positive reinforcement of drugs?
- operant conditioning
- reinforcing stimuli = more likely to repeat that behaviour
- gaining a reward e.g., euphoria feeling
411
How is timing important in the positive reinforcement of drug use?
- 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
How are neural mechanisms involved in substance abuse?
- 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
What do changes in the VTA lead to?
increased activation in a variety of regions that receive dopaminergic input from the ventral tegmental area
414
Where does the process of addiction begin?
- 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
True or false?
Synaptic changes that are responsible for the compulsive behaviour that characterise addiction occur before continued use
False
| They only occur after continued use
416
Where do important changes occur in the brain following substance abuse?
In the dorsal striatum (part of the basal ganglia)
| - plays a critical role in OC
417
Where does the mesolimbic pathway run from and too?
from ventral tegmental areas to nucleus accumbens
418
What is the negative reinforcement of substance abuse?
- operant conditioning
- reward = removal of an unpleasant stimuli
e. g., unpleasant feelings
419
How can negative reinforcement explain the start of addiction?
- drug reduces unpleasant feelings
- taking drug to deal with stress
- eliminating physical/ emotional pain = negative reinforcement
420
How can negative reinforcement explain the maintenance of addiction?
- drug produces unpleasant feeling
| - e.g., withdrawal --> drug removes these = negative reinforcement
421
What is tolerance in SA?
- 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
What are withdrawal symptoms in SA?
- when you stop taking drug
| - generally has opposite effect of the drug itself
423
When can craving and relapse occur?
Can occur after a long period of abstinence e.g., months/ years
- potentially due to long-lasting brain changes
- increases likelihood of relapse
424
What can craving and relapse be elicited by?
- drug related stimuli --> physiological and subjective
e. g., going to the pub
- stress
425
What role does dopamine play in craving and relapse?
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
What role does the PFC play in craving and relapse?
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
What are opiates?
- come from resin of opium poppy
- heroin, morphine, methadone, codeine
- pain killer effects
- can be eaten, smoked or injected
428
What is heroin?
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
What do opiates do to the brain?
Stimulate opiate receptors
1. ) Analgesia --> pain relief
2. ) Hypothermia --> low body temp
3. ) Sedation
4. ) Reinforcement --> release of dopamine
430
What is the positive and negative reinforcement of dopamine?
Positive:
- dopamine --> mesolimbic pathway
Negative:
- painkiller
- feeling of pleasure
- withdrawal
431
How do opiates lead to cravings?
- 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
What are the stimulants cocaine and amphetamine?
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
What is the positive reinforcement of cocaine and amphetamine?
- mesolimbic system
- potent and rapid effects --> most effective
e. g., rats are 3x more likely to die from cocaine OD than heroin
434
How can the reinforcing effects of cocaine and amphetamine be lost?
by blocking/ destroying dopamine receptors in the nucleus accumbens
435
How do cravings occur due to cocaine or amphetamine?
- related stimuli resulting in the release of dopamine
436
Is smoking a habit or an addiction?
- 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
What is the positive reinforcement of nicotine?
- mesolimbic pathway
- stimulates nicotinic ACH receptors
- associated with release of dopamine in nucleus accumbens --> reinforcing
438
What is the negative reinforcement of nicotine?
When people quit:
- appetite increases
- overeating and weight gain
Try to remove these things = negative reinforcement
439
How does nicotine lead to cravings?
- associated stimuli = dopamine
- nicotine stimulates orexin --> involved in drug-seeking behaviour (insula)
- damage to insula disrupts smoking addiction --> high correlation
440
What is the case study of Jimmie G?
- 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
What is Korsakoff syndrome?
- chronic memory disorder --> anterograde amnesia
- can't form new memories
- explicit memories affected, implicit not
442
What is Korsakoff syndrome caused by?
- 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
What are the societal costs of alcohol?
- accidents
- violence and aggression
- chronic alcoholism
- liver cirrhosis
- foetal alcohol syndrome
444
What are two theories for the actions caused by alcohol?
- disinhibition theory
| - alcohol myopia theory
445
What is disinhibition theory?
-alcohol = selective depressant on cortex and activated subcortical structures
446
What is alcohol myopia theory?
- tendency for people to respond to near and immediate cues while ignoring more remote cues and potential consequences
447
What is the positive reinforcement of alcohol?
- 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
What is the negative reinforcement of alcohol?
- anxiolytic and sedative effects --> reduces anxiety
| - disinhibition
449
How does alcohol lead to cravings?
opiate receptors --> level increases with abstinence
| - thought to be related to craving for alcohol
450
What are the withdrawal effects from alcohol?
- mild to serious
Seizures:
- increases sensitivity of NMDA receptors after suppressive effect of alcohol removed = seizures
- drugs that block NMDA receptors prevent seizures
451
What are the 2 natural components of cannabis?
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
What is the positive reinforcement of cannabis?
- THC stimulates dopaminergic neurons
| - Cannabinoid Type 1 (CB1) receptors mediate most psychotropic effects of THC
453
Do CB1 receptors also reinforce the effect of other drugs?
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
Why can some people use drugs and not become dependent?
- genetic and env. factors --> influence the likelihood of taking in the first place and likelihood of becoming dependent
- general and drug specific factors
455
What did a twin study find about the heredity of drug abuse?
- env. plays a stronger role in drug use
| - genetics play stronger role in who becomes addicted
456
What % of vulnerability to addiction can be attributed to genetic factors?
- 40-60%
- different for different drugs because they affect dopamine pathways differently
- env. still plays a role e.g., availability, stress, socioeconomic status
457
What is alcohol addition determined by?
- variability in metabolism
| - differences in brain chemistry --> sensitivity to reinforcing effects
458
What therapies are there for opiate addiction?
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
What is immunotherapy>
- vaccines specific to the SA
| - prevents substance from getting to brain
460
What is deep brain stimulation?
- DBS of nucleus accumbens has had promising effects but is risky
- invasive --> requires placing an electrode in brain
461
What is TMS for SA?
- 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
