Biological psychology Flashcards

1
Q

What makes up the nervous system?

A
  1. Central nervous system (CNS)
    - Brain
    - Spinal cord
  2. Peripheral nervous system (PNS)
    - Nerves
    - Motor/sensory pathways
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2
Q

The brain: 3 parts

A
  1. Cerebrum
  2. Cerebellum
  3. Brain stem
    - Two hemispheres (left and right)
    - Contralateral: opposite side
    - Ipsilateral: same side
    - Receives a constant flow of blood (approx. 20% of blood flow from heart)
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3
Q

Anatomical directions: 4 types

A

a) Superior/ Dorsal (Top)
b) Posterior/ Caudal (Back)
c) Inferior/ Ventral (Bottom)
d) Anterior/ Rostral (Front)
- Medial: towards the middle
- Lateral: towards the side

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4
Q

Planes and sections: 3 types

A

a) Frontal – parallel to forehead
b) Sagittal – ‘arrow’
c) Horizontal – parallel to ground

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5
Q

What is the difference between grey and white matter?

A
  1. Grey matter – cell bodies and dendrites
    e.g. cortex, basal ganglia, thalamus
  2. White matter – myelinated axons
    e.g. corpus callosum (the largest fibre bundle that connects the two hemispheres of the brain)
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6
Q

What are some protections of the nervous system?

A
  • Meninges: 3 layers of tissues that protect the brain and spinal cord
  • Cerebrospinal fluid (CSF): a clear liquid that fills the subarachnoid space (Function = shock absorber, buoyancy)
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7
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A
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7
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7
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8
Q

What is the ventricular system and function?

A
  • Ventricles: hollow cavities filled with CSF
  • Function = exchange of materials between blood vessels and brain tissue
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9
Q

What is the blood-brain barrier and purpose?

A
  • A semipermeable barrier
  • Lipid soluble substances can pass through but substances with large molecules (e.g. glucose) must be actively transported through the walls
  • Purpose = maintain stable environment and protection from potentially damaging chemicals
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10
Q

Features of Cerebral Cortex

A
  • Outer surface of cerebrum
  • 3mm thick and folded to allow a bigger surface area
  • Clefts/cracks/grooves = Sulci
  • Folds/bulges = Gyri
  • Major grooves = Fissures
  • 4 lobes: Frontal, Parietal, Occipital, Temporal
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11
Q

Frontal lobe: and function

A
  • The anterior area of the cortex, rostral to parietal lobe, dorsal to temporal lobe
  • Divided from parietal lobe by the central sulcus
  • Function = motor and cognition
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12
Q

Parietal lobe: and function

A
  • Caudal to frontal lobe, dorsal to temporal lobe
  • Function = somatosensory
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13
Q

Occipital lobe: and function

A
  • Caudal to parietal and temporal lobes
  • Function = vision
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14
Q

Temporal lobe: and function

A
  • Rostral to occipital lobe and ventral to parietal and frontal lobes
  • Function = hearing, vision, cognition, emotion
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15
Q

Primary areas in the brain

A
  • Primary somatosensory, visual & auditory cortex receive info from the senses
  • Primary motor cortex is connected to muscles in the body
  • All contralateral
  • Sensory association areas receive and analyse info from primary regions
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16
Q

What structures are in the brains subdivisions?

A
  1. Telencephalon:
    Cerebral cortex
    Basal ganglia
    Limbic system
  2. Diencephalon:
    Thalamus
    Hypothalamus
  3. Midbrain:
    Tectum
    Teamentum
  4. Metencephalon:
    Cerebellum
    Pons
  5. Myelencephalon
    Medulla oblongata
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17
Q

Telencephalon: Basal ganglia

A
  • Collection of nuclei (a group of cell bodies)
  • Important for control of movements, reward systems
  • Lesions in basal ganglia can cause disorders such as Parkinson’s and Huntington’s
  • Main structures: caudate nucleus, putamen (both make up striatum) & globus pallidus
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18
Q

Telencephalon: The limbic system

A
  • Limbic cortex, hippocampus, amygdala, fornix, mammillary bodies
  • Important for emotion and learning/memory
  • Hippocampus is important for consolidating memory (e.g. classic case study of H.M.) and spatial navigation
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19
Q

Diencephalon: Thalamus

A
  • Two lobes separated by massa intermedia
  • Receives info from and sends info the cortex
  • Divided into nuclei including lateral geniculate nucleus, medial geniculate nucleus, ventrolateral nucleus
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20
Q

Diencephalon: Hypothalamus

A
  • Controls autonomic nervous system
  • Connected to pituitary gland
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21
Q

Mesencephalon (mid brain)

A
  • Tectum: superior colliculi, inferior colliculi
  • Tegmentum: reticular formation, periaqueductal grey matter (involved in animal fighting and mating), red nucleus (limb movement), substantia nigra (connect to basal ganglia and initiate movement)
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22
Q

Rhombencephalon (hindbrain)

A
  • Metencephalon: pons and important for sleep and arousal. Relays info from cortex to cerebellum
  • Cerebellum is important for coordination of movement
  • Myelencephalon: medulla oblongata. Regulation of cardiovascular system, respiration, and skeletal muscle tonus
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23
Q

The nervous system: 3 types of neurons

A
  • CNS: brain & spinal cord
  • PNS: all other nerves
  • Neurons do all the information processing and information transmitting
  • Many different types of neurons
  • 86 billion neurons
    1. Sensory neurons = info from the body
    2. Interneurons = link sensory and motor neurons
    3. Motor neurons = info to the body
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24
Q

Structure of a neuron

A
  • Soma (cell body): contains nucleus
  • Dendrites: receive messages
  • Axon: carries info from soma to terminal buttons (axon potential)
  • Myelin sheath: wraps around axon
  • Terminal buttons: at the end of the axon branches
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25
Q

Supporting cells: Glia

A
  • Includes: astrocytes (star-shaped cells and provide structural support, provide nutrients to neurones, surround synapse)
  • oligodendrocytes (produce the myelin sheath that insulates axons)
  • microglia (provide support, waste services, supply of nutrients and chemicals)
  • Nodes of Ranvier: naked axon
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26
Q

Transmission within a neuron

A
  • An electrical process
  • All cells have an electrical charge
  • They have more negative on the inside than the outside
  • This results in a resting potential (a store of energy)
  • Neurones can reverse their electrical charge
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27
Q

Cell membrane and ion channel structures

A
  • All cells are covered in a membrane
  • Two layers of phospholipid molecules (hydrophobic tail, hydrophilic head)
  • Ion channel: spans the membrane
  • Cations: positively charged
  • Anions: negatively charged
  • Intercellular fluid contains potassium ions and anions
  • Extracellular fluid contains sodium and chloride ions
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28
Q

The membrane potential: 4 ions

A
  • The membrane potential is the difference in electrical potential inside and outside the cells
  • Balanced by diffusion and electrostatic pressure
  • Organic anions (concentrated inside the cell): cannot cross the membrane
  • Potassium ions (more concentrated inside the cell): wants to move out by diffusion, electrostatic is attracted to inside = overall forces balance so potassium doesn’t move
  • Chloride ions (more concentrated outside the cell): wants to move out by diffusion, electrostatic is repelled from inside = overall forces balance so chloride doesn’t move
  • Sodium ions (more concentrated outside the cell): wants to move in by diffusion, electrostatic attracted to inside = overall both forces sodium into cell but is kept under control by sodium-potassium pump (3 sodium out, 2 potassium in)
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29
Q

Resting potential

A
  • Inside = negative
  • Outside = positive
  • The resting potential of a neurone is -70mV
  • Maintain the resting potential is important so the neurone can respond rapidly to a stimulus
  • An action potential is a reversal in the potential and is how information is sent through an axon
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30
Q

Action potential: depolarisation & hyperpolarization

A
  • Is a rapid change in the membrane potential
  • Is an ‘all or none’ process
  • Depolarization: decrease from normal resting potential (brings membrane closer to 0)
  • Hyperpolarization: increase relative to resting potential (more negative)
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31
Q

Action potential: 6 steps

A
  1. sodium channels open, sodium begins to enter the cell
  2. potassium channels open, potassium begins to leave cell
  3. sodium channels become refractory, no more sodium enters cell
  4. potassium continues to leave cell, causes membrane potential to return to resting level
  5. potassium channels close, sodium channels reset
  6. extra potassium outside diffuses away
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32
Q

What is propagation?

A
  • The action potential is transmitted down an axon via propagation
  • The action potential is regenerated at points along the axon due to the entry of sodium ions at the neighbouring point
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33
Q

What is salutatory conduction?

A
  • Action potential regenerated along the axon at Nodes of Ranvier
  • The electrical conduction ‘jumps’ between the Nodes of Ranvier
  • Benefits: fast conduction, more energy efficient
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34
Q

Transmission between neurons

A
  • neurons send messages via synaptic transmission
  • neurotransmitters are released from one neuron and attach to another neurone
  • this initiates a reaction that ultimately results in postsynaptic potentials
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35
Q

What is synapse?

A
  • the junction between two neurons (terminal buttons & membrane)
  • synaptic vesicles contain neurotransmitters made in the stoma
  • synaptic cleft is 20nm wide
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36
Q

Synaptic transmission: 7 steps

A
  1. action potential arrives at the terminal buttons
  2. calcium channels open and calcium ions enter the neuron
  3. vesicles fuse with membrane and the pores opens
  4. the vesicles release the neurotransmitters into the synapse (exocytosis)
  5. neurotransmitters diffuse across the synapse and bind to the postsynaptic membrane
  6. postsynaptic channels open
  7. ions flow into the neurone which either results in an excitatory or inhibitory post-synaptic potential
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37
Q

Binding of the neurotransmitter

A
  • neurotransmitters bind to binding sites on post-synaptic membrane (lock and key)
  • postsynaptic potential depends in which ion channel is opened
  • EPSP – excitatory postsynaptic potential
  • IPSP – inhibitory postsynaptic potential
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38
Q

Receptors: 2 types

A
  • ionotropic receptor: contains a binding sit and an ion channel. This opens when molecule attaches to binding site. This a direct method
  • metabotropic receptor: contains a binding site. Initiates a chain reaction that eventually opens ion channels, and this requires energy. PSPs slower than those produced by ionotropic receptors
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39
Q

Termination of neurotransmitters: 2 ways

A
  1. Reuptake – transmitter is taken back by the presynaptic terminal vis transporter molecules
  2. Enzymatic deactivation – transmitter broken down by an enzyme (e.g. acetylcholinesterase breaks down Ach into choline and acetic acid
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40
Q

Neural integration

A
  • excitatory: increases likelihood of neuron firing
  • inhibitory: decreases likelihood
  • integration: summation of PSPs in control on neuron firing
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41
Q

Drugs and neurotransmitters

A
  1. Antagonist – a drug that blocks a neurotransmitter (e.g. Botox blocks the release the release of acetylcholine and prevents muscle contraction so paralyses muscles)
  2. Agonist – a drug that mimics a neurotransmitter and enhances synapse function (e.g. muscarine imitates acetylcholine)
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42
Q

Examples of neurotransmitters: 5 examples

A
  1. GABA – most abundant inhibitory neurotransmitter in CNS (reduces chance of neuronal firing)
  2. Glutamate – most abundant excitatory neurotransmitter in CNS. Can bind to several receptors. Learning and memory
  3. Acetylcholine – first neurotransmitter discovered. Focus on neuromuscular junction. Working primarily in muscles
  4. Serotonin – regulation of mood, eating and sleep
  5. Dopamine – motor control. Reward and addiction
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43
Q

Neurological diseases and cases

A
  • Stroke
  • Alzheimer’s disease (affects hippocampus)
  • Parkinson’s disease (deuteriation in the substantia nigra)
  • Patient Leborgne (had a stroke which affected his left frontal cortex and then had problems with speech)
  • Phineas gage (iron rod through his frontal cortex but his behaviour changed)
  • Patient HM (suffered from epilepsy and underwent temporal lobe surgery)
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44
Q

Methods to study the brain and its role in behaviour

A
  • Behavioural studies
  • Manipulations of brain function
  • Neuroanatomy and histology
  • Electrophysiology
  • Imaging (MRI & PET)
  • Computational models
    (brain-behaviour requires combination of many methodological approaches)
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45
Q

Case studies: Patient H.M.

A
  • Surgical resection of medial temporal lobe, mainly hippocampus, to stop epileptic seizures
  • Impairments in specific types of memory, including aspects of declarative and spatial memory
  • Other cognitive and memory functions were largely unaffected
  • Led to concept of memory systems (procedural, declarative, etc)
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46
Q

Experimentally induced lesions

A
  • Selective destruction of specific brain sites (mechanical, electrolytic, neurotoxic)
  • Temporary pharmacological manipulations via pre-implanted micro-cannulae to switch neurones or switch specific receptors on and off
  • Electrical stimulation of specific brain sites
  • Targeted mutations of brain-specific genes
  • Optogenetics (manipulate specific genes in the brain to make them light sensitive to either activate or inhibit these genes later)
  • Trans-cranial magnetic stimulation (TMS)
  • Morris et al (1982): selective place learning deficits after hippocampal lesions in rats using a water maze
  • Results: The hippocampus is necessary for spatial and declarative memory
47
Q

Neuroanatomical study of brain connectivity

A
  • Neuronal tract tracking: take a compound and inject it into one brain region where it travels along the axon away from the stoma or the opposite way (against action potential)
  • This shows the connections between the brain areas
48
Q

Electrophysiology: 2 types of recordings

A
  • Single unit recordings: recording the electrical activity of single neurons (e.g. ‘place cells’ in the hippocampus)
  • Local field potential (LFP) recordings: recording electrical potentials generated by many neurons (‘field potentials’)
  • Invasive single unit and LFP recordings in humans: only conducted in rare cases for pre-surgical evaluation of epilepsy patients
  • Surface EEG for humans: spontaneous and event-related (provoked)
  • Magnetencephalography (MEG) in humans: measures the small magnetic field changes accompanying electrical voltage changes due to brain activity. Better spatial resolution than EEG (<1cm)
49
Q

Magnetic resonance imaging (MRI)

A
  • Images are generated from MR signal that emanates from hydrogen nuclei in brain tissue when these are aligned by a strong magnetic field and then excited by a magnetic pulse
  • Structural MRI of the brain: non-invasive imaging of brain structure based on MRI contrast between different tissue types due to different densities of H nuclei
  • Functional MRI of the brain: non-invasive imaging of brain ‘activity’ based on MR signal changed associated with metabolic and cerebral-blood-flow changes. Most common is based on changes in the Blood-Oxygen-Level-Dependent (BOLD) MR signal
50
Q

Activation of human hippocampus during place memory task in virtual environment: an fMRI study

A

(Bohbot et al 2004)
- Results: didn’t conclude that hippocampus is necessary for place/ such memory
- Correlation does not mean causation

51
Q

What is Positron Emission Tomography (PET)?

A
  • Involves injection of radioactive tracers that resemble compounds of biological interest. Using dedicated detectors around the head, these tracers can be followed in the brain (e.g. to monitor metabolic activation)
  • Measure indirectly binding of dopamine and serotonin receptors
52
Q

Modelling the brain: spatial learning and navigation by Darwin X, a brain-based device

A
  • Spatial learning: the robot first didn’t have a clue, but overtime got mor precise where it was going – showing its learning
53
Q

What is the primary visual pathway? its journey

A
  • Primary visual pathway from eyes to primary visual cortex (striate cortex, V1) In the occipital lobe
  • Stimulates areas in retina called the fovea (where photoreceptors are located)
  • Travelled down the optic nerve through the lateral geniculate nucleus to the primary visual cortex
54
Q

Information-processing stages in primary visual pathway

A
  • Photoreceptors – bipolar cells – retinal ganglion cells
  • Experimental strategy to reveal mechanism at visual perception
  • By studying the different neuronal responses at different stages of the visual pathway, one may gain understanding of the different stages of visual information processing that mediate visual perception
55
Q

Experimental set-up to record visual responses of neurones along the visual pathway

A
  • Attach electrodes to the brain to study the neurones at the different stages
  • Performed whilst unconscious
  • Start at the retina and then move up to the lateral geniculate body and then visual cortex
56
Q

Facts about photoreceptors: 2 types

A
  1. Rods – more abundant and has no colour discrimination
    - Sensitive in low light levels (easy to see at night)
    - Higher density in periphery
    - Track high-rate changes
  2. Cones – less abundant and has 3 types of discriminate different colour wavelengths
    - Less sensitive to low light
    - Higher concentration in fovea
    - Cannot follow rapid changes
    Photoreceptors and bipolar cells vary their voltage as they are stimulated, whereas all subsequent cells vary spike rate (all-or-nothing)
    Photoreceptor detection of light is translated into excitation or inhibition of retinal ganglion cells via bipolar cells
57
Q

Receptive fields of visual neurons

A
  • The portion of the retina/visual fields in which visual stimulation will evoke a change in the firing rate of a given visual neuron
  • Substructure of a receptive field: A description of how visual stimuli need to be presented in the receptive field of a visual neuron to evoke firing-rate changes
58
Q

What do retinal ganglion cells do?

A
  • Receive input from multiple photoreceptors (via bipolar cells)
  • ON-OFF Centre-Surround receptive fields
  • Light presented in ‘ON’ regions, excites cell, and light in ‘OFF’ region inhibits cell
  • ON & OFF regions are organised in ‘centre-surround’ fashion
  • Response rate of cell is based on the sum of stimulation in ON region minus stimulation in OFF region
  • Enhancement of contrast and boundaries
  • Neurons in the lateral geniculate body respond to visual stimuli in similar ways to retinal ganglion cells
59
Q

Functional significance of centre-surround fields

A
  • The world has lots of things that stay constant, and we don’t need to keep responding to them (changes and boundaries counts the most)
  • So, responding only to changes and boundaries (edges) is efficient
  • The luminance of features is represented relative to their surround so it helps preserve appearance of objects regardless of light levels in the environment (newspaper looks basically the same in a dark room and in sunlight, despite hugely different levels of overall reflected light) but it can also result in illusions
60
Q

Colour sensitivity of retinal ganglion and LGN neurons

A
  • Retinal ganglion and LGN cells receive inputs from cones (that are differentially sensitive to different wavelengths) and are sensitive to colour
  • Colour-sensitive retinal ganglion and LGN neurons have receptive fields that dhow centre-surround colour opponency
  • Function significance of colour-opponency not clear
  • However, colour opponency, together with firing-rate adaption (rebound effects), in retinal ganglion cells can explain negative afterimages
61
Q

Orientation-selective cells in V1

A
  • Most V1 neurons respond to elongated stimuli with specific orientation and has two main types of orientation-selective V1 neurons
  • Simple cells = fields have inhibitory and excitatory regions and can be thought of as combining inputs from ON & OFF cells
  • Complex cells: fields have no discrete ON & OFF regions. Best responses to moving stimuli and can be thought of as combining inputs from simple cells
62
Q

Maps and modules in V1

A
  • Retino-topic map – orderly mapping of retina/visual field onto visual cortex
  • Modules – V1 is divided into small columnar modules that combine neurons sensitive to different aspects of stimuli presented in a small part of the visual field
63
Q

Further processing of visual information

A
  • To result in perception and memory of the ‘holistic’ visual properties of whole objects and visuals scenes, the visual information from the modules in V1 needs to be combined and further processed
  • This processing takes place in the visual association cortices (V2-V5, inferior temporal cortex, posterior parietal cortex) and other regions
64
Q

Facts about people with Blindsight

A
  • Subjects with lesions to primary visual cortex and apparent ‘blindness’ can show appropriate responses to visual stimuli of which they are not ‘conscious’ (e.g. ‘looking’ or pointing toward visual stimuli; detection of movement; etc.)
  • ‘Blindsight’ highlights that, apart from the primary visual pathway that is critical for conscious vision, there are additional visual pathways
  • Recent study suggests that direct LGN projections to extrastriate cortex are critical for blindsight
  • ‘Blindsight’ also highlights that the brain can perform visual information processing which can guide subjects’ behaviour without their conscious awareness
65
Q

Hierarchy and functional differentiation in visual information processing:

A
  • Processing of visual info by the brain is hierarchical, with the complexity of the visual representation increasing from retina to visual association cortices and beyond
  • At the different stages of info processing there is functioning differentiation, with different neuron types or different brain region processing different properties of visual stimuli
    1. Simple features: light intensity and wavelength, 2D position in visual field
    1. Combination and elaboration via parallel channels
    1. Complex visual representations for perception and memory: Integrated info (shape., colour, spatial, movement), integration with other sensory modalities
66
Q

Visual processing in extrastriate cortex

A
  • Neurons in extrastriate cortex signal ‘global’ properties of visual scenes and objects, rather than ‘component’ properties
67
Q

Global colour vs component wavelength

A
  • Perceived colour of an object depends not only on the wavelength reflected by the object, but also on the wavelength reflected by the surroundings (colour constancy: e.g. perceived colour of an object does not change when viewed during sunset)
  • Some neurons in V4 are ‘colour’-sensitive (i.e. respond to wavelengths in the centre of their receptive field, depends on the wavelengths reflected from the background), whereas neurons in primary visual pathway and V2 are only ‘wavelength’-sensitive
68
Q

Two visual information processing streams

A
  • Following V1 visual information processing is mediated by two streams that are anatomically and functionally differentiated
    1. Dorsal stream: visuo-spatial/ visuo-motor processing
    1. Ventral stream: object analysis
  • Inferior temporal lobe lesions (‘ventral stream’) in monkeys impair object-discrimination/recognition (‘what’), but not object location (‘where’)
  • Posterior parietal lesions (‘dorsal stream’) impair object location (‘where’), but not discrimination (‘what’)
69
Q

What are visual streams

A
  • (Milner & Goodale) proposed that the ventral stream processes visual information for object perception, whereas the dorsal stream processes visual information for visuo-spatially guided action
  • Key evidence: patients with occipital-temporal brain damage show severe forms of visual agnosia (i.e. deficits in aspects of visual perception without blindness) but intact visually guided actions, whereas patients with posterior-parietal lobe lesions show optic ataxia (i.e. deficits in visually guided reaching) with otherwise relatively intact visual function
70
Q

Visual perception and memory in inferior temporal cortex

A
  • The inferior temporal cortex receives inputs from extrastriate cortex and forms the final stage in the visual processing hierarchy of the ventral stream
  • Neurons in the inferior temporal cortex can respond very selectively to specific shapes and objects
  • These responses can show invariance to changes in size/ orientation & sustained activity in absence of visual object, reflecting short-term object memory
71
Q

What are face cells?

A
  • Some neurons in the inferior temporal lobe show highly selective responses to individual faces
  • The highly selective properties have been compared to those of ‘gnostic units’ or ‘grandmother neurons’ (i.e. hypothetical neurons at the end of a processing hierarchy that ‘recognise’ individual entities, such as your grandmother)
  • Areas showing selective responses to faces have also been identified in the human inferior temporal lobe using functional imaging
72
Q

The medial temporal lobe (MTL): further processing of visual information and multimodal integration

A
  • MTL is at the end of the visual-processing hierarchy, combining inputs from ventral and dorsal streams, and receives additional inputs from other sensory modalities
  • It is thus in position to elaborate visual representations further and to generate multi-modal representations (e.g. complex spatial representations \7 multimodal representations of experiences)
73
Q

Parietal lobe: Boundaries

A
  • Central sulcus (boundary with frontal lobe)
  • Parieto-occipital fissure (boundary with occipital lobe)
  • Macro-anatomical (based on sulci and gyri)
  • Lateral sulcus (boundary with temporal lobe)
  • Central sulcus, postcentral sulcus, postcentral gyrus
74
Q

Parietal lobe: Major anatomical subdivisions

A
  1. Primary somatosensory cortex
  2. Posterior parietal cortex (Superior parietal lobule, intraparietal sulcus, inferior parietal lobule, anterior parietal lobule)
75
Q

Primary somatosensory cortex

A
  • Function: processing information about body sensations (touch, pain, proprioception)
  • Can be divided into at least 4 subdivisions
  • Input – mainly from the thalamus and motor cortex
  • Output – mainly to motor cortex and posterior parietal cortex
  • Penfield and Boldrey (1937) inserted electrodes in the somatosensory cortex of epileptic pp’s just before operating on them and then he stimulated different parts of the cortex and recorded the sensation reported by the patients = led to creation of a simplified somatopic map (somatosensory homunculus)
  • Seelke et al (2012) while there is clear somatotopy, it isn’t as simple as depicted by Penfield
  • You can learn about brain reorganisation after injuries and through learning
  • Functional reorganisation of S1 can occur within just 24 hours (supported by Kolasinki et al 2016, where a little and ring finger were glued together)
76
Q

Intraparietal sulcus and superior parietal lobule

A
  • Overarching concept – vision for action (dorsal visual stream)
  • More anterior areas = coding in hand-centred coordinate system
  • More posterior areas = coding in vision-centred coordinate system
  • Classic neuropsychological syndrome after bilateral lesions (Balint syndrome):
  • A) Optic ataxia (deficit in visually guided reaching movements)
  • B) oculomotor apraxia (inappropriate fixation of gaze and difficulties in voluntarily shifting fixation to other objects)
  • C) simultanagnosia (impaired ability to perceive multiple items in a visual display)
  • Involvement in cognitive functions might derive from these rudimentary mechanisms:
  • A) visuospatial working memory – link to representing the location of objects, coding what is relevant
  • B) mental rotation/imagery – link to manipulating objects
  • C) arithmetic – link to moving eyes/hands to count, spatial layout
76
Q

Left anterior inferior parietal lobule

A
  • Reynaud et al (2016) understanding tool-use actions
  • Lesion in this area – apraxia with possible impairments (imitation of gestures, communicative gestures, real tool use)
77
Q

Left posterior inferior parietal lobule

A
  • Seghier (2012) semantic processing, reading, comprehension, number processing, default mode processing, memory retrieval, theory of mind
  • Integrative account for more posterior areas
  • Bottom-up attention to internally generated stimuli
  • Contrasts from the right inferior parietal lobule which relies on bottom-up information from environmental stimuli
  • One possibility why function could be difficult to understand – animal models might not work for these areas
78
Q

Frontal lobe: anatomy and main subdivisions

A
  • Primary motor cortex – giant Betz cells in layer V
  • Premotor cortex – no granular cells in layer IV
  • Prefrontal cortex – granular cells in layer IV
  • Brodmann’s (1909) classic cytoarchitectonic map
  • Strong evidence that there are more areas than identified by Brodmann
79
Q

Functions of motor and premotor cortex

A
  1. Motor cortex – control of skeletal muscles together with ither structures, roughly somatotopically organised
  2. Premotor cortex – movement planning, selection, sequencing, inhibitory control of motor cortex
80
Q

Neuropsychology of the prefrontal cortex: Traditional approach

A
  • Neuropsychological tests conducted on patients with frontal lobe lesions deficits
  • Verbal fluency & Wisconsin card sorting test (Milner, 1964)
  • Stroop task (Perret, 1974), Tower of London (Shallice, 1982)
  • Issues = sensitivity – ability of test to identify those with prefrontal lesions, specificity – ability of tests to not identify those impaired by lesions in other areas, not all patients have frontal lesions have difficulties, some patients with non-lesions have difficulties
81
Q

Neuropsychology of the prefrontal cortex: Recent approach

A
  • Stuss & Alexander (2007) basic approach – devise simple tests, manipulate difficulty and context, based on Norman and Shallice supervisory attention system
  • Lesion-symptom mapping
  • Conclusions: lateral pre-frontal cortex executive function (left – task setting, right – monitoring)
  • Dorsomedial pre-frontal cortex energisation (processing of initiating and sustaining any response)
  • Orbital PFC behavioural and emotional self-regulation
  • Polar PFC metacognition
  • Evaluations: Lesion-symptom mapping is interesting (Further refined with modern structural MRI)
  • Exact processes are still unclear
  • General problems with patient studies: small sample sizes, lesions restricted to grey / white but not both
  • Adaptivity per se is plausible but it is restricted.
  • Hierarchical organization per se is plausible but exact processes associated with the different areas are still quite unclear
82
Q

Basic emotion: Ekman

A
  • 7 basic emotions (anger, disgust, fear, surprise, happiness, sadness, contempt)
  • Basic emotions are universal (present in all human societies) and do not need to be learned
  • New Guinea and Borneo population:
    1. Most frequent response was predicted – only 50% accuracy
    2. Stimuli where more than 70% agreed – Less than 50% accuracy.
    3. Happy stimuli recognised consistently
    4. Fear and anger seem to be confused with each other.
    5. Surprise and Fear seem to be confused.,
  • Point – not as universal as Ekman claimed, his own research did not support this
83
Q

Criticisms to Ekman’s approach

A

(are basic emotions really universal?)
- Gendron et al (2014) tested this on the Himba tribe in Namibia
- Task: sort face pictures into piles – no labels given
- ‘happy’ and ‘fearful’ consistently recognised
- But not sadness, disgust and anger
- Basic emotions fail to describe the richness of human emotional experience (Cowen & Keltner 2017) – identified 27 ‘fuzzy’ categories
- You can replicate the study within the same lab with the same labelling
- Sorenson (1975) failed to replicate when using free labelling

84
Q

Ekman’s sketchy past

A

(why didn’t Ekman revise his theory given the failed replication by Sorenson?)
- Ekman was funded by DARPA, who has some ‘interesting; research that it funds (e.g. MAD-FIRES which is a program to develop self-guided bullets)
- - not that emotions were useless to DARPA, but they were more interested in using this deception detection for defence purposes
- So, they threw more money at the problem, repeatedly renewing grand with Ekman
- Ekman developed a tool for lie detection (METT) – people show fleeting expressions of ‘felt emotions’, so when people attempt to mask, emotions consistent with their ‘actual state’ will appear briefly as some facial muscles are difficult to control
- METT does not stand up consistently in testing and therefore dangerous
- 80-90% of emotion research view the following emotion as empirically established (anger, fear, disgust, sadness, happiness)

86
Q

From centres to distributed representations

A
  • Emerging view of emotions as dynamic, distributed representations in brain networks
  • Problem with human research: no neuroimaging method has (high spatial resolution, high temporal resolution, whole-brain coverage)
  • Representations are distributed but more fine-grained functional-anatomical understanding possible in theory
  • Animal research might be able to fill some gaps
88
Q

Emotion regulation: cognitive reappraisal

A
  • Anterior Insula (AI), Anterior cingulate cortex (ACC) and PFC (lateral and medial) are important for voluntary control over amygdala activation.
  • Oschner et al (2002) Participants were asked to reappraise negative images (E.g., crying in grief – change meaning – crying with joy)
  • Decreased activation in amgydala and increased activation in PFC (lateral and medial)
  • Vergallito et al., (2018) – brain stimulation – rVLPFC would regulate negative affect in preventing dangerous situations regardless of intensity
  • Coactivation between AI, ACC and PFC also shown in regulating and processing; Interoceptive (heartbeat, arousal) & Exteroceptive (environmental changes)
  • Important for anxiety disorders, depressive disorders, aggression, impulsivity
  • In everyday life, you could use cognitive appraisal strategies: Presentations, Public Speaking & Social communication
  • Brooks (2013) Reappraise anxiousness as excitement
89
Q

Who is Mendel and what did he discover?

A
  • He noted that peas get one version of each trait from each parent (alleles), some seemed to be dominant while others were recessive
  • Dominant traits are easily expressed in an organism’s phenotype
  • Recessive traits are only expressed in the absence of an overshadowing dominant trait
  • Many of your phenotype traits will depend on your parents, as you receive an allele of each gene from each
90
Q

Mendelian inheritance: 2 laws

A
  • Relies on two fundamental laws:
    1. Segregation – traits are either dominant or recessive
    2. Independence – varieties of each trait sort independently of each other
91
Q

DNA to chromosomes to genes

A
  • Deoxyribonucleic acid (DNA) can be found in the nucleus of every cell, and it composed of two strands of nucleotides that coil around each other to form a double helix
  • Adenine & Thymine, Guanine & Cytosine
  • The long strands of DNA in the nucleus are called chromatids
  • When mitosis occurs, the chromatids undergo condensation (act of coiling tight to form a chromosome)
  • Humans typically have 46 chromosomes (females have XX, males have XY)
  • Individual sequences of DNA on these chromosomes are called genes
  • Some phenotype traits may be programmed by a single gene (pleiotropic) or a combination of genes (polygenic)
  • Locus – position of gene on the DNA sequence
92
Q

Beyond Mendel: Sex-chromosome disorders

A
  • X-linked conditions: some recessive traits more prevalently expressed in males compared to females because they may not have a dominant allele on their Y chromosome
  • E.g. Colour-blindness, Turner syndrome, Klinefelter syndrome, Fragile X syndrome (all generally associated with learning disabilities, language delays, emotional issues)
93
Q

Beyond Mendel: Sporadic mutations

A
  • Caused by errors or interference in typical cell division and these mutations can happen naturally or be the result of environmental factors |(e.g. radiation)
  • Down’s Syndrome – effects 1/1000 and causes learning difficulties
  • Williams Syndrome – effects 1/18000 and causes earning difficulties
94
Q

Beyond Mendel: Polygenic traits

A
  • These conditions or disorders reply on coding from multiple genes and may not consistently follow Mendelian rules
  • Schizophrenia – effects 20m worldwide
  • Individuals are genetically predisposed to develop schizophrenia, suggesting a clear genetic basis
  • But some interaction with the environment
95
Q

Genetic research methods

A
  • Twin studies – compare monozygotic (genetically identical) and dizygotic twins
  • Genomic studies – inspect the genome of specific groups and identify allele commonalities (e.g. studying an extended family prone to Huntington’s helped identify the genetic markers)
  • Targeted mutations – mutated lab produced genes are inserted into chromosomes. Usually two types
    a) These can be defective and fail to produce a specific functional protein
    b) These can also produce new or different proteins
96
Q

Genetic engineering

A
  • Suggested to be on the verge of a genetic revolution
  • Technology such as CRISPR may allow us to directly edit our own genome
  • Currently being used to tackle big diseases such as HIV and cancer
  • Potential applications are huge
  • However, may be an ethical nightmare
97
Q

History of animals in biological research

A
  • Dates back 3000+ years
  • Systematic use picked up in the renaissance
  • Cruelty to animals’ act (1876) first introduction of ethical guidelines
98
Q

Historical benefits of animal use: 3 benefits

A
  1. Medical advancements e.g. to combat pandemics, understand anatomy
  2. Psychological advancements e.g. treatments of disorders
  3. Veterinary advancements
99
Q

Benefits: transplants

A
  • Fist successful transport in 1954
  • More than 50,000 people now alive thanks to organ donation & transplant
100
Q

History of humans in biological research

A
  • Experimented on: poor, blind, slaves, prisoners & mentally ill people
  • E.g. bloodletting, isolation practices, lobotomy & trephination
101
Q

University of Nottingham: Significant rules & guidelines

A
  • Code of research conduct and research ethics
  • WHO: declaration of Helsinki (2006)
  • UKRIO: code of practice for research
  • UK GDPR
  • NO long-term damage
  • Minimum number required to obtain valid use
  • More than slight pain = under anaesthesia
  • Reward clearly needs to be worth any risk
  • INFORMED CONSENT!
102
Q

Ethical hurdles

A
  • Research often uses animal subjects
  • Often done before birth or in early years
  • Potentially unforeseen long-term consequences
  • Ethics in biological research: ongoing process, ethics continues to change, keep a dialogue, stay transparent, be kind
103
Q

Learning from the past with ethics

A
  • Contemporary gynaecology: as with many medical practices devised in the 19t century, roots can be directly linked back to experiments conducted on slaves
  • The Los Alamos Plutonium Experiments: between 1945-1947, 18 people were unknowingly injected with plutonium during unrelated GP visits
  • Tuskegee Syphilis Experiment: individuals infected with syphilis and lied about treatments (placebos). One of many studies where people have been unknowingly infected. Fuelled congress-lead legislation within the USA
  • HeLa Cells: unknowingly had ‘immortal’ cells harvested and circulated
104
Q

What are the core concepts of evolution?

A
  • Darwin’s theory of evolution: he noticed that mockingbirds differed between islands. Characteristics of an organism had a useful function for its survival
  • Mechanisms of natural selection: differences are seen within species and inherited by offspring, favourable characteristics that help in survival get passed on to offspring so overtime, these become dominant. Mutations could occur and non-useful die out, favourable passed on
  • Adaptive radiation: single species rapidly evolves into multiple new species to match survival. Little competition and diverse resources
105
Q

Human evolution: Brief history

A
  • Earliest mammals – small nocturnal predators that fed on insects
  • The first hominids (humanlike apes) appeared in Africa and left around 1.7 million years ago.
  • Human evolution was a relatively late development – given overall timescale of primate evolution (some 60 million years ago.)
  • Rapid evolution of human brain and behaviour sets us apart but also seen as part of the evidence for our animal ancestry
  • Our closest living relatives – Chimpanzees, Gorillas and Orangutans
106
Q

Human brain evolution

A
  • Human useful functions and need for complex brain (i.e. Bipedalism – Mobility, energy efficiency and adaptability, Colour vision – Differentiate fruits from leaves, fruit decay & Linguistic abilities – Sharing information, propagation of species)
  • Neoteny – Slowing of maturation, allowing for time for growth, important for large brain and complexity
  • Not all neurons are coded at birth, allowing for learning based on environment.
  • Human brain weight for a neonatal = 350g & Adult human brain = 1400g
  • Hippocampal lesion in rats tell us which neuronal systems are key
107
Q

Evolution shaping psychological mechanisms

A
  • Game theory:
  • (Von Neumann & Morgenstern) Classic definition: Mathematical model of strategic decisions. Analysis of outcomes based on their own decisions and other players decision. No control on others’ decision
  • (Maynard Smith & Price) Applied in understanding evolution strategies. Evolutionary Stable Strategies (ESS) and Price Equation
  • Evolutionarily stable strategy (ESS) Once adopted by most of the population, cannot be invaded by alternative strategy. Best strategy for survival
  • Two Conditions: Strategy should do better with itself than any new competing strategy if it tried to invade, Strategy should have at least comparable pay off (benefit) than any other strategy
108
Q

Kin selection – Altruism towards relatives

A
  • Behaviour at a coat to oneself but benefit to others
  • Inclusive Fitness: Includes both direct fitness (offspring of an individual) and indirect fitness (offspring in the same species)
  • Hamilton’s Rule (Hamilton, 1963) : rB>C (r = genetic relatedness, B = benefit to recipient and C = cost to altruist’s fitness)
  • Price’s Equation: Mathematically explains how natural selection is connected to inclusive fitness
  • Even if there is a cost to individual fitness, if net effect (genetic line) increases (rB), altruism increases
  • Based on two mechanisms:
    1. Reciprocal altruism (Trivers, 1971): Benefits will be reciprocated in a similar situation. Price Equation – Past cooperation predicts future fitness. Iterated Prisoners Dilemma
    2. Group Selection: More cooperation – helps dominate selfish groups. E.g., humans giving to charity, vampire bats regurgitating blood for non-relative vampire bats
109
Q

Schizophrenia: an overview

A
  • Affects approximately 1:300 people (24 million)
  • Onset is most often during adolescence and 20s
  • Considered to be a type of psychosis; a loss of contact with reality (‘split mind’)
110
Q

Symptoms of schizophrenia: Positive, negative & cognitive

A
  • Positive – hallucinations, thought disorder, delusions
  • Negative – emotional response, social withdrawal, poverty of speech, lack of persistence, anhedonia (lack of interest)
  • Cognitive – difficulty sustaining attention, low psychomotor speech, deficits in learning/ memory, poor problem solving, poor abstract thinking
  • Ventricular enlargement is one of the earliest and most consistent finding in schizophrenia (130% the size of normal controls)
  • Other physical symptoms: fine electric hair, wide-set eyes, third toe longer than second toe)
111
Q

Causes of schizophrenia

A
  • Not entirely sure (could be linked to genetic and environmental factors) so suggest a genetic predisposition
  • Heritability – 46% chance of developing schizophrenia if both parents have it
  • Davis et al (1995) showed 60% concordance in MZ twins and 10.7% in DZ twins
  • Other environmental factors; cannabis use, prenatal infection, birth month, childhood trauma, chronic stress
112
Q

Treatments & pharmacology for schizophrenia

A
  • The dopamine hypothesis: pp with schizophrenia has an overactivity in dopamine neurons (as taken dopamine receptor medications alleviated psychotic symptoms)
  • Activity of Dopamine neurons in the accumbens strongly reinforce behaviour
  • Fibiger (1991) – Paranoid delusions caused by activity in Amygdala (fear responses, learning emotional responses)
  • Snyder (1974) – Schizophrenics report elation at the start of a schizophrenic episode
  • NMDA theory: glutamate hypoactivity in regions involved with cognition and executive function
  • Serotonin theory: serotonin dysfunction may disrupt typical cognitive abilities prompting the schizophrenic development
  • Non-medication treatments are also available (e.g. CHT/ Art therapy)
113
Q

Affective disorders: an overview

A
  • Categorised as a mood disorder, identified by disruption in emotions
  • Primary symptoms: Depression (low energy levels, loss of appetite, sleeping problems), Mania (euphoria, delusional, poor attention span, lack of sleep)
  • Currently unclear as no consistent neurological markers across conditions
114
Q

Affective disorders: 3 Main types

A
  1. Bipolar disorder - Alternating periods of mania and depression, 1% of the population afflicted at some point in their life, equally frequently in men and women
  2. Unipolar disorder - Depression without mania, 2 or 3 times more likely in women than men
  3. Seasonal affective disorder - Depression typically associated with the onset of winter months
115
Q

Causes of affective disorders

A
  • Clear link with both genetics and environmental factors (genetic predisposition)
  • Heritability: (Gershon et al 1976) MZ concordance = 69%, DZ concordance = 13%
  • (Rosenthal 1971) 10 times more likely to suffer from affective disorders if a close relative also does
116
Q

Treatments & pharmacology for affective disorders

A
  • The monoamine hypothesis: suggest depression is caused by faulty activity on monoamine neurons (e.g. deficits in serotonin = modulating mood, norepinephrine imbalance = bodies stress response, dopamine dysfunction = reward and pleasure pathway)
  • Non-medication treatments are also available