Biological psychology Flashcards

(158 cards)

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
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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7
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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7
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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8
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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9
Q

Parietal lobe: and function

A
  • Caudal to frontal lobe, dorsal to temporal lobe
  • Function = somatosensory
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10
Q

Occipital lobe: and function

A
  • Caudal to parietal and temporal lobes
  • Function = vision
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11
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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12
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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13
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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14
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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15
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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16
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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17
Q

Diencephalon: Hypothalamus

A
  • Controls autonomic nervous system
  • Connected to pituitary gland
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18
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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19
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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20
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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21
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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22
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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23
Transmission within a neuron
- 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
24
Cell membrane and ion channel structures
- 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
25
The membrane potential: 4 ions
- 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)
26
Resting potential: and its importance
- 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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Action potential: depolarisation & hyperpolarization
- 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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Action potential: 6 steps
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
29
What is propagation?
- 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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What is salutatory conduction?
- 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
31
Transmission between neurons
- 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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What is synapse?
- the junction between two neurons (terminal buttons & membrane) - synaptic vesicles contain neurotransmitters made in the stoma - synaptic cleft is 20nm wide
33
Synaptic transmission: 7 steps
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
34
Binding of the neurotransmitter
- 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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Receptors: 2 types
- 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
36
Termination of neurotransmitters: 2 ways
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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Neural integration
- excitatory: increases likelihood of neuron firing - inhibitory: decreases likelihood - integration: summation of PSPs in control on neuron firing
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Drugs and neurotransmitters
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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Examples of neurotransmitters: 5 examples
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
40
Neurological diseases and cases
- 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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Methods to study the brain and its role in behaviour
- 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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Case studies: Patient H.M.
- 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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Experimentally induced lesions
- 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
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Neuroanatomical study of brain connectivity
- 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
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Electrophysiology: 5 types of recordings
- 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)
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Magnetic resonance imaging (MRI)
- 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
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Activation of human hippocampus during place memory task in virtual environment: an fMRI study
(Bohbot et al 2004) - Results: didn’t conclude that hippocampus is necessary for place/ such memory - Correlation does not mean causation
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What is Positron Emission Tomography (PET)?
- 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
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Modelling the brain: spatial learning and navigation by Darwin X, a brain-based device
- Spatial learning: the robot first didn’t have a clue, but overtime got mor precise where it was going – showing its learning
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What is the primary visual pathway? its journey
- 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
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Information-processing stages in primary visual pathway
- 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
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Experimental set-up to record visual responses of neurones along the visual pathway
- 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
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Facts about photoreceptors: 2 types
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
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Receptive fields of visual neurons
- 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
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What do retinal ganglion cells do?
- 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
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Functional significance of centre-surround fields
- 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
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Colour sensitivity of retinal ganglion and LGN neurons
- 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
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Orientation-selective cells in V1
- 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
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Maps and modules in V1
- 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
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Further processing of visual information
- 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
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Facts about people with Blindsight
- 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
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Hierarchy and functional differentiation in visual information processing:
- 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 - 2. Combination and elaboration via parallel channels - 3. Complex visual representations for perception and memory: Integrated info (shape., colour, spatial, movement), integration with other sensory modalities
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Visual processing in extrastriate cortex
- Neurons in extrastriate cortex signal ‘global’ properties of visual scenes and objects, rather than ‘component’ properties
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Global colour vs component wavelength
- 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
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Two visual information processing streams
- Following V1 visual information processing is mediated by two streams that are anatomically and functionally differentiated - 1. Dorsal stream: visuo-spatial/ visuo-motor processing - 2. 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’)
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What are visual streams
- (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
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Visual perception and memory in inferior temporal cortex
- 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
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What are face cells?
- 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
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The medial temporal lobe (MTL): further processing of visual information and multimodal integration
- 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)
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Parietal lobe: Boundaries
- 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
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Parietal lobe: Major anatomical subdivisions
1. Primary somatosensory cortex 2. Posterior parietal cortex (Superior parietal lobule, intraparietal sulcus, inferior parietal lobule, anterior parietal lobule)
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Primary somatosensory cortex
- 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)
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Intraparietal sulcus and superior parietal lobule
- 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
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Left anterior inferior parietal lobule
- Reynaud et al (2016) understanding tool-use actions - Lesion in this area – apraxia with possible impairments (imitation of gestures, communicative gestures, real tool use)
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Left posterior inferior parietal lobule
- 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
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Frontal lobe: anatomy and main subdivisions
- 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
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Functions of motor and premotor cortex
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
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Neuropsychology of the prefrontal cortex: Traditional approach
- 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
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Neuropsychology of the prefrontal cortex: Recent approach
- 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
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Basic emotion: Ekman
- 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
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Criticisms to Ekman’s approach
(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
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Ekman’s sketchy past
(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)
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From centres to distributed representations
- 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
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Emotion regulation: cognitive reappraisal
- 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
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Who is Mendel and what did he discover?
- 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
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Mendelian inheritance: 2 laws
- Relies on two fundamental laws: 1. Segregation – traits are either dominant or recessive 2. Independence – varieties of each trait sort independently of each other
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DNA to chromosomes to genes
- 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
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Beyond Mendel: Sex-chromosome disorders
- 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)
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Beyond Mendel: Sporadic mutations
- 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
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Beyond Mendel: Polygenic traits
- 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
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Genetic research methods
- 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
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Genetic engineering
- 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
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History of animals in biological research
- Dates back 3000+ years - Systematic use picked up in the renaissance - Cruelty to animals’ act (1876) first introduction of ethical guidelines
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Historical benefits of animal use: 3 benefits
1. Medical advancements e.g. to combat pandemics, understand anatomy 2. Psychological advancements e.g. treatments of disorders 3. Veterinary advancements
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Benefits: transplants
- Fist successful transport in 1954 - More than 50,000 people now alive thanks to organ donation & transplant
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History of humans in biological research
- Experimented on: poor, blind, slaves, prisoners & mentally ill people - E.g. bloodletting, isolation practices, lobotomy & trephination
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University of Nottingham: Significant rules & guidelines
- 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!
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Ethical hurdles
- 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
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Learning from the past with ethics
- 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
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What are the core concepts of evolution?
- 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
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Human evolution: Brief history
- 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
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Human brain evolution
- 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
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Evolution shaping psychological mechanisms
- 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
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Kin selection – Altruism towards relatives
- 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
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Schizophrenia: an overview
- 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’)
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Symptoms of schizophrenia: Positive, negative & cognitive
- 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)
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Causes of schizophrenia
- 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
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Treatments & pharmacology for schizophrenia
- 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)
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Affective disorders: an overview
- 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
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Affective disorders: 3 Main types
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
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Causes of affective disorders
- 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
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Treatments & pharmacology for affective disorders
- 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
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What is cognitive neuropsychology?
- The study of the relationship between brain regions and behaviour - Historically linked to evidence from damaged brains - Generally, now includes other methods (e.g. imaging, lesion studies) - Missile wounds, tumours, impact, injury, surgery, disease, strokes
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Aims and assumptions of cognitive psychology
- Aims to assign specific psychological functions to particular brain structures - Assumption: brin function is ‘localised’ or ‘modular’ with different structures performing different roles - Many functions rely on distributed brain systems (i.e. language, memory) - Brain regions are specialized to perform roles, but these may not map neatly onto ideas of ‘brain functions’
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Cognitive neuropsychology: History
- (Gall & Spurzheim) as a youth, Gall was annoyed by students with a good memory but poor original thinking - Recalled these students had protruding eyes - Developed a theory of brain function: Localisation of function - Here, different parts of the brain responsible for variations in individual differences - Studied individuals with skills in maths, music, sense of colour, combativeness, discovered “bumps” in some areas - Depressions in skull indicate underdevelopment - Launched phrenology: the study of skull structure as indications for mental faculties (e.g., Amativeness (sex drive) behind lower part of ears) - Soon invited quackery and ridicule by association, most assessments entirely subjective - Outside of the skull does not mirror even the inside of the skull, let alone the underlying brain
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Cognitive neuropsychology: Recovery from start to finish
- Lesioned parts of the cortex of different animals and observed hoe it behaved - At first = moved very little, refused to eat and drink - Later = recovery of function to the point of appearing ‘normal’ - Pattern of loss and recovery seemed inconsistent with the assumption of localisation
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Cognitive neuropsychology: Localisation
- Hemispheres - Lobes (frontal, parietal, temporal, occipital) - Subcortical structures (e.g. limbic system, basal ganglia) - Broadman areas
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Mapping the brain
- Brodmann (1868-1918) German neurologist and died of septic infection after pneumonia - Appearance of the cortex under microscope - Labelled zones based on cell organisation (e.g. density), cell type, and number of connections
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Neuropsychology & Language
- Bouilaud (1796-1881) proposed that certain functions were localised & lateralized - Physicians noted that damage to left hemisphere resulted in impaired movement on an individual’s right - Writing was also disrupted, so language on the left? - His son in law reported as a case of a patient who lost the ability to speak when pressure was applied to the exposed frontal lobes - He died a few years later and autopsy revealed a lesion to the left frontal lobe, thus demonstrating lateralization, localization - Anterior speech region = Broca’s areas - Syndrome that results from damage to this area = Broca’s aphasia
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Neuropsychology: Wernicke (1848-1904)
- Investigated region of the cortex that receives information from the ear - His patients spoke fluently, but with no sense - Could hear, but could not understand what was said to them - This region of temporal lobe = Wernicke’s area - Syndrome that results from damage to this area = Wernicke’s aphasia - Wernicke’s Model of Language processing: auditory information sent to 1. Wernicke’s area 2. Sound images transmitted along arcuate fasciculus to 3. Broca’s area - Conduction aphasia: impairment in the ability to repeat words or phrases despite intact comprehension and present speech production
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Neuropsychology & memory: 4 types of memory
- Memory is not a single function - Episodic = memory of specific events - Semantic = memory for facts - Working = short term, rehearsal - Procedural = motor memory - These types of memory can be dissociated from each other and disrupted independently - Damage to memory is often referred to as amnesia - Hippocampus, amygdala and related structures in the medial temporal lobe (MTL)
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Memory: Anterograde Amnesia
- Poor ability to acquire new information - Information acquired before damage is relatively spared, especially further back in time (info in working memory is spared) - Impaired declarative (explicit) memory: episodic and semantic - Relative preservation of non-declarative (implicit) memory: - A) perceptual (familiarity with stimuli) - B) procedural (motor skills & habits) - Causes: Disorders (e.g. Korsakoff’s syndrome) thiamine deficiency, due to alcoholism, produces bilateral degeneration of mamillary bodies - Temporal lobectomy (e.g. for patients with intractable seizures) bilateral removal of temporal lobes
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Anterograde Amnesia: H.M. case study
- Major seizures (epilepsy) since 16 years of age - Drugs failed to contain seizures - Surgical bilateral removal of anterior hippocampal regions at age 27 - Important case in neuropsychology of memory: circumscribed lesion, surgery successful in combating epilepsy - Pure deficits: IQ unaffected by surgery, no personality change or other deficits outside memory - Even within memory, deficits are specific to the formation of new memories - Intact working memory, semantic memory disrupted, absence of new episodic memory - Could earn new motor tasks. Improvements in short term. Lost when pushed to LTM. Deficits specific to semantic & episodic memory
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Retrograde Amnesia: History
- Anterograde amnesia = since lesion & Retrograde amnesia = prior to lesion - Hippocampus, amygdala and related structures in the medial temporal lobe - H.M.: old memories are still intact and memory immediately before lesion lost - Suggest hippocampus doesn’t store memories, old memories are preserved - Role of hippocampus in memory not yet completely understood - It may enable consolidation of new memories, which are stored elsewhere - This consolidation process must take time possibly decades
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Neuropsychology & Visual perception: and what's optic ataxia?
- Occipital lobes and surrounding temporal and parietal (including PVC, ventral & dorsal stream) - Damage to these systems can cause agnosia (damage to the ventral) or - optic ataxia (damage to the dorsal) - Agnosia = the inability to recognize. A lack of knowing or perception - Optic ataxia = deficits in spatial perception, visuospatial processing and visual guidance of action
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Visual Agnosia: and its 3 types
- The inability to recognise. A lack of knowing or perception (can be visual, auditory, etc) - Modality specific: individuals with visual agnosia would be able to name an object through touch 1. Apperceptive – unable to perceive full shape of object despite intact low-level processing. Inability to extract global structure. Intact low-level perception (acuity, brightness discrimination, colour vision) 2. Associative – ability to perceive shape, but inability to recognise it. No problem copying figures, however inability to draw from verbal instruction 3. Prosopagnosia – Apperceptive prosopagnosia is defines as the inability to even perceive and cognitively process faces, associative prosopagnosia is defined an inability to recognise or apply any meaning to the face, despite perceiving it. Tends to involve damage to the fusiform gyrus in the lower part of the occipital and temporal lobe
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Are faces special?
- Faces tend to include all the same features (eyes, nose, mouth), and very similar features are present in different individuals (e.g. family members), but we still recognize individuals well - The configuration of features is unique to an individual - Face-processing involves perception of the configuration as well as the features - A specialized face-processing system in the brain may process faces ‘holistically’ (as a whole), including configural information - Most ‘prosopagnosics’ have difficulty recognizing differences within other categories: types of cars, breed of dog, cows in a herd - The FFA is not only concerned with faces: - Also, active when observing pictures of birds or cars (Gauthier et al., 1999, 2000)
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Three principal measures of sleep
- Electro-encephalogram (EEG) – head - Electro-oculogram (EOC) – eye - Electro-myogram (EMG) – neck
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Key features of measurement and stages of sleep
- Pre-sleep Alpha waves – bursts of 8-12Hz activity in low amplitude/ high frequency waves - Four stages of sleep EEG: - Each cycle lasts around 90 min - Progressive: increase in amplitude, decrease in frequency - Sleep spindle: 1-2s burst of 12-14Hz waves - K complex: single large upward, then downward deflection - As night progresses, spend more time in stage 1
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Stage 4 (REM sleep) evidence with dream recall
- Early studies of REM sleep indicated high rates of blood flow, oxygen consumption and neural firing - Increase in variability of the ANS (blood pressure, pulse and respiration) - These REM sleep episodes seemed emotionally charged - Is it correlated with dreaming? Dement (1978) - Results: 80% awakenings during REM sleep = dream recall, 93% awakenings during non-REM sleep = no dream recall, Non-REM dream recall = isolated experiences, REM dream recall – narrative - Derment & Kleitman (1975) pp’s awoken 5 or 15 min after onset of REM and were asked, based on their dream events, how long they had been dreaming - Results: 92/111 cases correctly answered
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Theories of sleep: 2 theories
1. Recuperation Theories – being awake disrupts homeostasis and sleep restores this e.g. sleep restores energy levels 2. Evolutionary Theories – sleep is not a reaction to homeostatic disruption. Sleep evolved to prevent accidents and predation at night. Sleep is like sex (we don’t need it to stay alive nut we are still motivated to have it)
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Sleep in animals
- All mammals and birds’ sleep - Fish, reptiles and amphibians have periods of inactivity too - Large species differences in sleep – not related to body size/ temperature - Sloths hardly move, yet need 20hrs a day - Little/ no effect of exercise on sleep duration in human - Not consistent with recuperation theories of sleep - Evolutionary theories – sleep related to: how vulnerable you are asleep, time spent eating a day
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Effects of sleep deprivation: Humans
- Recuperation theories predict that with sleep deprivation: - A) increases in physiological/ behavioural disturbances - B) after deprivation, missed sleep must be regained - Deprivation influences: mood, physiological function, molecular function, induce anxiety - Effects in executive function: assimilating changing information, updating plans, reference memory - BUT people recover well after sleep deprivation (e.g. 260 awake but went back to normal after 1st recovery night of 14 hrs)
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Depression and sleep deprivation: 4 research evidence
1. Vogel et al. (1975, 1990): Preventing REM sleep acts as an antidepressant 2. Scherschlicht et al. (1982): Examined effects of 20 antidepressants. All reduced REM sleep. Most increased slow-wave sleep 3. Preventing REM sleep makes the body want it more, so it tries to enter REM sleep quicker (Webb & Agnew, 1967) 4. Deprivation of REM sleep causes a transient rebound (Brunner et al., 1990)
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Effects of sleep deprivation: Animals
- After several days, experimental rats died - But post-mortem revealed swollen adrenal glands, gastric ulcers, and internal bleeding - possibly a consequence of stress and physical damage?
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Brain areas involved in sleep: 2 areas and research evidence
1. Hypothalamus – victims who had difficulty sleeping showed damage to anterior region, victims who had difficulty staying awake showed damage to posterior region. Confirmed in lesion studies in animals 2. Reticular System - Bremer (1936): Cerveau isole transection = slow-wave sleep pattern, Encephale isole transection – Normal sleep-wake cycle. Thus, “wakefulness” area = somewhere in between the two Mouzzi & Morgan (1949): Stimulation of the reticular formation of sleeping cats woke them. Area became known as the Reticular Activating system – low activity = sleep, high activity = wakefulness
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Sleep disorders
- Narcolepsy is a rare long-term brain condition that can prevent a person from choosing when to wake or sleep - - the brain is unable to regulate sleeping and waking pattern normally, which can result in: a) Excessive daytime sleepiness (feeling very drowsy throughout the stay and finding it hard to concentrate and stay awake) b) Sleep attacks (falling asleep very suddenly and without warning) c) Cataplexy (temporary loss of muscle control resulting in weakness and possible collapse, often in response to emotions such as laughter and anger) - REM sleep without core muscle Antonia
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Digestion: The Basics
- Start with eating/chewing the food - Down the oesophagus into the stomach, where it’s broken down by stomach acid - Passee through large and small intestine where the food is broken down into simple sugars and water is absorbed - Leaves the body via anus
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Theories of hunger: Set Point Theory (Keesey & Powley, 1986)
- Hunger is a consequence of an energy deficit - Everyone has an optimal level of energy resources (a set point) - Bodies inherently seek to return to this set point (i.e. homeostasis) - As energy levels drop, hunger increases, and a meal is initiated - Issues: 1. Evolutionarily unlikely – need to cope with inconsistent resources in the environment and not a system that just responses to energy deficits 2. Not supported by evidence – reductions in blood glucose needed to start a meal are substantial. Drinking a high calorie drink prior to mealtime does not stop the meal. Beliefs about the content of the drink had more of an effect 3. Ignorance of environmental factors – effects of learning, preference and social factors
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Theories of hunger: Positive Incentive Theory (Berridge, 2004)
- Anticipation: animals driven to eat by the expected pleasure of eating. Expected pleasure = positive-incentive value - Craving: eating (and the perception of hunger) is initiated by craving. This may be for something specific. Enables you to take advantage of goof food - Multiple factors: flavour of the food. Knowledge about the food. Time since last meal, amount of food in gut, blood glucose levels
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Eating factors: WHAT do we eat?
- Learning food preferences and aversions - Test 1: Rats were given flavour A (glucose) and flavour B (nothing). When given both, rats favoured flavour A (known as a ‘conditioned taste preference’) - Test 2: Rats were given flavour A (LiCL) and flavour B (nothing). When given both, raths avoid flavour A (known as a ‘conditioned taste aversion’) - Food preferences can also be socially acquired (e.g. animals will prefer a certain type of food if they’ve seen other animals eating it) - Learning to eat vitamins and minerals: - Associating salt with flavours (Fudim, 1978) – rats preferred banana with sugar than almon with salt. However, this was reversed when the banana with sugar with now being administered with an injection - So why do some people have such a poor diet? One possibility is that we have too many choices to form specific associations. This suggests eating is susceptible to overshadowing
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Eating factors: WHEN do we eat?
1. Pre-meal hunger – eating a meal stresses the body: influx of fuel moves it away from homeostasis. Signals for a meal (e.g. time of day, smells) evokes a cephalic phase. Insulin is released into blood which lowers blood glucose levels. Thus, hunger isn’t a cry for energy, it’s the body preparing for homeostasis disruption 2. Conditioned hunger for rats – rats ate more food when the CS was subsequently presented
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Physiological research: the hypothalamus
Ventralmedial hypothalamus (VMH) – a satiety centre (inhibits eating) - VMH lesion = hyperphagia (overeating & obesity) - VMH syndrome: 1. Dynamic phase – excessive eating, weight gain 2. Static phase – body weight maintained. Oversight state returns following diet - VMH syndrome rats will not work for food. Sensitive to unpalatable food Lateral hypothalamus (LH) – a feeding centre - LH lesion = aphagia (cessation of eating) - LH syndrome: 1. Aphagia if often accompanied by adipsia (cessation of drinking) 2. Recovery is possible; tube feeding, milk-soaked cookies, dry food pellets Issues: 1. VMH lesions in fact damaged the PVN (this region produces hyperphagia & obesity) 2. Hypothalamus regulated metabolism, not eating. VMH lesions increases blood insulin increases production of fat (lipogenesis) and decreased breakdown of body fat (lipolysis). Thus, the rats must consume more calories to meet demand 3. LH lesions produce a variety of motor disturbances, and lack of responsiveness
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Physiological research: the stomach
- Cannon & Washburn (1912): contractions caused by empty stomach correlated with hunger. But patients without stomachs still get hunger. Thus, stomach is not necessary for hunger - Koopmans (1981): transplanted an extra stomach & length of intestine into rats and joined the major arteries and veins. Food injected into the stomach so reduces eating. Transplanted stomach had no functioning nerves. Satiety signal must have reached the brain through blood flow (can’t have been nutrients as not absorbed by the stomach)
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Physiological research: Peptides
- Short chains of amino acids (can function as either a hormone, or a neurotransmitter) - Ingested food stimulates receptors in the gastrointestinal tract to release these into the bloodstream and can pass through the blood-brain barrier - Leptin: discovered as a spontaneous genetic mutation in a mouse colony. Low leptin mice ate much more converted calories to fat more efficiently, suggests it’s a negative feedback signal to lower appetite & encourage fat metabolism - Humans typically have high levels of leptin and leptin injections in obese people do not decrease eating or body fat
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Distribution of learning in humans?
- Humans can learn during their sleep - 1200Hz tone = deodorant - 400Hz tone = rotten fish - Recorded how many times humans sniffed during their sleep (higher tone & better odor = more sniffs) - Effect is only established if learning was acquired during REM sleep
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What is learning?
- A relatively permanent change in behaviour as a consequence of experience - The acquisition of information - The problem of behavioural silence (i.e. learning something that doesn’t change your behaviour)
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Why do organisms learn?
- Reflex arc is fast/ automatic and doesn’t require the brain - However, many organisms live in environments that have predictive relationships between events - But predictive relationships may change (e.g. finding food in summer vs winter) - To survive animals must modify their behaviour as a consequence of their experience with the environment
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Habituation: 3 research support
- “The relatively persistent waning of a response as a result of repeated stimulation which is not followed by any kind of reinforcement” (i.e. getting used to it) - (Whitlow, 1975): Rabbits were exposed to 530 or 4000 Hz tones for 1 second. Measured vasoconstriction (blood volume) in rabbits’ ear. Results = vasoconstriction increased when exposed to tone, but increased less when repeatedly exposed - (Cross): neonatal rats split into two groups (a – Mozart group, b – Schoenberg group). 12 hrs a day exposure to vocal and non-vocal selections of both musicians for 52 days. Response: choice of entering a box playing Mozart or Schoenberg music. Results: rats preferred the group that was pre-exposed. Conclusion: avoidance of some aversive aspect of the music habituated with exposure - (Domjan): water deprived rats split into two groups (S & W). Group S had 30 min access to sweetened water then 30 min of normal water. Group W had 30 min access to just water and recorded consumption each day. Conclusion: shows how learning and innate behaviour can work together to be adaptive as rats are cautious about novel flavours to reduce poisoning. But with experience, diet can be widened through habituation
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Classical Conditioning & its 4 main components
- First reported by Pavlov (1927) 1. Unconditioned stimulus – a biologically significant stimulus 2. Unconditioned response – the response evoked by the US 3. Conditioned stimulus – a previously neutral stimulus that acquires a response by being paired with the US 4. Conditioned response – the response evoked by the CS - (Martin): Blue block = cornea air puff, red block = nothing. CR was blinking. At first relatively little evidence of blinking during the lights (CS). Blinking elicited by the CS that predicted the air puff (US). Very functional. Eyelid responses anticipate irritations and protect the eye - (Smith): rats allowed to drink sucrose solution (CS) then given 1 dose of radiation to make them feel nauseous (US). Control group had no X rays delivered. Final test- choice between sucrose and water in both groups
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Learning how to detect a lie
- People have a more positive view on the side of their body that is their dominate hand (i.e. you spend more time interacting with your dominant hand, so u have a more positive view about that side) - More likely to use the non-dominant side of their body when telling a lie
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Features of Classical Conditioning: 3 features
1. Acquisition – the initial increase in responding to a CS when it’s paired with a US 2. Extinction – the weakening of conditioning responding if the C is subsequently presented without the US 3. Spontaneous Recovery – an increase in an extinguished conditioned response due to the passage of time
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Exposure therapy: an application of extinction
- Part of CBT and helps to reduce fear by severing association - Simply presents the cue in this maladaptive behaviour
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The spread of learning: Generalization
- Stimuli: 4 groups of pigeons had different-coloured key lights paired with food. Conditioned response – pecking at the key light - Test: presented with lots of different coloured key light and food was not delivered - Results: pigeons pecked most at the coloured light that had been paired with food. They also pecked at wavelengths at light that were SIMILAR to learnt colour, suggesting generalisation of learning
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Learning to control the world: Instrumental Conditioning
- (Thorndike, 1898): at first cats would take 60-120 s to escape the box after a dozen trials = 20 s - Connections are formed between a stimulus and a response (S-R) - Reinforcement merely strengthens the S-R association - Widespread as all manner of species can be trained to do something for reward - Sometimes hard to get started because if the animal doesn’t respond, then it will never encounter reward (use shaping) - Although superstitions are common, they do not dominate our behaviour & life a) Continuous reinforcement – reward is delivered every time animal makes a response b) Ratio schedule – reward is delivered after a certain number of responses are made (fixed or variable) c) Interval schedule – reward is delivered after the first response is made after a certain interval is passed (fixed or variable)
155
What is learnt during learning?
- Associations/ connections in classical and instrumental condition - Why this conservative approach to learning? 1. Physiology – brains are mostly made up of connections between neurons 2. Occam’s Razor – other things being equal the simplest explanation is best - Adams (1982): behaviour transitions from being a goal directed action to a stimulus-response habit. Implies that something that isn’t present is influencing behaviour (conditioning results in a representation being activated & can a representation of something not present also be conditioned?)