Biological Psychology All Lectures PDF

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Lecture 1 – Why and how we study the Brain Background The brain is studied in order to:  Help explain behavioural disorders  Help us “understand its place in the biological order of our planet”  Discover how it produces behaviour and consciousness Psychology was preceded by Philosophy Hippocrates (460-379 BC)  “Brain the seat of intelligence and involved in sensation”  4 humours approach – Yellow bile, black bile, phlegm, and blood – illness was caused by an imbalance of these  Bloodletting and other forms of purging were thought to help balance out the levels of these humours similar to the Egyptians who used trepanation to relieve headaches or mental illness  However, unlike Hippocrates they believed the “seat of the soul” was the heart Aristotle (384-322 BC)  No role for the brain – only cooled the blood  Believed the mind lived in the heart because:  The brain is peripheral and must therefore cool the blood – the heart is central and must therefore heat up the blood  Invertebrates have sensation but no brain  The brain is bloodless  The brain is cold  The brain is insensitive to touch the heart is  The heart forms before the brain  The brain was not essential for life but the heart is  The heart was involved in emotion whereas the brain is emotionless  The heart was connected to the sense organs via blood vessels and the brain had no sensory function as it was not connected  However:  You can live for a period without no heartbeat, if your brain ceases to function you are legally dead  Sensory connections are neural so we need our brains to sense touch  The brain is heavily involved in emotion with areas such as the amygdala unlike the heart

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Galen (130-200 CE)    

Treated gladiators after arena battles saw brain and spinal injuries Dissected animal brains – poked them with a finger Two main parts are the soft and hard cerebellum Cerebral Cortex – Sensation, perception and memory, Cerebrum – Movement Control, this is limited but correct  However, he did also state that the ventricles corroborated Hippocrates’ theory and that the humours flowed from ventricle to ventricle via hollow nerves and that this caused movement and sensation

Descartes (1596-1650)  “Tried to explain the brain in terms of machines”  Used ideas from hydraulically powered machines – “fluid being forced through the ventricles brings about movement”  Linked the mind and brain and the mind with the body  The brain is controlled by the mind which flows through the pineal gland – actually involved in biological rhythms  The pineal gland also directs fluid which travels from the ventricles through nerves into muscles causing them to expand and contract  Dualism – “behaviour is controlled by two entities”  To have a mind required the presence of language and reason  Language and action tests:  Language test – “describe and reason about things that are not present”  Action test – “display behaviour based on reasoning”  Led to poor treatment of mentally ill patients – no mind meant no pain Gall (1758-1828)    

Examined localisation of function Each area of the mind must have a separate seat in the brain The size of this seat determines its power Phrenology – “as the skull takes its shape from the brain, the surface of the brain can be read as an accurate index of psychological aptitudes and tendencies” – not seen as credible by the scientific community  Lavery’s Electric Phrenonmeter was popular despite the lack of scientific credibility

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Golgi (1843-1926) and Cajal (1852-1934)    

Golgi created a stain for neurons so that there structure can be seen They were shown as a “network of interconnecting tubes” Cajal showed that nerve cells were “separate entities” Golgi believed the nerve cells acted like blood vessels and Cajal saw them as “separate entities with their own functions”

Brodmann (1868-1918)  Grouping of neurons was shown to suggest localisation of different functions  Neuropsychology – inference can be used to suggest the function of areas of the brain through looking at brain damaged patients

Broca (1824-1880)  Tan (1861) – Showed that Broca’s area was crucial in speech production

Kleist (1879-1960)  Used 1600 head wound casualties from the First World War to create a functional map of the cerebral cortex However, Neuropsychology required the patient to die before they could be examined and due to large areas of damage it was difficult to accurately determine the particular function of small areas of the brain.

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Methods Since Galvini’s (1737-1798) frog experiments it has been clear electricity plays a role in muscle contraction and his nephews work was a “direct precursor” to ECT. Electroencephalography  This allows us to examine brain waves by listening for the electrical activity that tells us part of a brain is active  Involves wearing a cap with 64-128 electrodes on and these can pick up the brain waves Imaging  Less messy than EEG  Computerised Tomography scans produce cross- sectional pictures of the brain  Magnetic Resonance Imaging – A strong magnetic field aligns the water molecules in the brain in one direction then sees how they react when a radio wave is applied  It takes images at 1mm intervals producing pictures of the brain  These can be used to look at structures at any angle when fed into a computer programme  functional Magnetic Resonance Imaging – allows blood flow to be tracked – see what part of the brain is being used in a task  The software shows how high the levels of activity are by using different colours  But this is only correlative – don’t know which area caused the behaviour Transcranial Magnetic Simulation  Sends and electrical pulse through the skull  About 1cm of the brain is turned on for about 0.001 of a second  Reduces the speed of a task as the part of the brain involved is switched on by the TMS  Because “the brain is active with response to the magnetic pulse and will not be able to respond to the task at hand”  Makes up for the problems associated with large brain lesions

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Lecture 2 – The Neuron and the Action Potential Neurons Neurons are one of the smallest subunits in the nervous system and there are several main types which are motor neurons, sensory neurons and interneurons.

Motor Neuron

Interneuron

Sensory Neuron

Motor Neurons  Involved in movement – all outgoing motor information passes through them  The cell body is located at the beginning of the axon  Extensive dendritic network to receive information from multiple sources Interneurons  Associate sensory and motor activity  Can either be:  Stellate cells (thalamus)  Pyramidal (the cortex)  Purkinje (the cerebellum) Sensory Neurons     

Simplest neurons structurally Take information from the body to the brain for interpretation Dendrites on the bottom Axon takes information to terminals Cell Body halfway along length

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   

Neurons are insulted by Schwann Cells – allows for saltatory conduction Myelin Sheath does this in the brain Glial cells “look after” neurons – Schwann cells and oligodendroglia Cells communicate in an electrochemical manner – electrical then chemical then electrical  Dendrites collect information  Terminal boutons link with other neurons Neuronal Membrane  Separates intra/extracellular fluid  Phospholipid bilayer – fatty and hydrophobic – keeps water out of the membrane and prevents fluids from leaving  Special proteins act as pumps/channels to control movement in and out of the cell  This movement causes electrical signals  Channels can be:  Resting (open)  Voltage gated – open when a certain voltage is reached  Ligand gated – open when a certain substance is present  Mechanically gated – open as a result of a mechanical deformation Movement of Ions     

Sodium/Potassium/Chloride and large negative ions are in the intracellular fluid Chloride – reduces the charge Sodium and Potassium – increase the charge Inside more negatively charged due to the large negative ions (anions) Movement in and out of cells occurs along concentration and electrical gradients through channels specific to ions

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Resting Membrane Potential    

Sodium ion channels are closed – no movement of sodium across the membrane Potassium ion channels open – can move in/out of the cell Potassium is attracted into the cell due to the more negative potential inside the cell Also attracted outside of the cell due to the lower concentration of potassium outside  This gives an resting membrane potential of -65/-70 mV  Neuron has a more negative charge inside due to the large negative ions at rest  Sodium-Potassium pump keeps the imbalance by pumping three sodium ions out for every two potassium ions that are pumped in Action Potential  At rest the neuron is more negatively charged inside (-65/-70mV)  Excitatory stimulation – injection of positive ions upsets the equilibrium and can cause an action potential if this is large enough (must rise above -50mV)  At -50mV sodium rushes into the cell down a concentration and electrical gradient  The inside of the cell becomes more positive (+40mV)  This is depolarisation  The potassium voltage gated channels that only open at this voltage open and the sodium channels close  As the outside of the cell is more negative potassium ions are attracted and move out of the cell  As positive ions are leaving the cell the inside becomes more negative than before (hyperpolarisation)  The voltage gated channels shut  The Sodium-Potassium pump acts to readdress the balance The Refractory Period  Action potentials are all or nothing events  Strength of stimulus denoted by the rate of firing  Another action potential cannot begin until the previous action potential has finished – absolute refractory period  Neurons can fire many action potentials per second

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Nerve Impulse  Can occur slowly by a domino effect with the neurons depolarising section by section  Or the myelin sheath can allow for action potentials to be quickly propagated down axons to terminal buttons  The myelin sheath and nodes of Ranvier allow for saltatory conduction  Myelin produced by glial cells (oligodendrocytes in the brain and spinal cord or Schwann cells in the peripheral nervous system)  Without this nerve conduction would be very slow and possibly break down completely as happens in multiple sclerosis

The Synapse  When the action potential reaches the presynaptic terminal the depolarisation causes a the voltage gated calcium channels to open causing a calcium influx  The calcium binds with vesicles containing the neurotransmitter which then move to the pre-synaptic membrane  The neurotransmitter is then released into the synaptic cleft  Different neurotransmitters bind with different ion channels and these can have different effects  These are called ionotropic channels  This effect can be excitatory or inhibitory:  Excitatory – Causes and influx of positive sodium ions increasing the chance of an action potential  Inhibitory – Opens chloride channels causing an influx of negative ions – reduces the likelihood of an action potential (excitatory)  Metabotropic receptors – similar to an inhibitory effect but results in longer term effects like smell  Epilepsy – balance between excitation and inhibition breaks down causing neurons to be to active creating uncontrollable patterns of electrical activity  Correct balance of EPSPs (excitatory post-synaptic potential) and IPSPs (inhibitory post-synaptic potential) must be reached for an action potential to continue (-50 mV) and this occurs at the axon hillock  Spatial/temporal summation can occur at the synapse

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Lecture 3 – Synapses and Nervous System Organisation The Synapse  When an action potential reaches the presynaptic terminal a vesicle releases a neurotransmitter into the synaptic cleft  The neurotransmitter can be inhibitory or excitatory  The action potential causes calcium ion channels to open at the presynaptic terminal 9

 This enters the cell and binds with the neurotransmitter vesicles.  When the calcium binds to the vesicles they move towards the terminal membrane and then merge releasing the neurotransmitter into the synapse  Can be seen by electromicroscopy  Made clear the fact that there are well defined junctions between neurons  Formed by the termination of an axon from one neuron onto a dendrite  Most occur between neurons  However, they can also occur at neuro-muscular junctions  Amyotrophic Lateral Sclerosis – affects the neurons, restricting movement and eventually causes death  A lack of calcium in the diet can make it difficult to relax muscles Neurotransmitters  Made in the cell body, packaged in vesicles and transported along the axon to the presynaptic terminal  Remain dormant until an action potential occurs then they can release the neurotransmitter into the synaptic cleft  Different neurotransmitters open different ligand-gated ion channels Sea Slugs  If the gill-withdrawal reflex in a sea slug is stimulated several times rapidly the withdrawal response intensity decreases  Less glutamate is released by the sensory neurons at the synapses with the motor neurons as less calcium is released as the habituation occurs

Ionotropic Neurotransmitter Receptors  Neurotransmitter receptors are proteins found on dendrites  Ionotropic neurotransmitter receptors have two parts – one part binds to the neurotransmitter the other is an ion channel  When the neurotransmitter binds the ion channel opens allowing ions into the cell

Metabotropic Neurotransmitter Receptors  Receptor is separate to the ion channel  Receptor has G proteins with alpha/beta/gamma subunits  The alpha subunit detaches when the neurotransmitter binds and can bind to the ion channel and alter its structure, allowing or preventing the movement of ions 10

 Allows for a more graded response to stimuli  Effects also last beyond the initial stimulus for example smell Excitatory and Inhibitory Postsynaptic Potentials  Excitatory – released at type one synapses and bind to receptors causing an influx of positive sodium ions causing an excitatory post synaptic potential  Inhibitory – released at type two synapses and cause an influx of negative chloride ions causing an inhibitory post synaptic potential Neurotransmitter removal and inactivation  Tetanus – caused by prolonged activation of muscles and paralysis as inhibitory neurotransmitters are prevented from being released  Mustard Gas – prevents deactivation of acetylcholine via acetylcholinesterase in the motor system and causes paralysis through the hyperactivity of muscles Synaptic Integration     

Spatial integration of EPSPs Temporal integration of EPSPs EPSPs – can be added together at the axon hillock Action potentials never degrade but EPSPs can degrade over space/time Summation reduces this by combining a number of EPSPs from an area or from a period of time  The threshold of -50mV must be reached to cause an action potential

Neurons and Neurotransmitters  Different neurons use different neurotransmitters  Glutamate – the main excitatory neurotransmitter in the brain forms links between neurons – the basis of learning and memory  GABA (gamma-Aminobutyric acid) – main inhibitory neurotransmitter in the brain  Dopamine – involved in movement control and reward circuits  Serotonin – affects mood and anxiety  Acetylcholine – involved at the neuromuscular junction and alertness in the brain Parkinson’s Disease  Loss of dopaminergic neurons in the substantia nigra causes rigidity and trembling 11

 Levodopa (a dopamine precursor) acts as an agonist and relieves symptoms temporarily  Progress made through discovery of effects of MPTP, a neurotoxin which causes the symptoms of Parkinson’s  Link to schizophrenia – too much dopamine FROM Toxins  Tetrodoxin – inactivates sodium ion channels preventing action potentials and causing paralysis  Scorpions – activate sodium ion channels which end the equilibrium between sodium and potassium causing paralysis  Wasps/bees – inactivate potassium channels  α-latrotoxin – massive release of neurotransmitter at the neuromuscular junction causing paralysis  Botulism – stops the release of excitatory neurotransmitters preventing muscular contraction  Tetanus – prevents inhibitory neurotransmitters from working causing hyperactivity of the muscles and therefore paralysis  α-Bungrotoxin – blocks neurotransmitters on the neuromuscular junction causing paralysis Drugs  Mimic the effect of neurotransmitters  LSD and psilocybe (mushrooms) – mimic serotonin  Alcohol – stimulates GABA receptors to give a sedative effect and also blocks glutamate receptors  Cocaine – prevents reuptake of dopamine prolonging its effects  Prozac – prevents the reuptake of serotonin by inhibiting the enzyme involved in its breakdown this enhances its effects and giving a feeling of well-being Addiction  False feeling of well-being and reward  Many highly addictive thought to be

Nervous

drugs affect dopamine which is important in reward circuits

System Organisation

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Autonomic Nervous System  Sympathetic:  Fight or flight  Pre-ganglionic – acetylcholine,  Post-ganglionic – noradrenaline  Parasympathetic:  Rest and digest  Pre/post-ganglionic – acetylcholine The Brain  2 hemispheres with 7 layers  Weighs around 1.8kg  Cerebro-Spinal fluid cushion between the brain and the skull  Gyri (tops) and sulci (valleys) – used as landmarks  Cerebral cortex forms a layer of nerve cells that cover the entire brain  4 lobes:  Occipital – visual Processing  Parietal – touch, balance, movement  Temporal – hearing, speech, comprehension, memory and visual recognition  Frontal – movement, thinking and planning Bail Ganglia/Limbic System  Important in the control of voluntary movement 13

 Limbic system is important in navigation and spatial memory formation Brainstem      

Includes the hindbrain, midbrain and diencephalon Evolved 500 million years ago Acts as a relay station Clumps of cells for motor control, hearing etc. Contains 10 if the 12 pairs of the cranial nerves Controls general level of alertness/homeostatic functions

Cranial Nerves  Part of the somantic nervous system  Allows the brain to communicate with the muscles and the sensory organs of the head and neck  12 cranial nerves:  Olfactory  Optic  Oculomotor  Trochlear  Trigeminal  Abducens  Facial  Vestibulocochlear  Glossopharyngeal  Vagus  Spinal accessory  Hypoglossal

Nerves from the spinal cord  The brain communicates with the body via the spinal cord and cranial nerves  Sensory information about touch and pain is relayed to the body via the spinal cord  Motor commands go via to spinal cord to the muscles to produce movement Anatomical Locations Anterior – towards the front Caudal – towards the tail (animals) 14

Dorsal – towards the back Frontal – the front Inferior – underneath Lateral – towards the side Medial – towards the middle Posterior – towards the tail (animals) Rostral – towards the beak (animals) Sagittal – parallel to the length Superior – above Ventral - below

Lecture 4 – The Senses The Senses     

Touch Taste Audition Smell Sensation – registration of physical stimuli from the environment by sensory organs 15

 Perception – interpretation of sensations by the brain  Somatosensation:  Hapsis – touch (skin)  Nociception – pain and temperature (skin)  Proprioception – body awareness (muscles containing the sensory organs) Hapsis        

Meissner’s/Pacinian/Ruffini corpuscle are fast adapting Meissner’s – touch Pacinian – fluttering sensations Ruffini - vibrations Merkel’s/Hair receptors are slow adapting Merkel’s – steady skin indentation Hair...