Psychobiology Flashcards
Learn it all :)
Degrees of reductionism (3)
Macro-anatomical (brain areas)
Micro-anatomical (brain cells)
Macro molecular (individual protein molecules)
Blindsight
Patients with damage to the visual cortex declare they cannot see but can actually instinctively reach for objects
(superior colliculus intact - where sight functions)
Function of 1) Broca’s area 2) Wernicke’s area
1) Speech production
2) Speech perception
Three characteristics of neurons
Fully differentiated
Cannot undergo mitosis (cell division)
Generally, cannot be replaced in a mature nervous system
Dendrites
Branch like processes that receive information from other neurons
Axons
Long filament like processes that convey information away from the cell body to other neurons (through the terminals)
Longest axon in body
Sciatic nerves’ axons run from the end of the spinal cord to the toes
Myelin Sheath
Insulating fatty layer that coats the axons to speed transmission
How does myelin sheath speed transmission
Made from oligodendrocytes, it enables the action potential to decrease as it travels underneath the sheath and fully regenerate at each node (conserving energy)
Schwann cells
Makes the Myelin in the peripheral nervous system (PNS) - similar to oligodendrocytes
Nucleus (3 functions)
Contains chromosomes and DNA, produces neurotransmitters and receptors, makes modifications to dendrites
Microtubules
Transport system moving proteins up and down axons (damage can cause Alzheimer’s)
Mitochondria function
Takes in nutrients, breaks it down and converts it into energy to be used
Function of cell body
Cell maintenance, one way being protein production
How information is passed through a neuron to the other
Electrical signal (action potential) comes in through dendrites into cell body, then passes through the axon to the terminals where neurotransmitters are released into the synapse ready for the neighbouring neurons receptors to pick up
A multipolar neuron
One axon and many dendrites
Bipolar neuron
One axon, one dendrite tree (usually in sensory systems)
Unipolar neuron
One axon divided into 2 branches. One branch receives info and the other sends it
Afferent neuron
Carries information towards the CNS (A for arrival)
Efferent neuron
Carries information away from the CNS (E for exit)
Types of glial cells (3)
Astrocytes
Oligodendrocytes
Microglia
Function of glial cells (3)
Support neurons
Take away waste
Give neurons nutrients
Astrocytes function (2)
Some limit exchange of substances between blood and brain (barrier)
Others regulate ion concentration and extracellular concentration of neural signalling
(are star shaped)
Oligodendrocytes function
To wrap around axon to create myelin sheath (multiple layers of cell membrane)
Microglia funtion
To remove waste, viruses and fungi
mostly inactive unless repair is needed
Cell membrane and function
A barrier surrounding cells made up of membrane lipids (not perfect, a bit leaky)
Can open its channels to certain chemicals and not others in particular circumstances
Resting membrane potential (full explanation)
When the neuron is inactive, it is a state in which neurons can become active at any moment (requites a lot of energy for the brain).
Inside the cell is more negatively charged (-70mV).
There is electrostatic pressure of positively charged ions (Na+) from out to inside the cell
Force balanced by the K+ inside the cell attempting to diffuse outwards
Electrostatic pressure
Ions with a different charge to nearby them naturally move towards or away to balance the charges (attract like magnets)
Action potential (full explanation)
The mV shifts from -70 to -55 due to neighbouring action potentials or sensory inputs. This causes the Na+ channels to open and positively charged ions to flood the cell. Then the K+ channels open and it diffuses out. Once the mV is +40, repolarisation begins as charge inside cell now more than outside. Na+ leaves the cell and K+ enters.
mV overshoots -70 slightly before returning to the resting membrane potential state
How is cognition speed often measured
Action potentials per second
Diffusion
Movement of ions from a high to low concentration area
Why depolarisation of neuron occurs (3) - mV from -70 to -55
Action potential in neighbouring neuron
Sensory receptors
Chemical transmission between neurons
Synaptic cleft
Gap (20nm) between a neurons terminals and another’s dendrites
Synapse
Gap between neurons, including receptors etc.
What is different in an electrical synapse compared with a chemical one
Neurons touch each other (no cleft), so ions diffuse across adjoining pours
Pre-synaptic neuron
Input neuron that brings information to the synapse
Vesicle
A bubble type thing that neurons package molecules in to transport them
How neurotransmitters are released from the neuron into the cleft
The vesicle is encapsulated by the cell membrane and the neurotransmitters are then released onto the other side into the cleft
What happens when a neurotransmitter bind to a receptor
Certain ion channels open, allowing the conductance of the neuron to change
Post-synaptic neuron
Receives information at the synapse from the receptors on the dendrites
Hypopolarisation
Opening of the cation channels (+ve) - is excitatory
similar to depolarisation
Hyperpolarisation
Opening of anion channels (-ve), is inhibitory
Ligand and two examples
Chemical that interacts with a receptor (E.g. neurotransmitters, drugs)
Binding site
Location on receptor that ligands interact
Why will only some ligands bind to some receptors
They need to match each others 3D shape (at least roughly)
Affinity
How well a ligand binds to a receptor
high affinity receptors are saturated by very dilute ligands
Types of receptors (2)
Ionotropic
Metabotropic
Ionotropic receptor
Directly coupled to ion channel (ligand binds and ion channel opens)
Metabotropic receptor
The ligand binding changes its 3D shape and activates a G-protein inside its neuron, causing a signalling cascade which can change excitability and protein synthesis
Why are there receptors at pre-synaptic neurons as well
To provide negative feedback in order to stop neurotransmitter release when beneficial (called retrograde signalling, important for plasticity)
Glutamate neurotransmitter characteristics (4)
Derived from glutamic acid
Excitatory
Most abundant in brain
Bind to at least 8 receptor types
GABA neurotransmitter characteristics (3)
Made from glutamate
Most abundant inhibitory neurotransmitter in brain
Binds ionotropic and metabotropic GABA receptors
Glycine neurotransmitter characteristics (3)
An amino acid (unusual)
Binds to inhibitory receptors in the spinal cord
A co-agonist
Monamine neurotransmitter characteristics (3)
Includes dopamine, serotonin and neuropeptides
Mostly bind to metabotropic receptors
Found in a restricted group of neurons
Synaptic transmission explanation in steps
1) Neurotransmitter made in cell body, stored in vesicles
2) When action potential arrives, vesicle fuses with cell membrane and releases transmitter into cleft
3) Binds with post-synaptic neuron’s receptor
4) Ion channel opens or closes
5) Excess neurotransmitters then recycled, vesicles reconstructed
What receptor does 1) caffeine 2) alcohol 3) nicotine bind to
1) Adenosine receptors
2) GABA and NMDA receptors
3) Nicotinic receptors
Pharmacokinetics
How drugs get to their site of action and are handled by the body
Stages of pharmacokinetics (4)
Absorption
Distribution
Metabolism
Elimination
Absorption, and method of absorption
How drugs get into the body, always through a membrane (nasal, intestine, skin) or injected
How do water soluble drugs absorb into the body
Not by membranes, but cross pores in capillaries
How do lipid soluble drugs absorb into the body (3)
Pores in capillaries, cell membranes and blood-brain barrier
Slower routes of drug absorption (4)
Oral, suppository, topical (skin), mucous membranes (nasal, chewing etc)
Faster routes of drug absorption (3)
Inhalation, Injection, directly into brain (the fastest)
Methods of injection (3)
Subcutaneous (under skin), Intramuscular (in muscles) and intravenous (in vain)
Blood-brain barrier
Made of astrocytes, it separates the brain from the bloodstream
How drugs become less likely to pass the blood-brain barrier
They bind to plasma proteins, making them too big to get through capillary pores
Why do fat soluble drugs take longer for the body to eliminate
Get deposited in fat tissue (e.g. THC)
Metabolizing a drug
Converting it into another compound (can be inactive, active or even more active) - often essential for elimination
(Mainly in liver, but everywhere)
Methods of eliminating a drug (4)
Urine, Breath (e.g. alcohol), sweat and hair
Drug half life
Measures the duration of action of a drug by the time taken for blood plasma levels of the drug to fall by half
Pharmacodynamics
The effect the drug has on the body
Direct agonist drug and example
Mimics the effect of a particular neurotransmitter (nicotine)
Indirect agonist drug and example
Enhances the action of a natural neurotransmitter (not affecting the binding) - (cocaine blocks dopamine reuptake/recycling)
Direct antagonist drug and example
Binds to receptor with no physiological effect (blocks endogenous transmitters (meloxone - used to treat opium, an agonist, overdoses)
Indirect antagonist drug
Inhibits neurotransmitter release and synthesis without binding
Allosteric modulator drug and example
Alters the action of a binding natural neurotransmitter, binding to a secondary binding site (alcohol increases the effect of principle ligand on GABA receptors)
Inverse agonist drug
Has the opposite effect of a natural neurotransmitter on the receptor
Therapeutic index
Quantifies the difference in doses for desirable and toxic effects of a drug
Therapeutic index equation
Doses that produce desirable effects in 50% of animals (ED50) / Doses that produce toxic effects in 50% of animals (LD50)
Alcohols effect on the brain (3)
Enhances GABA transmission by binding to GABAA receptor (secondary binding site), increasing the flow of Cl- ions
Acts as antagonist at NMDA receptor, reducing Na+ into neuron
Indirectly increases neurotransmission in serotonin and dopamine systems (at cannabinoid receptors)
Long-term brain effects of alcohol consumption (2)
Korsakoff’s syndrome (damage to thalamus and hypothalamus)
Withdrawal (addiction)
What happens to the brain when alcoholics try to detoxify
Becomes overactive to try and regain its normal state. Causing: anxiety, hyperexcitability, tremors etc
Cocaine’s effects on the brain (2)
Blocks dopamine transporter, reducing reuptake/recycling and prolonging duration of dopamine in the synapse (repeatedly binding)
Indirectly increases dopaminergic transmission
Why is methamphetamine one of the most addictive amphetamines?
Is more liquid soluble so can cross the membrane more easily
Amphetamines effects on the brain (2)
Blocks dopamine and noradrenaline reuptake (indirect agonist)
Doubles release of dopamine and noradrenaline by reversing transporters to push more out into synapse
Effect of nicotine on the brain
A direct agonist, it mimics nAChRs receptors in the presynaptic neuron - increasing neurotransmitter release
Why desensitisation to nicotine is so easy
nAChRs receptors change shape every time they are activated, it binds worse the more it is taken, building up a tolerance
Effect of caffeine on the brain
Direct antagonist, it binds to adenosine receptors (which inhibit dopamine receptors activation through co-localisation), caffeine reduces this inhibition, increasing dopamine signalling
Why heroin is more addictive than morphine
Crosses blood-brain barrier more easily, then is metabolised into morphine in the brain
Opiates effects on the brain (3)
Direct agonist, naturally produced opiod ligands bind to mu and kappa receptors
Inhibits neurotransmitter’s responsible for pain release
Indirectly inreases dopamine release: by inhibiting GABA neurons, reducing dopamine inhibition
How is THC eliminated in the body
In urine, lipid soluble so metabolism is essential for elimination (some in fat stores makes elimination slow)
Cannabis effects on the brain (3)
Direct agonist, it binds to CB1 and CB2 receptors
Complex interactions with cannabinoid and opioid systems
Results in dopamine release
Two examples of cannabinoids
THC, CBD
How do dopamine and addiction link together
Dopamine release is found rewarding, creating motivational ‘wanting’ (seen in rats, and humans)
Why is memory biologically useful
Allows us to make predictions for the future and act accordingly
What does the learning curve show
The law of diminishing marginal returns (1st time something is learnt has a larger level of learning than later times - diminishing!)
Rescorla-Wagner rule of learning
The amount learnt is proportional to the amount of surprise at the outcome
(if the outcome is fully predicted, there should be no learning)
Blocking
If stimulus X creates and outcome, and then stimulus X and Y create the same outcome, follows that X should fully predict the outcome (blocking learning from Y)
What/where is the mesolimbic pathway
Pathway that fires dopamine neurons from the ventral tegmental area to lots of outer brain areas (particularly the nucleus accumbens)
Experiment that gives evidence for Rescorla-Wagner rule
Monkey associates images with reward, action potentials in mesolimbic pathway decrease as reward becomes predicted. Much more action potentials for unpredicted reward and a pause in them (another prediction error signal) when predicted reward not given
Critical analysis of Rescorla-Wagner rule
Only correlational evidence, prediction error signals seem to act the way one would expect, but is that the actual function?
Can these dopamine signals be important for reward and learning simultaneously?
Stages of visual memory (2)
Immediate (iconic) memory and visual short term memory
Immediate (iconic) memory
Visual images in the retina and brain lasting 0.25 seconds (retained on eyes until decay)
Visual short term memory
Events that just occurred and are still in consciousness
How to find causal evidence for the function of something in the brain (3)
Studying lesions, damaged brains or temporarily inactivate parts
How to find correlational evidence for the function of something in the brain (and disadvantage)
Brain imaging, it doesn’t tell us if it is significant for the behaviour, just shows its presence (need to remove the part and study behaviour)
Difference between short term memory and long term memory
Short term memory lasts for minutes/hours while decaying whereas long term memory emerges over time and persists
Consolidation
The time dependent stabilisation of LTM
Evidence for Arc protein involvement in learning and memory (2)
Appear to increase in amygdala after learning (correlational)
Inhibition (using anisomycin or DNA strand) impairs fear memory consolidation (rats) (causational)
(STM intact with inhibition)
Why are NMDA receptors thought to be more involved in memory acquisition rather than consolidation?
Inhibition of them inhibits STM and LTM (fear in rats)
Evolutionarily, why is it beneficial to forget certain memories?
Remembering everything would be very energy inefficient, particularly as many have no survival benefit for remembering
Donald Hebb’s famous quote
Neurons that fire together, wire together
synaptic plasticity
Long term potentiation (LTP)
Long lasting increase in signal transmission between two neurons based on the strength of synapses
Early and late LTP
Early LTP is equivalent to STM as it comes fast and decays. Late LTP equivalent to LTM as it comes later and persists
Tetanic stimulation
High frequency stimulation
Summary of 1st LTP study (Bliss and Lomo 1973)
A still active (in artificial spinal fluid) slice of a rats brain was given tetanic stimulation which massively increased excitatory post synaptic potential (is a non-associative LTP study)
How to induce associative LTP
Concurrent brief tetanic stimulation of neurons connected to the same post synaptic neuron
How LTP was found in the amygdala
Tetanisation of axons innervating it resulted in LTP
How NMDA receptors were found to be required for LTP (and detail)
APV (NMDA antagonist) was applied and then both E-LTP and L-LTP were found impaired after tetanisation
(more for acquisition than consolidation)
Correlational evidence for LTP role in memory
Fear conditioned rat who underwent tetanisation froze in response to the tone and had an increased synaptic response in amygdala
How Arc proteins link to LTP (correlational)
Tetanisation in amygdala induces activity of Arc proteins (similar mechanisms)
Causational evidence for LTP’s role in memory and criticism
Successful artificial insemination of a fear memory (using optogenetics in LA pyramidal neurons) used instead of shock in fear conditioning rats saw freezing to just a tone
(however less percentage freezing than normal)
Long term depression (LTD)
Low frequency stimulation causes decrease response to test stimulation (most commonly in cerebellum). Can, along with LTP, lead to increase in synaptic response
How LTD increases output (synaptic activity)
Depresses the excitatory synapse from the input neuron to an inhibitory interneuron, resulting in a weaker response by the inhibitory neuron’s synapse onto the output neuron
(basically inhibiting the inhibitory neuron!)
How are memories consolidated more
The Adrenergic system (adrenaline and nor-adrenaline) is known to modulate memories when there is arousing stimuli, consolidating more
Memory extinction
Not a process of unlearning, it is forming a new memory not to associate the CS with the US
Why can memories be recovered much faster/stronger than if it was formed again
extinct memory is not actually lost, it is just overpowered by the association not to associate the CS and US. If conditioned again, spontaneous recovery is strong
2) Extinction based on the context of which the new (non-association) memory is formed. Memory can recover in different contexts
In fear memories, what areas are involved before and after extinction
Before extinction, the fear memory is located in the amygdala and the pre-frontal cortex inhibits it after extinction
??
When is memory consolidation vunrable and how do we know this
In the first few hours after the event or for a short period after retrieving a memory, known as it is the only time NMDA receptor/Arc protein inhibitors have an effect
Memory reconsolidation
After a memory is retrieved, there is a period where it is vulnerable to extinction (stress increasing chances) and needs to maintain its integrity
If successfully re-consolidated, it is generally stronger than before
Example of memory re-consolidation (gone wrong!)
Researcher put pictures of Bugs Bunny (Warner Bro’s) at Disneyland around a university campus and when he asked later, many students gave detailed accounts of their childhood experience with Bugs Bunny at Disneyland
Example of therapy for phobias based on memory reconsolidation
Fear memory (of spider) is reactivated and a pill of an adrenergic inhibitor is taken right after to interfere with the re consolidation. proven effective but is correlative
What are emotional responses characterised by, and examples based on fear emotion
Physiological changes (heart rate, pupil size) Behavioural responses (facial expression, avoidance behaviour) Cognition changes (enhanced attention and memory) Subjective feelings (feeling of fear)
Function of emotional responses
Behaviour that adapts to emotional response is biologically useful for survival
(however can be maladaptive: disorders etc)
Classic example of human fear conditioning
Little Albert classically conditioned to associate rat with loud noise (fear)
Explain James-Lang Theory (emotion/response)
After a stimulus is perceived, it causes a peripheral response in the body. This is then interpreted by the brain and an emotion is formed
Supporting reasons for and against James-Lang Theory (emotion/ response) (2 / 1)
Enhances survival as response is done before emotion is processed
Makes evolutionary sense as we evolved from less complex animals that appear to respond without emotion (response 1st)
Against: paraplegics who cannot feel from neck downwards… can they not feel emotion as cannot peripherally respond?
Explain Cannon-Bard Theory (emotion/response)
After a stimulus is perceived the peripheral response and emotion appear in unison. Emotion then being able to influence peripheral response once processed
Explain Schachter-Singer two factor theory (emotion/response)
After a stimulus is perceived, it causes a peripheral response in the body. The context of the environment along with the bodily interpretation both decides what emotion is then felt. Response can then be altered
Real world applications of the emotion/response theories (2)
Lie detectors record peripheral responses (sweat conductance)
Responses thought to be more involuntary when fear and guilt emotions at play
Phineas Gage example
Tamping iron when right through his ventral prefrontal cortex. Still had motor reflexes but became emotionally dysregulated and engaged in reckless behaviour
Kluver-Bucy syndrome
Lesions in the amygdala/temporal lobe causes one to be emotionally dulled, placid and have less expressive facial and vocal expressions
Commonly thought most key area involved in emotion
The limbic system
Amygdala involvement in emotion, and how it is known (2)
Thought the area that regulates fear. Stimulation in it elicits fear responses in animals and fear/aggression responses in people with amygdala stimulation prior to neurosurgery
Emotional effects of bilateral lesions in the amygdala (3)
Tameness, reduced stress hormone release, reduced responsiveness to threatening stimuli
Urbach-Wiethe disease, and patient example
Bilateral amygdala degeneration. SM, middle aged woman, tried to pick up a venomous snake and laughed though fearful situations
Amygdala damage effect on memory and study example
Memories of emotive content appear impaired, cannot remember an event emotionally. Found by interviewing people with Alzheimer’s in Japan about the 1995 Kobe earthquake
(LTP increases in amygdala after fear conditioning also supports)
What was also found to increase amygdala activity other than fear?
Food, drugs, sex etc - it appears biologically beneficial things (lower pleasures)
Studies showing the pre-frontal cortex’s role in emotion (3)
Phineas Gage
Decreased activity found in young people with violent histories
Decreased activity in murderers (increase in amygdala)
The pre-frontal cortex link with extinction and how it is known
Appears important for extinction as damage to rats medial PFC impairs the extinction process
Amygdala link with anxiety and how it is known
Amount of axons in amygdala predicts trait anxiety levels (the more axons the more anxious)
Periaqueductal grey (PAG) and function
Located around the central aqueduct deep in brain, involved in the selection of defensive emotional responses
Periaqueductal grey (PAG) two parts and their separate functions
Dorselateral part (above) control running away responses Ventralateral part (below) controls freezing responses
How the network of emotional responses is believed to work
The PFC regulates the amygdala which coordinates the appropriate response, amygdala activates the PAG
How do anti-anxiety drugs tend to work, and example
They inhibit the amygdala (GABAergic receptor agonists) E.g. benzodiazepines
How are emotions in others recognised (3)
A composite of facial, vocal and postural elements
How recognition of emotional facial expressions can be impaired (and evidence)
Damage to the amygdala (especially fearful ones) as patients do not look at the eyes nearly as much
Imaging shows activation in amygdala when faces shown (especially fearful ones)
Evidence that facial expressions are processed unconsciously
Can been shown subliminally and subjects will guess the correct emotion
Evidence that producing emotional facial expressions may not depend on amygdala
Patient SM (bilateral amygdala damage) can voluntarily produce all facial expressions Implying regions for production and recognition of facial expressions differ
Six core expressions
Happiness, surprise, fear, sadness, disgust and anger
Evidence that facial expression production may take place in the right hemisphere more than the left
Generally, mirror imaging studies show a more expressive left side of the face in primates and human
What are the implications of humans having similar facial expressions to animals (2)
Evolutionary basis, genetic component
Volitional facial paresis ** and cause (2)
Emotions elicit facial movements that cannot be reproduced voluntarily. Caused by damage to motor cortex regions that control facial muscles or to the neurons connecting them
Emotional facial paresis ** and cause (2)
Emotions don’t elicit facial movements though they can be produced voluntarily. Caused by damage to specific PFC regions or to Thalamic region between PFC and hindbrain regions controlling muscles
Evidence that facial expressions are innate (3)
Similarity with animals, blind children and remote cultures
Evidence that facial expressions are not innate (or completely innate) (2)
East Asians confuse Western fear and surprise faces. Shows they focus much more on the eyes
Maybe blind children learn facial expressions through trial and error
Evidence of non-facial emotional expressions
Subjects drew a body map for each different emotion. After averaging them, a hierarchy could be constructed of how similar each were to each other (anger and fear surprisingly similar)
PTSD causes and symptoms (4)
Caused by direct or indirect experience of a traumatic event.
Symptoms include: re-experiencing, avoidance, negative cognitive effects (depression) and high arousal (increased startling and/or attention)
Brain differences in PTSD patients (2) and how we know
Increased amygdala activity (higher response to fearful faces)
Low ventromedial prefrontal cortex activity (shown by imaging)
Why PFC and amygdala activity negatively correlate in terms of fear emotions
PFC inhibits amygdala activity, therefore low PFC activity will mean high amygdala activity
Why PTSD patients may have enhanced fear memories (3)
People with high nor-adrenaline seem susceptible to PTSD, known to enhance consolidation
Imaging studies show ‘unconditioned’ activation of the amygdala in patients (role in fear memories)
Cortisol release (responds to stress) is reduced in PTSD patients, enabling more nor-adrenaline
How is PTSD often treated
Using beta-blockers (propanolol), which blocks beta receptors to prevent the over-activity of nor-adrenaline (weakening the consolidation/re-consolidation of the traumatic memory)
How an impaired PFC may contribute to the enhanced traumatic memory in PTSD patients
May mean a weaker ability for extinction (Patients do not recall extinction as well as traumatised controls)
What area are grasp and pain withdrawal reflexes mainly elicited in
The hind-brain, including the brain stem and spinal cord
Define motivation
The internalised directioning of behaviour (not just reacting to stimuli)
Homeostasis
Maintenance of an ideal, stable physiological environment (the ‘set point’)
Drive theory
Deviations from homeostasis mean physiological deprivation, which causes a psychological ‘drive state’ which directs behaviour until homeostasis is achieved again. An essential negative feedback system
Supporting evidence for drive theory
Drug addicts experiencing withdrawal require the drug to return to their own ‘set point’ or homeostasis (demonstrating that ones set point is always changing)
Critical analysis of drive theory
It assumes the existence of a ‘set point’ which there is no evidence for. Set point is always changing and is unclear, more likely ‘settling points’
Anticipatory motivational drives
An extension of drive theory, is that people get drives to maintain their ‘set point’ before deviation occurs (Based off learning, E.g. drinking water while eating)
Drive reduction and reward hypothesis
‘Drive states’ are associated with unpleasant emotional states. Reducing these may be rewarding, this reward drives behaviour
Incentive theory
Actions are motivated by external, personalised intensives (not reducing negatives, actually attracted to stimuli)
Evidence supporting incentive theory
May come down to learning: rat given food/drug/sex in one compartment and placebo in the other. When given the choice, it stays much longer in reward compartment
How incentive theory turns back to drive theory
If motivated behaviour was purely incentive based, it would be very habitual. Ones drive state still plays an important role in motivated behaviour, making it flexible (e.g. a sour taste is more palatable with sodium depletion)
Evidence against drive theory
Often removing drive states does not alter behaviour: intra-gastric food did not satisfy a man’s appetite - he still chewed it up, spat it out and then put it in his stomach (rewarding taste)
Evidence that reward is more link to hedonistic pleasure than achieving homeostasis
Rats obsessively drank non-calorific sweeteners. Humans also put them in hot drinks (but this may be associative behaviour by humans)
Preparatory and consummatory behaviour, and their brain areas shown by imaging
Preparatory behaviour enables access to the goal (amygdala)
Consummatory behaviour, more reflexive, consumes the goal (hypothalamus)
Case study for preparatory and consummatory behaviour
Male rat presses lever several times and releases a female rat to mate with. With hypothalamus lesion, the rat will press the lever but choose not to mate (no consummatory behaviour). With amygdala lesion, rat doesn’t press the lever but will mate when presented with the female (no preparatory behaviour)
Reward
A mixture of liking and wanting
Physiological mechanisms for liking
??
Brain-stem areas show facial effective responses but for-brain mechanisms overrule it for expressions of taste (unconscious, can be conditioned)
Physiological mechanisms for wanting
??
Increased dopamine (in mice) shows higher levels of wanting, but not liking. They run faster for the reward Mesolimbic subconscious motivation
Why is knowing the difference between liking and wanting useful
It shows, when thinking about the reason for flexible behaviour, we should focus on wanting and not liking or reward (drug addicts want a drug but often do not like it anymore)
Principles of the development of neurons (6)
Formation of nervous system (neurulation), neurons form (proliferation), neurons move, neurons connect, circuits are refined, neurons are myelinated
What happens during neurulation
Embryos elongate and neural plates fold into a neural tube, creating the basis for the brain and spinal cord
What happens during proliferation
Progenitor cells divide to form neurons (or more progenitor cells which will eventually form into neurons)
What could happen if proliferation is disrupted
Can cause substantial cognitive problems later on, evidence shows giving pregnant rats MAM chemical causes schizophrenic tendencies in their offspring
What happens (with detail) after proliferation in the development process
Neurons specialise by differentiating and migrating into areas of the brain with other similar neurons
What happens after neurons specialise in the development process (give detail)
Neurons axons extend to the correct target regions to connect together, also forming synapses to connect with neighbouring neurons through synaptogenesis
What could happen if the stage of connecting neurons is disrupted during the development process
Evidence shows it could cause ADHD or autism
What happens during apoptosis (detail)
Circuits are refined: 50% of neurons are intentionally killed after neurons connect in the development process
What may apoptosis explain about early childhood
Why so many early memories are lost
What is apoptosis critical for
Visual development (especially spatial awareness, identifying vertical edges)
What happens during myelination
Myelin sheath created to insulate axons and save energy
Fast (2) and slow (3) causes of degeneration
Fast: stroke and hypoxia (lack of oxygen in brain)
Slow: disease, age-related decline, repeated concussions
What physically happens during degeneration
The brain physically gets smaller as neurons and axons (white matter) die. There is also a loss of synaptic connections
Causes of degeneration (5)
Lack of oxygen
Cannot generate enough energy (underactivity)
Neural disfunction causing apoptosis
Strokes and transient ischaemic attacks
Overactivity causes lesions (to rid of troubled neurons_
What causes transient ischaemic attacks and what is it
Loss of blood flow, has the same symptoms as a stroke
What causes Huntington’s diseases
Is monogenetic: caused by the Huntington gene which alters the function of the Huntington protein, creating apoptosis in affected neurons
Where in the brain does Huntington’s disease usually originate
Degeneration focused in the basal ganglia
Symptoms of Huntington’s disease (4)
Impulsivity, balance problems, depression, involuntary movements
How regeneration occurs in the peripheral nervous system
Axons regrow and connect to sensory cells/muscles (only if cell body remains intact
Why regeneration in the CNS is more abnormal (3)
Due to the complexity of connections (have to reconnect perfectly)
Astrocytic and fibrotic scars
Myelin debris
Hope for regeneration of neurons in the CNS (2) and a problem
Proliferation occurs in some brain areas throughout our lives
Meaning more neurogenesis and stem cell research are possible
…but how do the new neurons connect and differentiate correctly for their function?
Commonness of 1) Parkinson’s and 2) Alzheimer’s disease
1) 2nd most common neurodegenerative disease (1:500)
2) Most common, 1:6 people over 80
Parkinson’s disease types (3)
Idiopathic (most common, no clear cause)
Drug induced (often anti-psychotic medication)
Genetic (less than 5%)
Environmental cause and non-cause of Parkinson’s
Exposure to certain chemicals a cause, exercise can reduce risk
Clinical motor function characteristics of Parkinson’s (3)
Tremor, slowness (bradykinesia) or absence (hypokinesia) of movement, early symptoms in facial expression
Clinical non-motor function characteristics of Parkinson’s (2)
General slowing of cognition, emotional effects
symptoms start physical and spread
Usual initial brain area of degeneration for Parkinson’s
Basal Ganglia (dopaminergic midbrain), specifically the Substantia Nigra and nigrostriatal pathway
How Dopamine problems (loss of transporter activity) are known key to Parkinson’s
Initial degeneration in Basal Ganglia
People taking MPTP (opioid drug) suddenly stopped moving, similar symptom to Parkinson’s
Why Parkinson’s is rarely caught in time for effective treatment
80% of neurons degenerate before symptoms appear
Other neurotransmitters besides dopamine hindered by Parkinson’s (2)
Serotonin and Noradrenaline
Secondary brain area affect by Parkinson’s and its effects
The Basal nucleus of Meynert, affecting Cholinergic transmission
Treatments for Parkinson’s (3) and a problem with each
Levodopa drug, aiming to increase dopamine but is rapidly metabolised
Cell transplantation to replace dopamine neurons, but may not develop correctly
Deep brain stimulation to enhance remaining dopamine, however stimulating inhibitory neurons has undesirable effects
Types of Alzheimer’s disease (2)
Sporadic (no obvious cause, most common)
Early onset / genetic (less than 10%)
Alzheimer’s clinical characteristics (5)
Speedy memory decline Spatial navigation deficits (often 1st symptom) Potential personality changes Aggression/apathy Depression
Physiological effects of Alzheimer’s (5)
General neuronal loss (apoptosis)
Initial degeneration often in temporal lobe
Neurofibrillary tangles
Plaque build ups
Synaptic loss (cholinergic and glutamatergic synapses)
Potential reasons for memory loss in Alzheimer’s (2)
Due to neuronal loss
Glutamatergic synaptic loss (NMDA receptors attach to these)
Potential cause of genetic Alzheimer’s
Weak link with ApoE gene: variants make it more likely for plaque to build
Treatments for Alzheimer’s (2) and problem with each
Acetylcholinesterase inhibitors to boost cholinergic transmission and prolong its synaptic presence, however nicotine has the same effect
Targeting pathology to create antibodies for amyloid and stop plaque formation, but unclear if amyloid’s actually cause Alzheimer’s
Cause of phantom limb syndrome
Neurons take time to degenerate after a limb has been amputated
Why blind people who read brail have a greater sense of touch
Sensory space in visual cortex area of the brain for other similar function
