PS121 Brain & Behaviour Term 1 Part 1 Flashcards
What does dualist mean?
Mind is different & separate from matter
What does materialist mean?
“Mind” is what brains do
Define behaviour
An organism’s internally coordinated response to its internal or external environment.
What is a nervous system good for?
- To interact flexibly with the environment:
- Register (‘sense’) the environment
- Transform (interpret ‘make sense of’ those signals;
- Generate an appropriate response
Label an axon with the following labels:
- Dendrites
- Axon Hillock
- Cell body
- Soma
- Axon terminals
What is the output of the Somatic Nervous System?
Skeletal muscles (voluntary control)
What is the output of the Autonomic Nervous System?
Eithet sympathetic part ‘fight or flight’ or ‘rest and maintenance’
Final output: muscles and glands - involuntary control
Label cross section of spinal cord with the following labels:
- Grey matter
- White matter
- Ventral roots
- Dorsal roots
- Sensory neuron
- Motor neuron
- Dorsal root ganglia
Monosynaptic Reflex Arc (e.g knee-jerk reflex)
- Inside each muscle fibre, specific sense organs (muscle spindles) activate a sensory neuron when muscle is quickly stretched
- Their axons enter spinal cord (via dorsal root), connecting directly with
- Motor neuron, which send their axons out (via ventral root)
- Activating the same muscles from which signals originated
What is a polysynaptic reflex arc?
- Sensory and motor neurons connected via one or more interneurons
- Sensor and effector in different locations (e.g withdrawal response)
Spinal Cord Resection
- Spinal cord neurons can even generate complex movement patterns (e.g walking - see stepping reflex in young infants)
- but CANNOT VOLUNTARILY initiate movements - patterns are only elicited in response to appropriate responses
- Experimental evidence: cat with spinal cord section CAN still walk on a treadmill
Long myelinated axon of sensory neurons from all over the body (except the head) enter the spinal cord via the dorsal root of the spinal nerves
- Neurons transmitting precisely localised information send axons to the top of the spinal cord
- Neurons transmitting poorly localised information synapse immediately with other neurons upon entering the spinal cord
True or false sensory neurons from the head send axons directly into the brain via cranial nerves (e.g optic nerve)
True
What does the brainstem consist of?
Hindbrain and midbrain
Hindbrain
- Medulla and pons: where the spinal cord enters the brain (Functions: contains several nuclei of the autonomic nervous system)
- Cerebellum - not part of the brain stem (Function: balance, motor learning)
Midbrain (mesencephalon)
Above the pons (functions include combination of information from different sense modalities: direction of attention)
What does the forebrain (diencephalon) include?
Thalamus and hypothalamus
Thalamus
Massive structure on top of the midbrain, deep in the centre of the brain.
- Main relay station for incoming sensory signals
- Recieved downward-going input from higher areas, modulating the relay of sensory signals
Hypothalamus
Small structure in front and below thalamus
- Directly connected to pituitary gland (‘master gland’ of the ES, controls activity of all other glands)
- ‘Gateway to endocrine system the nervous system can influence endocrine system via hypothalamus - pituitary connection
The Forebrain - Telencephalon
- From the diencephalon, incoming signals go up to cerebum
- Divided into two highly similar (but not identical hemispheres)
- Each covered in cerebral cortex (thin layer of neurons covering each hemisphere) also contains several groups of sub-cortical nuclei (tight cluster of neuron’s cell bodies)
What is grey matter?
Cortex and sub-cortical nuclei
What is white matter?
Myelinated axons of neurons
Each hemisphere mainly receives input from and sends output to the ________ side of the body
Contralateral
Basal Ganglia
Group of nuclei surrounding the thalamus
Involved in motor control process
Consist of globus pallidus, putamen and caudate
Putamen and caudate often referred to as corpus striatum (‘striped body)
Amygdala closely connected to this system, therefore sometimes described as being part of the basal ganglia.
Limbic System
Several interconnected cortical and sub-cortical areas - playing a crucial role in memory and emotion.
Sub-cortical: almost complete circle formed by fornix and hippocampus, ending in mammillary body and amygdale
Cortical: cingulate cortex directly above corpus callosum (evolutionary older, more primitive than rest of the cortex)
Connected to hypothalamus (septum) and olfactory system
Cortex and Corpus Callosum
Cerebral cortex: thin layers of neurons covering the whole hemisphere, i.e., not just
the outside, but the inner (‘medial’) surface as well
Corpus callosum: thick bundle of axons connecting the two hemispheres
Virtually all signal transfer between the cortices of the hemispheres done via CC!
Highly folded, forming gyri (s. gyrus, outward folded areas) and sulci (s. sulcus, inward folded areas)
o Longitudinal fissure: Largest sulcus, separating left and right hemisphere
o Smaller sulci used to define boundaries of cerebral lobes:
Occipital lobe
At the back of the brain and function is visual perception.
Temporal lobe
At the sides function is auditory perception
Parietal lobe
At the top of the brain function is somatosensory perception: inter- sensory and sensory-motor integration
Frontal lobe
At the front of the brain and function is planning and motor output
Everything is reversed!
Sensory input from the right side of the body (or the right visual field) is processed in the left half of the brain (and vice versa). Motor output to the right side of the body is generated in the left half of the brain and vice versa.
Sensory signals from the diencephalon are relayed to their appropriate primary sensory cortex
Visual signals > visual cortex (occipital lobe)
Auditory signals > auditory cortex (temporal love)
Signals from skin, muscles and joints > somato-sensory cortex (pariental lobe)
Inside the specific sensory areas, signals arrive at positions corresponding to the position
of the receptor cells what is this called?
Topographic representation
Motor output
Cortical motor areas: Located in the frontal cortex, at the boundary to the parietal cortex
o Supplementary motor cortex & premotor cortex: involved in planning, monitoring, &
sensory guidance of movements
o Primary motor cortex: final execution stage – its motor neurons send axons directly
down the spinal cord (the pyramidal tract)
Cortical motor areas are massively interconnected with two sub-cortical structures, forming complex motor control circuits:
o Basal ganglia: modulate movements, particularly in-volved in selective inhibition of
movements
o Cerebellum: involved in maintaining posture & balance, timing of movements, & motor learning
o Both receive input from motor cortex, sensory cortex, and from other sub-cortical
structures!
True or false motor signals are ultimately sent around the brain
False - motor signals are ultimately sent down the spinal cord
Why do more complex organisms need a nervous system?
o cells on the inside of the body are not in direct contact with the outside world
o cells live in different environments
o cells have become specialised
Neurons have no possibility to store energy
Therefore glucose and oxygen MUST be constantly supplied. Without supply, neurons stop working within seconds and die within minutes.
Neurons do not divide
They develop from neural stem cells.
o cells on the inside of the body are not in direct contact with the outside world
o cells live in different environments
o cells have become specialised
Glia cells
- Provide ‘protected environment’ for neurons to survive
- Develop – like neurons! – from neural stem cells
- About as many glia as neurons in the brain
Astrocytes
o star-shaped
o physical & nutritional support for neurons (‘Blood-Brain-Barrier’):
▪ transport nutrients from blood vessels to neurons
▪ waste products away from neurons
▪ hold neurons in place
o take part in neural signalling (!!)
Microglia
o small
o mobile for defensive function
▪ produce chemicals that aid repair of damaged neurons
▪ digest dead neurons (‘phago-cytosis’)
Oligodendroglia
o large, flat branches, wrapping themselves around axons
o consist of fatty substance, insulating the axon (‘myelin sheath’)
Membrane hyperpolarisation and depolarisation
- All based on movement of electrically charged particles (ions):
o Ion-specific channels in cell membrane are ‘gates’ that can open (either by chance or in response to stimulation)
▪ If positive ions enter (or negative ions leave): membrane depolarises (inside less negative
than usually)
▪ If negative ions enter (or positive ions leave): membrane hyperpolarises (inside more
negative than usually)
Action potential
- Voltage gated membrane channels:
o Na+
channels open or close in response to
electrical changes at the membrane
o Sequence of events:
Start: Membrane depolarised
→ Na+
channels open
→ Na+
ions enter the cell
→ Membrane depolarises further
Threshold potential and the Hodgkin-Huxley cycle:
o IF membrane potential at axon hillock remains below ~ -50mV
=> resting potential returns
o IF membrane at axon hillock depolarises beyond ~ -50mV
=> all Na+
channels (at axon hillock) open
=> action potential generated (‘triggered’)
Electrochemical processes during an action potential
o Enough positive ions have arrived that threshold has been reached:
▪ so many Na+
ions enter the cell that inside becomes
more positive than outside (complete depolarisation)
o complete depolarisation causes
▪ Closing of Na+
channels: No more Na+
ions enter the
cell
▪ Opening of K+
channels => K
+
ions rush out =>
membrane repolarises
o K
+
channels close when resting potential is restored
▪ briefly, fewer K
+
ions inside than outside the cell =>
membrane hyperpolarized (inside more negative
than usual)
Conduction of the action potential
o Originates at axon hillock and travels down the axon
o Each burst of depolarisation = trigger that opens Na+
channels in adjacent sections of the
membrane
Why does the action potential not travel backwards?
▪ During hyperpolarisation (after AP has just passed through), membrane more difficult to
depolarise
▪ whereas membrane ‘in front of’ AP is still at resting potential and hence relatively more
easy to depolarise
Properties of the action potential
o Does not decay during transmission
o Always strong enough to depolarise next area of membrane ahead of it
o ‘All-or-nothing’ phenomenon: either generated or not - can not be generated with different
intensities!
o Can not be produced continuously (minimal time bet-ween subsequent APs 2 - 5 ms)
o Fast
▪ However, for some purposes they might not be fast enough =>
Saltatory conduction
- Saltatory conduction
o In mammals, the axons of sensory and motor neurons are myelinated, resulting in much faster transmission
▪ Myelin (fat) prevents inflow and outflow of ions
▪ Electrical charges are transported inside the axon, without the need to produce an AP (for
a rough analogy, think Newton’s cradle)
▪ Every 1 or 2 mm, myelin sheath interrupted by small gaps (Nodes of Ranvier)
▪ Only at these nodes, a new AP is generated - the action potential ‘jumps’ from node to
node
How strong a stimulus is represented in a neuron’s _______ ___
Firing rate - a strong input will cause the neuron to send out signals more quickly
Voltage gated ion channels open in response to a change in membrane potential
Examples:
o K+ channel and Na+ channels in
axon hillock & axon,
o Ca++ channels in membrane of
axon terminal;
All of these respond to a positive
charge on the inside of the membrane (depolarisation
Transmitter-gated ion channels open in response to a NT molecule binding with the channel’s receptor site
Ionotropic transmitter channels open directly and metabotripic transmitter channels open indirectly
Excitatory synapse
Positive ions enter (depolarisation) and new AP becomes more likely
Inhibitory synapse
Negative ions enter (hyperpolarisation) and new AP becomes less likelt
For an action potential to be triggered the membrane potential at the axon hillock must depolarise beyond _____ mV
-50 mV
Post-synaptic summation:
GP integrates (‘sums’) changes caused by several APs at one post-synaptic neuron:
o Temporal summation: Combines PSPs occurring in rapid succession;
o Spatial summation: Combines PSPs from different synapses (of one post-synaptic neuron)
Neurotransmitter Removal (degradation and re-uptake)
o Degradation:
- Special enzymes in the synaptic cleft break down (inactivate) NTs
- Components are (partly) ‘recycled’ to make new NTs
o Re-uptake:
- Receptor molecules at pre-synaptic axon terminal take up NTs
- return them into pre-synaptic cell
Schizophrenia and Parkinson’s Disease
Schizophrenia therapy: anti-psychotic drugs and possible side effects: parkinsonism
Parkinson’s disease therapy: L-Dopa and possible side effects: psychotic episodes
Quaternary- and Mono- Amines
Dopamine, Serotonin, Noradrenaline and Acetlycholine
Amino Acids
GABA and glutamate
Peptide transmitters
Endorphins and oxytocin
Gas transmitters
Nitric oxide and carbon monoxide - not stored inside the neuron, but synthesised as needed
Neurotransmitters function
Glutamate: excitatory (e.g., all sensory systems [except pain])
GABA: inhibitory (esp. local inhibitory interneurons)
ACh: excitatory (activates muscle fibres -> muscle contracts)
Neurotransmitters information modulation
ACh: activates cerebral cortex, facilitates learning
Dopamine: voluntary movement, action planning & control
Noradrenalin: increases vigilance & readiness to act
Serotonin: calming, reduces impulsive behaviour
Neurotransmitter synthesis:
Neurotransmitters are complex molecules and cannot be stored in large amounts. Therefore need to be constantly synthesised by the neurons, e.g.:
1. Produce tyrosine (amino acid) in the liver;
2. Transport tyrosine in the bloodstream into the brain
3. Convert tyrosine into L-DOPA (L-DihydrOxyPhenylAlanine) in the brain [use tyrosine
hydroxilase]
4. Convert L-DOPA into dopamine [use aromatic L-amino acid decarboxylase]
5. Store dopamine in the neuron’s vesicles. OR:
5. Convert dopamine into noradrenalin [use dopamine-beta-hydroxylase]
6. Store noradrenalin in the neuron’s vesicles
What is a drug?
A substance that even in small quantities has a major effect on bodily functions
o Psychoactive drug: a drug that
- Affects the CNS and
- Alters alertness, perceptual, cognitive, and/or emotional processes
All psychoactive drugs interfere with the brain’s NT systems
Categories of Psychoactive Drugs
o Stimulants: Increase neural activity or bodily functions (e.g., Caffeine, Nicotine, Amphetamine, Cocaine)
o Depressants: Decrease neural activity or bodily functions (e.g., Alcohol, Diazepam)
o Analgesics: Relieve Pain (e.g., Morphine, Heroin)
o Hallucinogens: Cause hallucinations (e.g., Magic Mushrooms, Marijuana, LSD)
All of these potentially have euphoric effects and affect the body’s reward system
The Reward System
- Orbitofrontal cortex - frontal lobes: decision making
- Anteriror cingulate cortex - limbic system: emotion and memory
- Ventral striatum - basal ganglia: movement
Agonists direct interference
Agonists: Mimic the action of ‘their’ neurotransmitter:
Bind to the receptor site and open the channel
Antagonists direct interference
Antagonists: Prevent the action of ‘their’ neurotransmitter:
Block the receptor (i.e., no neurotransmitter molecule can bind to
it), but don’t open the channel
Agonists indirect interference
Agonists: Increase the availability of a neurotransmitter
(increase production, or prevent re-uptake)
Making it more likely that a ‘gate’ will open
Antagonist indirect interference
Antagonists: Decrease the availability of a neurotransmitter
(disrupt production processes)
Making it less likely that a ‘gate’ will open
Neurons are not distributed randomly in the nervous system
Cell bodies cluster together
CNS: nucleus & cortex
PNS: ganglion & retina
Axons travel in parallel to a common target structure
CNS: tract
PNS: nerve
Example: the visual pathway
Schizophrenia - how two pathways interact
Severe mental disorder with delusions, hallucinations, emotional &
cognitive dysfunction, etc.
Associated with overactivity in the
MLC (Meso-Limbic-Cortical) pathway:
Overabundance of dopamine
and/or over-sensitive dopamine receptors.
Treatment: antipsychotic drugs,
esp. dopamine antagonists
=> MLC system returns to normal
levels of activity
Side effects: Movement problems.
Parkinson’s disease - how two pathways interact
Severe movement disorder with
trembling, slowness, problems initiating voluntary movements, etc.
Underactivity in the NS (Nigro-Striatal) pathway
(caused by degeneration of the substantia nigra)
Lack of dopamine
Treatment: L-DOPA (a dopamine
precursor).
=> Striatum return to normal levels of activity
Side effects: Psychotic symptoms
At different synapses the same neurotransmitter can have completely different effects
o D1-receptor: dopamine molecule activates second messenger release -> opens channel
o D2-receptor: dopamine molecule inhibits second messenger release -> closes channel
Can we design a dopamine antagonist that selectively affects frontal cortex and limbic system?
Possibly not, as the distributions are too similar to each other
Development of Precursor Structure
In order to produce neurons, a precursor structure must be in place!
o The neural tube will develop into the CNS (brain & spinal cord)
Early in development, the main divisions of the CNS appear as distinct sections
These will form the ventricles (cortico-spinal fluid-filled chambers in the brain)
and their surrounding brain structures
Note: Retina & optic nerve are really part of the CNS!
Producing neurons
Neurons & glia develop from neural stem cells at the ventricular surface and travel to
their eventual destination.
o From 5 weeks to 5th month after gestation (approx..)
Step 1: Cell proliferation
o Division:
Undifferentiated stem cell
grows an extension to the surface
Cell nucleus moves up & duplicates its DNA
Nucleus moves down
Cell retracts extension
and divides in two
o Cells behave differently depending on whether split was vertical or horizontal:
Vertical split: Both daughter cells repeat the process
Horizontal split: One daughter cell repeats the process, the other moves away and
will not divide again
o These processes stop almost completely weeks before birth
Vertical split
Both daughter cells repeat the process
Vertical split
Both daughter cells repeat the process
Horizontal split
One daughter cell repeats the process, the other moves away and
will not divide again
Step 2: Cell Migration
Step 2: Cell Migration
Different cells have different places of origin
o Pyramidal cells & astrocytes
- originate from dorsal areas
- migrate vertically
o Inhibitory interneurons & oligodendroglia
- originate from more ventral areas
- migrate laterally
Structure of the cortex
Cortex is not a single, homogenous sheet
o Many different types of neurons
o Organised in structured layers
Step 2: Cell Migration (in-depth)
Radial glia cells in the ventricular zone extend thin processes towards the surface
o in an ordered pattern – the ventricular zone is a ‘proto-map’ of the cortex.
Developing neurons crawl along the processes towards
their destination
o First cells to migrate take up residence in the subplate layer (disappears later)
o Next cells migrate to cortical plate:
o first to layer VI, then V, then IV etc.: “inside out”
o Recall: interneurons move in sideways!
Connecting Neurons - Finding the right direction
Recall: each hemisphere receives signals from and sends commands to the contralateral
side, e.g.:
o The right hand is sensed and controlled by the left hemisphere,
o The right half of the visual field is represented in the left visual cortex.
Growing axons are guided by chemical signals in the environment
o Depending on a neuron’s location, it has different
chemical affinities (different ‘likes’ and ‘dislikes’)
o These affinities can be modified (again, by chemical signals in the environment).
Neurons - find the right target structure
How do axons connect with the right structure (instead of with other, nearby structures)?
o Again, chemical signals seem to guide axon development:
o Axons from a specific ‘source’ structure are only attracted to chemicals from a specific
‘target’ structure (chemo-affinity hypothesis, Roger Sperry 1940s)
Neurons - finding the right target cell
Even harder: How could chemical cues differentiate between neighbouring cells?
o Recall: sensory- & motor cortices form ‘maps’ (retinotopic map etc.)
o These are important for action control:
o Input and output must be systematically linked.
o Wiring of the NS seems to depend on dynamic,
coordinated electrical activity (rather than on
slow, overall chemical signals)
Overabundance and pruning
o Axons synapse with nearby cells in their target structure indiscriminately
=> Initially, far too many synapses develop
o Pruning:
o ‘Supported’ synapses are strengthened – unsupported ones disappear
‘Support’: when both the presynaptic and the postsynaptic neuron are active at the
same time – “correlated activity”
The more often that happens, the stronger the connection grows
The less often that happens, the weaker the connection gets
o ‘Anti-support’: when pre- and postsynaptic neuron are active at different times – “uncorrelated activity”
o A neuron that has lost too many connections dies
Learning to see
Prenatally, correlated activity is established through spontaneous ‘waves’ or retinal activity (Carla Shatz, 1990s)
This only works for each eye separately
To coordinate both eyes, actual visual input is needed!
New-born babies literally have to learn to see
Neural Signalling
Baseline activity
o A neuron’s activity without stimulation
o Spontaneously & randomly generates action potentials (APs)
Neural signalling:
o Change in activity relative to baseline
APs more frequent than usual or
APs less frequent than usual
Synaptic Plasticity
Persistent signalling causes the synapse to change
Increased activity causes short-term molecular changes
o Increased neurotransmitter (NT) release
by presynaptic axon terminal
o Increased number of channels in
postsynaptic membrane
o Neither lasts very long!
Sustained increased activity causes long-term structural changes
o Growth of new synapses
New axonal growth mostly during development
New dendritic spine growth all through
adulthood
o Synaptic take-over
Behavioural consequences and synaptic plasticity
o Optimising existing behaviour
Increased transmission rate: react more quickly / reliably to important changes in
the environment
Decreased transmission rate: better able to ignore unimportant changes in the environment
o Acquiring new behaviour:
Growth of new synapses: combine information from previously unrelated sources
Respond to old stimuli in a new way
Synaptic ‘take-over’: ‘re-route’ information to new pathways
Respond to old stimuli in a new way
Learning
Forming new connections
Evidence from brain lesion - cortex
o Lesion studies in animals:
No specific place in cortex where new memories are formed or stored
First formulated as the ‘Law of Mass Action’ (Karl Lashley, 1930-50s)
Loss of memory corresponds to size of lesion
(the more cortex destroyed, the worse the memory performance)
Loss of memory not specific to site of lesion:
(no single cortical area solely responsible for memory storage)
o BUT: Certain cortical lesions can destroy types of memories:
Example 1: lesion in V4 may cause
loss of colour perception
together with loss of colour memory
Example 2: lesion of the right fusiform gyrus may cause
loss of face perception
together with loss of memory for faces
The case of H.M
Structures of both medial temporal lobes surgically removed to treat severe epilepsy:
Amygdala
Hippocampus (pus some surrounding cortex)
Since the surgery, he developed severe anterograde amnesia:
unable to consciously remember anything new that happens to him
unable to learn new facts
BUT was able to
remember things that happened before the surgery
learn events implicitly (to some extent)
learn new skills
No general impairment of intellect and reasoning
Was aware of his condition
Evidence from brain lesion - Diencephalon: Kosakoff’s Syndrome
Thiamine deficit (typically from chronic alcoholism) can lead to the degeneration
of neurons in nuclei of the thalamus and in the mammillary bodies due to thiamine
deficit.
Like H.M., these patients
develop from anterograde amnesia (although less severe)
can learn new skills
learn events implicitly (to some extent)
Unlike H.M., they
also develop retrograde amnesia, i.e., lose most memories of their past
show impairment of intellect
seem to be unaware of their condition
PTSD
Intense negative experiences can damage our brains o especially when they combine
threat – the need to deal with something and
helplessness – the inability to deal with it
PTSD: when the memory of a traumatic experience does not ‘fade away’ over time, but
begins to dominate the patient’s life:
o Patients suffer from ‘flash-backs’ of the traumatic experience
o concentration problems, depression, nightmares, etc.
As yet incompletely understood, e.g.,
o unknown why some people develop PTSD symptoms, while others don’t
o exact causes and mechanisms of PTSD not yet known
Stress hormones may play a critical role
Adrenalin and noradrenalin affect memory
o In a memory test, pictures were remembered better when presented together with an
exciting story than when presented together with a neutral story.
o This advantage disappeared when participants were given a noradrenalin antagonist.
Amygdala and hypothalamus
Amygdala
o part of the limbic system
o crucial for emotional memories: when damaged, animals
appear emotionally ‘flat’ no longer learn a ‘fear response’ (fail to learn that a particular stimulus signals
danger)
over-sexed
o direct contact to…
Hypothalamus
o gateway from nervous to endocrine (hormonal) system
A simplified psychobiological model of PTSD
CYCLE
1. Stress/traumatic experience
2. Amygdala
3. Activates hypothalamus
4. Activated endocrine system which releases
5. Adrenalin and noradrenalin
6. This improves memory of stress and traumatic experience
Plasticity of the Nervous System
o Critical Period
Begins when the critical structures are in place
Ends when the required structural changes are no longer possible
the more elaborate the necessary structural changes, the more restricted the critical
period
Plasticty and development
o Plasticity linked to development, but
o Some forms of development are extremely long-lasting in humans:
o Frontal lobes
The last part of the NS to mature
(still maturing in your early 20s!)
Case Study: Phineas Gage
Survived severe brain injury - major damage to frontal (pole went through his skull)
lobe(s) (possibly only left FL)
o Behavioural effects:
Little impact on perceptual, motor, or intellectual skills
Initially, substantial personality change (but note: this is only anecdotal evidence!)
Later, apparently recovery of cognitive control / social skills
o Frontal lobes assumed to be crucially involved in ‘cognitive control’
Further Research on Frontal Lobe Injury
Evidence from clinical studies (‘frontal lobe syndrome’: impaired ability to maintain intentional, goal-directed behaviour);
Evidence from experimental research (e.g., brain imaging during cognitive control
tasks)
Cortical Reorganisation After Brain Lesion
Brain injury from stroke:
o Neuron death within a larger or smaller area
due to
Lack of oxygen & glucose because of a
blocked blood vessel
‘Drowning’ in blood from a ruptured blood
vessel
o Initial symptoms often far more severe than
final outcome: Significant recovery possible!
o But dead neurons cannot be replaced…??
o Initial wide-spread symptoms because of lack
of input to areas connected to the damaged tissue
o With sufficient training, remaining healthy areas can form new connections with each other
Thereby recovering some of the lost functions
Brain injury from accidents: Rehabilitation according to the same principle
Cortical reorganisation after loss of input
After amputation of a limb, the cortical area representing this part of the body no longer
receives input from it
o The corresponding synaptic connections stay silent and wither away (recall: ‘use it or
lose it’)
o Making room for axons from nearby active areas:
o Recall: Information is interpreted depending on where in the brain it is processed,
therefore:
‘Phantom sensation’ from stimulation of body parts with adjacent cortical representation!
Take-home message: Substantial reorganization of the cortex is possible even in adulthood
o Even if no neurons grow, axons and dendrites keep ‘sprouting’ and form new connections
o (recall that all forms of learning depend on such processes)
Old age associated with loss of structures
o Loss of muscle mass, bone density, etc.
o Cortex and subcortical structures atrophy
Death of neurons
Loss of synaptic connections
Old age associated with loss of function
Old age associated with loss of function:
o Decline in physical fitness and motor skills
Everything becomes more difficult…
o Increased reaction times (slower responses)
Less likely to catch something, catch yourself when you stumble…
o Decrease in memory capacity
Forgetfulness, more difficult keeping several tasks in mind at once…
o Decrease in mental flexibility
More difficult to switch between tasks…
Does an older brain no longer form new connections?
Influence of the environment on cortical neurons: rats reared in an ‘enriched’ (interesting) environment have better developed cortical neurons
more and larger dendritic branches
longer axons with more
collaterals
resulting in visible
thicker cortex:
o The same is true even when
rats are placed in an EE only as adults!
even old neurons can
sprout more dendrites &
axon collaterals
How to minimise cognitive decline in old age?
Grow up in an environment that is interesting, varied, and stimulating.
Learn a lot!
Practice various different skills – physical, social, and cognitive.
Remain physically active throughout your life.
Remain mentally active throughout your life.
