Synaptic Plasticity Flashcards
What is synaptic development?
The increase in both brain size alongside speed of neural processing.
Specifically the number of synapses in the cerebral cortex peaks within the first few years, declines by about 30% between early childhood & adolescence.
When is the brain fully developed?
- Brain size:
new born brain is 1/4 of the size of an adults
brain size is 80% of an adults at the age of 3 and then 90% by the age of 5
growth is mostly due to changes in individual neurons.
- Speed of neural processing:
a newborn transmitts info less efficiently than an adult therefore their brain is slower
increases dramatically during infancy & childhood, maximum at about age 15.
Brain development: Nature vs Nurture?
Does experience change the actual structure of the brain?
– Brain development is “activity-dependent”
– Every experience–whether it is seeing one’s first rainbow, riding a bicycle, reading a book, sharing a joke–excites certain neural circuits and leaves others inactive
– As neuroscientists sometimes say, “Cells that fire together, wire together.”
What is neuroplasticity?
The brain’s lifelong ability to change its structural & functional architecture in response to learning & experience.”
Post-natal brain development
*overall brain volume quadruples between birth and adulthood
*increase size and complexity of dendritic trees of most neurons- this is called dendritic arborisation
Dendritic arborisation of cells in visual cortex shows the increase
in dendritic length between birth to adulthood
*increase in density of synapses (synaptogenesis)
*increase in fatty sheath around neuronal fibres (myelination)- this increases the efficiency of electrical transmissions
- In the newborn brain there are also regressive changes that occur after birth.
- Synaptic densities undergo a loss of synapses, called pruning.
- The timing of these processes varies between cortical regions.
Synaptic density of visual cortex VS prefrontal cortex
synaptic density in the visual cortex begins to reach adult levels after about 2 years of age, however synaptic density of prefrontal cortex does not reach adult levels until the teenage years.
Define cognition
Processes by which knowledge is acquired and manipulated – i.e., thinking.
All mental activities involved in acquiring, understanding & modifying information.
This separates humans from other species
- A reflection of what is in the mind.
- Not observed directly –inferred from behaviour.
- Includes unconscious and non-deliberate processes involved in routine activity (e.g., reading).
Define cognitive development
Development: Changes in structure or function over time.
Define STRUCTURE with regards to cognitive development
Structure: a substrate of the organism
–e.g., nervous system tissue, muscle, limbs (physical structures) or
–mental knowledge that underlies thinking e.g., schemas or concepts
–hypothetical
Define FUNCTION with regards to cognitive development
Function: actions related to the structure
– Most commonly, something that the child does e.g.retrieving a memory, pressing a computer key, etc.
– Cognitive development; assimilation of info into schemas, performing addition.
Why is structure and function bi-directional?
Structures enable function, and function (e.g., activity) feeds back to
drive further development of structure
Function maintains the structure and allows for proper development
Give an example of when structure and function are bi-directional in newborn infants?
Newborn infants have very poor vision
– Growth of cells in the visual cortex (structure) leads to better visual
acuity
– Better acuity (sharpness) leads the baby to look at more patterns, objects (function)
– More looking stimulates further cell growth (structure)
Most development of the infants visual cortex occurs from birth to 6 months
Dynamic & reciprocal transaction of internal & external factors
Nature (biology) & Nurture (environment)
- Oldest, most fundamental issue in psychology
- Which one drives development? (genes or environment)
Currently, not an either-or issue
Genetic potential for development established at conception
Genotype is not a “blueprint”
Sets a range of potential outcomes
Phenotypic (observed) outcome depends on interaction with environment
New techniques has provided the means to address new questions about cognitive development- such as:
what does a baby know before birth? Does an infant understand the grammar of language?
The nature vs. nurture debate continues … At every stage of development, there are important genetic effects and biological
constraints at work in the unfolding of the human brain and mind. Similarly, at each stage there are critical effects of the surrounding
environment, whether at the level of a cell, a system, or the brain itself.
What is plasticity?
The ability to adapt to our environment & store information
Useful for:
1. Development
2. Learning & Memory
3. Disease & Addiction
Plasticity suggests that the nervous system is modifiable
What are the 2 areas where plasticity play an important role
- Macroscopic
Lesion studies – areas of brain damaged by injury (e.g. stroke, head injury) or surgical procedures (e.g. tumour removal, treat epilepsy) lead to changes in brain function and memory/learning
- Microscopic
a. How do individual brain areas encode new information?
– brain made up of neurones so likely that change in neuronal
function involved
b. What can we change?
–Action potentials
* APs are ‘all or nothing’ so can’t change size
* Could change probability of action potential being fired
–Synaptic transmission
Donald Hebb’s Postulate: “When an axon of cell A is near enough
to excite cell B or repeatedly or persistently takes part in firing it,
some growth process or metabolic change takes place in one or
both cells such that A’s efficiency, as one of the cells firing B, is
increased.”
State a case study that support the idea of plasticity on a macroscopic level
Patient HM (Henry Molaison)
- Developed epilepsy at age of 16
- Seizures increased in severity & frequency until he was suffering
around 11 seizures per week - Decision made to remove region of temporal lobe (where seizures
originated) - Fist-size area removed, including hippocampus, amygdala,
entorhinal and perirhinal cortices. - Epilepsy cured
- But HM lost ability to form new memories
- Researchers concluded that hippocampus is involved in learning &
memory
– Declarative – episodic and semantic (facts and events)
– Spatial (based on rodent studies) but HM had more than hippocampus removed
Why use the hippocampus to study learning & memory?
– has an identified role – spatial learning in rodents
– has a “simple” neuronal structure
check slide 30
Long term potentiation LTP (Slide 31)
Bliss & Lomo (1973)
Recorded from hippocampus of anaesthetised rabbits in vivo
Stimulation of axons at a low basal rate produced a stable synaptic response
Application of a single high frequency stimulus train resulted in a persistent increase in response size - LTP
Basal stimulation – e.g. one stimuli every 15s
*LTP induction: high frequency stimulus train
State the important basic properties of hippocampal LTP
- Long Lasting
- Input specificity
If you stimulate two independent inputs and deliver a high frequency
stimulus to one input, only that input shows LTP.
HEBBIAN PLASTICITY - Cooperativity
There is a threshold for LTP induction
e.g. 20 stimuli @ 100 Hz doesn’t induce LTP but 100 stimuli @ 100 Hz does induce LTP - Associativity
If a weak tetanus, which does not induce LTP, is delivered to one input at the same time as a strong tetanus is delivered to a second
input, the subthreshold tetanus now induces LTP – the two sets of
synapses act associatively. - Can be reversed
- Can be saturated
Induction on LTP
*CA3-CA1 hippocampal synapse is glutamatergic
* Different classes of glutamate receptors
AMPA receptor – responsible for basal transmission at this synapse
NMDA receptor – responsible for LTP induction
(also kainate and metabotropic glutamate receptors)
γDGG = AMPA and NMDA receptor antagonist
APV = NMDA receptor antagonist
When NMDA receptor binds glutamate and channel opens, magnesium ions block the channel unless the cell is depolarised.
When cell is depolarised magnesium is expelled from the channel and sodium and calcium ions enter cell
Depolarisation needed to remove magnesium is achieved by activating synapse repeatedly
Expression of LTP
Calcium influx through NMDA receptor is essential
for LTP induction
Calcium activates intracellular signalling molecules
–e.g. calcium calmodulin dependent protein kinase II - CaMKII
How is transmission increased?
– increased amount of glutamate release
– increase in the number of AMPA receptors
– increase in the current passing through each AMPA receptor
– increase in the number of synapses
Variety of mechanisms, dependent on developmental stage,
brain region, induction parameters
