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Week 8
Define neuroplasticity and outline its function and effects.
Definition: the physical and chemical change in the nervous system in response to changes in the external environment
Function:
Underlies Learning and Memory
Adaptation to the vast array of situations we find ourselves in – experience
Effects:
Can be good and bad
Effects can be local or widespread in the brain
Explain the signal cascade in neuroplasticity
Signal cascade:
Outside the body →Outside the CNS (e.g. muscle) → brain → back to outside the CNS
Outline what shapes the capacity and magnitude neuroplasticity
The capacity and magnitude shaped by:
Age (developmental stage)
Brain area
Past experience
Genetics
Outline whether neuroplasticity is unique to the brain and give two examples.
Not Unique to Neurons or the CNS:
Adaptation occurs in other systems of the body.
But unique to us as individuals
Muscle Adaptation:
Prolonged physical exercise increases muscle cell fibres—hypertrophy.
Differences between males and females are influenced by genetics (e.g., XY chromosome).
Skin Adaptation:
Exposure to the sun increases melanin production.
Response varies with prior sun exposure.
Age impacts melanin production.
Some individuals naturally have more melanin than others.
Outline the types of changes in the brain demonstrating neuroplasticty.
Neuronal Numbers:
Apoptosis (cell death, including in diseases).
Neurogenesis (creation of new neurons).
Axon:
Changes in number and length.
Synapse:
Changes in number and type.
Re-configuration of existing circuits.
Creation of new circuits.
Dependent on needs: some circuits/synapses aren’t being used anymore and can be removed
Outline the factors driving neuroplasticity
Driven By:
Experience-Dependent Changes:
Linked to neuronal activity.
Drug-Dependent Changes.
Developmental Program.
Disease or Injury.
Outline the results of neuroplasticity
Results In:
Subtle chemical changes at the synapse
Large-scale macrostructural changes detectable by MRI.
Transient or permanent irreversible changes, such as altered patterns of gene expression.
Outline an example of macrostructural brain changes in episodic memory.
Example: The spatial navigation of London Taxi drivers
Know all the roads in London (the Knowledge test)
Brain Changes:
Structural MRI showed increased grey matter in the anterior hippocampus (before taking the Knowledge test)
Outline an example of macrostructural brain changes in procedural memory.
Example: Learning a new skill, such as juggling
Brain changes:
Structural MRI showed increased grey matter in (before and after 3 months of training):
mid-temporal area
left posterior
intraparietal sulcus
Outline an example of microstructural brain changes from environmental enrichment.
Example: Improved environmental enrichment (e.g. increasing room to roam for mice—novelty) → better outcomes following a stroke
Brain changes → Increased:
Dendritic spines
Synapses per neuron
Expression of trophic factors
Altered cortical maps
Neurogenesis
Describe an example of microstructural brain changes from drug-induced neuroplasticity.
Behavioural Sensitisation:
Progressively greater behavioural response following repeated administration of psychostimulants.
Characterised by synaptic plasticity that builds on previous changes.
Sensitisation Pathways:
Involves the reward-seeking dopaminergic mesocorticolimbic system.
System projects to the nucleus accumbens and interacts with complex circuits.
Circuits involve the amygdala, hippocampus, and the bed nucleus of the stria terminalis.
Neurotransmitter Plasticity:
Plasticity occurs across various neurotransmitter pathways.
Includes activation or disinhibition of some pathways.
Includes inhibition or loss of activation in others.
Outline an example of macrostructural brain changes from childhood maltreatment.
Example: Physical and sexual abuse and neglect
Higher risk of post-traumatic stress disorder and major depressive disorder
Brain changes:
Decreased:
Surface areas and cortical thickness in frontotemporal regions.
Increased:
Cortical thickness in occipital regions and surface areas in frontal regions
Outline an example of microstructural brain changes in developmental neuroplasticity.
Late gestation – early adulthood characterised by:
Neuronal Loss: Apoptosis.
Axon Loss.
Net Synaptic Loss with some new synaptic connections.
Synaptic Processes:
Rearrangement: Synapses reorganize during development.
Segregation:
Dependent on neuronal activity.
Involves a "winner takes all" competition.
Driven by experience.
Convergence: Synaptic inputs combine into shared pathways.
Describe an example of microstructural and macrostructural brain changes from mindfulness.
Definition:
A type of meditation with beneficial effects on physical and mental health, and cognitive performance.
Enhanced Self-Regulation:
Improves attention control, emotion regulation, and self-awareness.
Brain Structure Changes:
Anterior Cingulate Cortex: Related to attention.
Posterior Cingulate Cortex & Prefrontal Cortex: Associated with self-awareness.
Fronto-Limbic Networks: Responsible for emotional control.
Mechanism:
Complex and not fully understood.
Involves dendritic branching, synaptogenesis, myelinogenesis, neurogenesis, autonomic regulation, and immune activity.
Promotes neuronal preservation, restoration, and/or inhibition of apoptosis.
Clinical Benefits:
Effective for reducing risks of:
School failure.
Attention deficit disorder.
Anxiety and depression.
Drug abuse.
State an overview of what chromosomes, DNA, and genes are and do.
DNA Structure:
Double helix with labelled 5' and 3' ends.
Base pairs: Adenine (A) pairs with Thymine (T), Cytosine (C) pairs with Guanine (G).
Nucleotide Components:
Composed of:
Phosphate group.
Sugar.
Nitrogenous base.
DNA and Chromosomes:
DNA wraps around histone proteins to form nucleosomes.
Microscopic visualisation shows DNA organised into chromosomes.
Key Facts:
Length: DNA, when unravelled, measures approximately 102 cm.
Nucleotides: Composed of around 6 × 10⁹ nucleotides.
Complexity: Representing the sequence would require about 1,000,000 pages of a typical book.
Describe the impact of genetics in variation between individuals.
Genetic Similarity:
Humans share 99.9% of their genetic makeup.
We are genetically more similar to biological parents and siblings than others in the population.
Complexity of Genetics:
Family members also share similar environments, influencing traits beyond genetics.
The remaining 0.1% genetic variation explains subtle differences in physical and behavioral traits, and can also play a role in diseases.
Genetic Variation:
A single nucleotide difference (genotype) can sometimes greatly affect traits.
In most cases, the impact of genetic variations is subtle and complex.
Combined Genetic Impact:
Hundreds of genotypes work together in combination to influence traits.
Outline an example of how genetics influences height.
Influence: Many SNPs in combination influence height (the difference between individuals’ height → 164 cm vs 183 cm)
Each SNP has a very small effect
Contribution:
20% of the variation in adult height explained by genetics
423 genes & 697 variants
Describe impact gene and environment interactions on variation between people.
Genetics and Environment Interaction:
Genetics alone doesn’t explain all variation between individuals.
Genetics and environment together make each person completely unique, including identical twins.
Environmental Contributions to Phenotypic Traits:
Total environmental variation responsible for a trait includes:
Specific Environmental Variance: Unique factors affecting an individual.
General Environmental Variance: Broader environmental influences.
Genotype by Environment Interaction: How genetic makeup interacts with environmental factors.
Outline an example of how the environment influences height.
Environment impacts:
Example: nutrition can have a large impact on height
Varies for the whole population or specific individuals
Environment and Genetics together:
Example: males may have a different diet –appetite, satiety, hormones, and metabolism.
State an example of how genetics influences on schizophrenia.
The closer the relation the higher the chance of schizophrenia.
State the importance of understanding genetic and environment contributions.
To better treat and prevent:
Anxiety and Depression
Childhood Stress
ADHD
Learning Difficulties
To better diagnose and stratify diseases
Describe the role of DNA methylation on epigenetics.
Methylation on CpG DNA Nucleotides:
Plays a crucial role in controlling synaptic scaling and glutamate receptor trafficking.
These processes are central to learning and memory formation.
Irreversibility:
Methylation is generally considered irreversible.
Evidence from Fear Conditioning:
After 24 hours of fear conditioning in rats:
Approximately 9.2% of genes in hippocampal neurons are differentially methylated.
This involves around 1,000 “C” residues in the DNA.
Outline methylation and acetylation of histone proteins in epigenetics.
Methylation (Me):
Affects the expression of genes involved in the structure and function of synapses.
Can lead to changes in:
Spine number.
Dendritic branching.
Behaviour (e.g., increased hypersensitive passive avoidance behaviour).
Irreversibility: Generally considered irreversible.
Acetylation (Ac):
Affects the expression of genes.
Reversibility: Generally considered reversible.
Outline the transgerenational effects of the environment.
Unique Memories:
Memories themselves are not inherited, but environmental influences can have transgenerational effects.
Environmental Exposure:
Exposure in one generation can impact subsequent generations.
Not all methylation patterns are stripped off during fertilisation
Examples:
Nutrition: Nutritional experiences can affect offspring.
Fear Conditioning: Learned responses to fear may be passed down.
Sex Differences:
Impacts can differ depending on whether the exposure originates from the mother or the father.
Transgenerational Effects:
Changes can:
Be transmitted across multiple generations.
Potentially skip generations before reappearing.
Outline neurotrophic factors in neuroplasticity
Stimulation: Active stimulation of a neuron→ increases BDNF
Growth factor: Brain derived neurotrophic factor (BDNF)
Impact: strengthened synapse and better neuronal survival
Outline the change in circuit activity in neuroplasticity.
Example: Fear conditioning in the Amygdala-vmPFC circuit
Unconditioned stimulus leads to fear response due to changes in inhibitory and excitatory inputs, after conditioning
Outline habituation in neuroplasticity
Stimulation: leads to less neurotransmitter release and a weaker onward response
Impact: synpase weakened
Outline the compensatory/ remapping neuroplasticity types.
Homologous area adaptation:
A particular cognitive process is taken up by a homologous region in the opposite hemisphere
Cross-modal reassignment:
Structures previously devoted to processing a particular kind of sensory input now accept input from a new sensory modality
Map expansion:
Enlargement of a functional brain region based on performance
Compensatory masquerade:
Novel allocation of a particular cognitive process to perform a task
Outline cross-modal plasticity in neuroplasticity
Compensatory Enhancement:
Often enhances functions related to the ability that is lost (e.g., improved hearing in blind individuals).
Unused Brain Region:
Deprived, unused brain regions are repurposed and taken over by other senses.
Supra-Modal Skills:
These are skills shared across senses (e.g., identifying a letter by feeling it in a bag of letters).
Developmental Window:
May occur within a limited developmental period.
Outline how recovery following a stroke works with neuroplasticity.
Complex Recovery Process:
Recovery operates within a window of opportunity.
Functional recovery rarely returns to pre-stroke levels.
8 Weeks Following Stroke:
Synaptic Refinement: Connections become more refined.
Improved Sensory Specificity: Sensory responses become more specific.
Neuronal Rewiring:
Some neurons are rewired to process information from damaged regions.
Rewired neurons become selective for sensory input.
Behavioural compensation
The restoration of performance through the use of modified or alternative response strategies, such as relying on the unimpaired limb or incorporating postural changes (for example, shoulder and trunk rotations) to perform motor tasks.
Homeostatic plasticity
Definition: A negative feedback-mediated form of plasticity, also known as synaptic scaling, that serves to keep network activity at a desired set point.
Importance: Homeostatic plasticity might be important after stroke for setting into motion pathways that restore synaptic activity.
Hebbian plasticity
A positive feedback-mediated form of plasticity in which synapses between presynaptic and postsynaptic neurons that are coincidently active are strengthened. Hebbian plasticity might be important after stroke for strengthening and retaining properly wired connections.
Ipsilateral pathways
Pathways that are present in the brain hemisphere or spinal cord on the same side as the body part to which they connect.
Motor engram
A putative memory trace for a motor action or movement.
Plasticity
Changes in the strength of synaptic connections in response to either an environmental stimulus or an alteration in synaptic activity in a network.
Remapping
The transfer of incoming sensory or motor output signals from one cortical region to another. This might not necessarily involve new structural circuits.
Representation
An area of cortex dedicated to processing a sensation from a particular body part
Rewiring
Changes to the structure of neuronal axons or dendrites that might affect neuronal function
Note 
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