Neuroplasticity and Habituation Quiz

Neuroplasticity

• Neuroplasticity is the brain's ability to reorganize itself in structure and function.
• This reorganization is continuous and influenced by experiences.
• Neurogenesis is the continuous generation of new neurons in certain brain regions.
• New synapses are created with new skills and experiences.
• Existing synapses are strengthened with repetition and practice.
• Synapses that are unused weaken.

Habituation

• Habituation is a simple form of neuroplasticity.
• It's a decrease in response to a repeated, harmless stimulus.
• This response returns to normal after a period of rest.
• Habituation is short-term, reversible, and caused by a decrease in synaptic effectiveness.
• Reduced excitatory neurotransmitters and less free intracellular calcium contribute to habituation.

Experience-Dependent Plasticity

• Experience-dependent plasticity involves persistent long-term changes.
• These changes occur between the strength of synapses or within neural networks.
• fMRI studies show large regions of activation during learning, which become smaller with skill proficiency.
• Protein synthesis, new synapse growth, synapse modification are required for this phenomenon.
• Repeated stimulus pairing between presynaptic and postsynaptic neurons alters excitability and potentially affects the number of synapses, mainly seen in dendritic spines.

Experience-Dependent Plasticity: Long-Term Potentiation (LTP)/Long-Term Depression (LTD)

• Long-term potentiation (LTP) occurs at excitatory glutaminergic synapses.
• LTP can occur presynaptically (changes in neurotransmitter release) or postsynaptically (receptor density or efficiency changes).
• Extensive hippocampus and cortex studies have been conducted to observe LTP.
• Transcranial magnetic stimulation can manipulate synaptic plasticity.
• Astrocytes and gliotransmitters play a particularly noticeable role in impacting the postsynaptic membrane.
• Long-term depression (LTD) involves the removal of AMPA receptors from the membrane into the cytoplasm, causing the synapse to become silent.

Synaptic Changes Following Axonal Injury

• Synaptic changes include changes in synaptic effectiveness, denervation hypersensitivity, synaptic hypereffectiveness, and the unmasking of silent synapses.

Metabolic Effects of Neuronal Damage

• Oxygen deprivation leads neurons to release glutamate.
• Glutamate activates NMDA receptors, causing a rush of calcium into neurons.
• Potassium diffuses out during this process.
• The sodium-potassium pump needs to work harder during this.
• Lactic acid build-up can damage the cell membrane.
• High intracellular calcium triggers protease release.
• Arachidonic acid generates inflammation and free radicals.
• Water influx causes cell edema.

Excitotoxicity

• Excitotoxicity is cell death caused by overexcitation of neurons.
• It's observed after stroke, TBI, and neurodegenerative diseases.
• Increased lactic acid-acidosis can degrade cell membranes.
• High levels of intracellular calcium trigger protease release.
• Arachidonic acid promotes inflammation and free radical production.
• Water influx causes cell swelling.
• Pharmacological blocking of NMDA receptors and the IP3 pathway are potential treatments.

Functional Reorganization of Cortex

• Neurons can reassign their function.
• This process is observed in adults after CNS injury.
• In some cases, areas of the brain that were assigned for one function will change and take on a different function.
• Studies have shown that individuals with specific variants in the BDNF gene experience worse outcomes after CNS injuries.

Clinical Approaches

• Rehabilitative exercises can stimulate neurotransmitter release.
• Gene therapy can be potentially used for nerve cell regeneration.
• In one instance, stem cells can migrate to injury areas and promote the survival of injured brain cells.

Peripheral Nerve Regeneration

• Neuronal survival and growth promoting molecules like NGF contribute to regeneration.
• Signal integration at the growth cone is key.
• Neuron damage can possibly block neuroma formation and long distance regeneration

Wallerian Degeneration

• Axonal injury causes segment retraction.
• Distal axon terminal degeneration occurs.
• Myelin breakdown is common.
• Glial cells clear the debris.
• The proximal segment of the axon experiences significant changes, including loss of Nissl substance, eccentric nucleus, and chromatolysis.
• Presynaptic terminals retract and postsynaptic cells degenerate.

Axonal Sprouting

• Axons in the peripheral nervous system (PNS) can regenerate through sprouting.
• Collateral and regenerative axonal sprouting are observed.
• Schwann cells play a guiding role in this pathway.
• Bungner bands and NGF promote axonal growth.

Timing of CIMT (Constraint-Induced Movement Therapy)

• Intervention timing is crucial following brain injury.
• Treatment is most effective when started between 1 and 7 days or 1 to 15 days post-injury.

Plasticity in Somatosensory Cortex

• Areas of the somatosensory cortex respond to different body parts.
• Sensory input changes in this area.
• Changes cause specific skin surfaces to be represented in different areas in the brain after injury.
• There is plasticity between cortical regions after injury.

Ocular Dominance Columns

• Visual experiences impact the growth of these columns.

Test your understanding of neuroplasticity, including its mechanisms and types, such as habituation and experience-dependent plasticity. This quiz will cover the brain's ability to adapt through reorganization and the development of new neurons. Dive in to enhance your knowledge of these fascinating processes!