Unit 25 Flashcards
Chronic traumatic encephalopathy
A progressive degenerative disease following multiple concussions
Levels of analysis of plasticity
Behavior, neural imaging, cortical maps, physiology, synaptic organization, mitotic activity, molecular structure
Focal hand dystonia
Loss of motor control of one or more digits due to fusion of digit motor maps. After repetitive, synchronous movements
Two methods of studying plasticity through physiology
Long term potentiation and kindling
Kindling
Development of persistent seizure activity after repeated exposure to a sub convulsant stimulus. Like LTP. Involves production of neurotrophic growth factors
Studying plasticity through synaptic organization
Using Golgi type stains to show dendritic arborization and using electron microscope’s to inspect synapse number and size. Requires post Mortem tissue.
Mitotic activity of olfactory bulbs cells
Stem cell mitosis along walls of lateral ventricles in sub ventricular zone. Migrate along rostral migratory Stream
Location of precursor cells in the hippocampus
Located between granule cell layer and the hilus
Gene chip arrays
Miniature grid exposed to neural tissue. Particular genes present in the tissue react with a substance at various locations on the chip. Detect epigenetic changes following life experiences
Experience expectant plasticity
Occurs during development. Certain brain systems require specific types of experience to develop. E.g. ocular dominance columns
Experience dependent plasticity
Brain changes in response to experiences throughout the lifetime. E.g. problem-solving, response to drugs,
Meta-plasticity
The attempt to determine how the experiences of a lifetime interact
Series of events following ischaemia
Changes in pH and properties of cell membrane. Causes massive release of glutamate an opening of calcium channels. Influx of calcium instigates second messenger pathways, resulting in mRNA stimulation, protein production. Inflammation, swelling, diaschisis
Neuroprotectant drugs
Can block calcium channels, prevent ionic imbalance, reduce swelling, or enhance metabolic activity.
Stages of recovery from motor cortex damage
Return of reflexes, development of rigidity, grasping facilitated by other movements, development of voluntary grasping. Sequential from shoulder to hand. First flexor, then extensor.