Consolidation, Plasticity and LTP Flashcards
1
Q
Synaptic plasticity
A
- The ability of synapses to change as a result of experience
2
Q
Hebbian learning
A
- The principle that learning involves strengthening the connections of coactive neurons
- Can also enhance the ability to recognize stimuli (incomplete version of stimulus activates still the whole network)
-> Neurons that fire wire together: Neurons that often fire together become better connected in a sense that when neuron A fires Neuron B is more likely to fire too.
3
Q
Long-term potentiation
A
- A process in which synaptic transmission becomes more effective as a result of recent activity
- When a synapse has NMDA and AMPA receptors, the NMDA receptors are blocked by Mg2+ blocks which are removed when the AMPA receptors already depolarized the cell.
4
Q
Protein kinase
A
- can change the properties of many protein molecules (PKA, PKC, Cam kinase, TK)
- Blockage of these kinases can prevent the induction of LTP
5
Q
Cam kinase
A
- remains activated once it is put into a state by CA2+even if the level of CA2+ subsequently falls
- Could play a role in maintaining LTP
- It also enhances influx of NA+ and K+ ions and increase the number of AMPA receptors
6
Q
Immediate early genes (IEG)
A
- a class of genes that are rapidly but transiently expressed in response to extracellular signals such as neurotransmitters and growth factors
- Many IEGs code for transcription factors that govern the growth and differentiation of cell types by regulating the expression of other genes.
7
Q
IEG and LG
A
- these IEGs in turn produce other RNAs and Proteins
-> These protein trigger the activation of so-called ‘Late Genes’ (LGs)
-> Late genes produce the RNAs and in the end the proteins that contribute to the structural changes in the neuron that can support long-lasting changes in synaptic efficiency (more receptors), or even the building of entirely new synapses from scratch.
8
Q
Long-term depression
A
- A process by which synaptic transmission becomes less effective as a result of recent activity
-> Requires the entry of Ca2+ through NDMA receptors
-> A large surge of Ca2+ in the postsynaptic neuron triggers the induction of LTP by activating Ca2+—dependent protein kinases. In contrast, small increases of postsynaptic Ca2+ induce LTD by selectively activating the opposite kind of enzyme
9
Q
Hebbian synapses
A
- a kind of hippocampal synapses which show kinds of conditional changes that could mediate aspects of associative learning
10
Q
Cell assamblies
A
- Large groups of cells that tend to be active at the same time because they had been activated simultaneously or in close succession in the past
11
Q
Physiological changes at synapses may store memory
A
- Greater release of neurotransmitter or the receptors become more numerous or more sensitive
12
Q
Structural changes at synapses my provide long-term storage
A
- new synapses can be formed or eliminated as a function of training, could also lead to rearrangement of synaptic connections (taking over endings from less used competitor)
-> neurons that fire to the same spot tend to get connected and fire together
13
Q
dual trace theory
A
- Learning experience sets up activity that tends to reverberate through the activated neural circuits. This activity holds the memory for a short period. If sufficient, the activity helps build up a stable change in the nervous system a long-lasting memory trace
14
Q
Enriched experiences
A
- Enriched experience has beneficial effects on brain anatomy
-> Develops new synapses and more elaborate information-processing circuits (20% more)
-> Length of synapses gets bigger too
15
Q
Filopodia
A
- fine extensions from the axon that are promoted by electrical activity. They only occur In development
-> They may become dendritic spines if they make contact with an axon
16
Q
CA1 and tactile stimuli
A
- rats with hippocampal damage are hyperactive in new environments
- resistante to extinction
- poor spatial task
- animal was restrained and pushed counterclockwise: hippocampus provides brain with spatial reference map, activity of cells specify direction
17
Q
genes and long-term placticity
A
- dogma of molecular biology: DNA - RNA - protein - permanent
- gene expression leads to neuronal modifications under coactivation
18
Q
sleep and memory consolidation
A
- during SWS, hippocampus produces specific activity that activates cortex
- neurons connected to it also get activated
- over time hippocampus establishes cortical network leading to LTM
19
Q
roles of NMDA and AMPA receptors in induction of LTP in CA1 region
A
- AMPA receptors: glutamate antagonist, first actived
- NMDA: selective ligant, enough AMPA receptors need to be stimulated first, neuron needs to be partially depolarized
20
Q
cerebral changes resulting from training
A
- changes in neurochemistry and neuroanatomy of a rodent’s brain
- three conditions: standard condition (SC), impoverished condition (IC), enriched condition (EC)
- EC greater activity of enzyme AchE than IC
- different weight of cortical samples: EC greater cortical thickness, especially occipital and somesthetic cortex
- EC: promotes learning, expression of genes, compensatory for diseases, new synaptic connections, growth of dendritic spines (number increased in EC, most basal dendrites)
- experiment of formal training
21
Q
kinds of neural circuits underlying memory
A
- neural chain: monosynaptic reflex arc, some learning, intrinsic changes
- superordinate circuits: modulatory circuits, no change during training
- cell assembly: complex network, show changes, depends on plasticity
22
Q
Neuromodulators
A
- adjust the message
- alter/modulate how neurons interact
- decline leads to Parkinson (dopamine) or Alzheimer (acetylcholine)
