Memory Systems Flashcards
Two ways that memory is classified?
- Based on Consciousness:
- Based on Processing mode
- Based on consciousness
- declarative memory
- episodic and
- semantic)
- Non-declarative memory (
- Procedural memory;
- Priming;
- Simple Classical Conditioning;
- Habituation sensitization)
- declarative memory
- Based on processing mode
- Rapid encoding of flexible association
- Slow encoding of rigid associations
- Rapid encoding of single or unitized items
Two ways that memory is classified?
- Based on Consciousness:
- Based on Processing mode
- Based on consciousness
- declarative memory
- episodic and
- semantic
- Non-declarative memory
- Procedural memory
- Priming
- Simple Classical Conditioning
- Habituation sensitization
- declarative memory
- Based on processing mode
- Rapid encoding of flexible association
- Slow encoding of rigid associations
- Rapid encoding of single or unitized items
Pre-frontal cortex encodes ________ memory
Pre-frontal cortex encodes short-term, working memory
- In Each, list the part(s) of the brain responsible
- declarative memory
- episodic
- semantic
- Non-declarative memory
- Procedural memory
- Priming
- Simple Classical Conditioning
- Habituation sensitization
- declarative memory
- In Each, list the part(s) of the brain responsible
- declarative memory
- episodic
- Medial temporal lobe, diencephalon
- semantic
- Medial Temporal Lobe
- episodic
- Non-declarative memory
- Procedural memory
- Basal ganglia
- Priming
- Neocortex
- Simple Classical Conditioning
- Amygdala, cerebellum
- Habituation sensitization
- Reflex pathways
- Procedural memory
- declarative memory
What is the circuitry within the hippocampus
Old memories become independent of the _____ and rely primarily on ______ for their retrieval
Old memories become independent of the MTH (Medial Temporal Hippocampal) system and rely primarily on neocortical activity for their retrieval
Define neuronal plasticity
Enduring change in the functioning of a neuronal network in response to use, or associated with recovery from injury
What are five mechanisms of neuronal plasticity
- Altered strength of existing synapses
- Formation of new synapses
- Changes of cellular properties of nerve cells
- Neurogenesis in select brain regions
- changes in glia and myelinated pathways (g)
How is hippocampal slice preparation done for studies of synaptic plasticity
Stimulate region in the hippocampus and record in the CA1 area
What are the 4 types of LTP properties as shown in the image?
-
Normal synaptic transmission = no LTP
- single AP in one or a few axons (weak input) leads to a small EPSP that is insufficient to expel Mg++ from NMDA glutamate Receptor-channels and thus cannot induce LTP
-
Cooperativity
- near-simultaneous activation of of several weak inputs during strong activation
- produces suprathreshold EPSP that triggers AP firing and results in LTP in all pathways
-
Associativity
- Stimulation of strong and weak inputs together
- causes LTP in both pathways
- in this way a weak input becomes significant when paired with a strong one
-
Synapse Specificity
- An unstimulated synapse does not undergo LTP in spite of the strong stimulation of neighboring synapses
- ensures that memories are selectively formed at active synapses
- An unstimulated synapse does not undergo LTP in spite of the strong stimulation of neighboring synapses
Define LTP cooperativity
-
Cooperativity
- near-simultaneous activation of of several weak inputs during strong activation
- produces suprathreshold EPSP that triggers AP firing and results in LTP in all pathways
Define Associativity (LTP Property)
Associativity
- Stimulation of strong and weak inputs together
- causes LTP in both pathways
- in this way a weak input becomes significant when paired with a strong one
Define Synapse specificity in the context of LTP
-
Synapse Specificity
- An unstimulated synapse does not undergo LTP in spite of the strong stimulation of neighboring synapses
- ensures that memories are selectively formed at active synapses
- An unstimulated synapse does not undergo LTP in spite of the strong stimulation of neighboring synapses
Define Normal Synaptic Transmission and it’s involvement in LTP
-
Normal synaptic transmission = no LTP
- single AP in one or a few axons (weak input) leads to a small EPSP that is insufficient to expel Mg++ from NMDA glutamate Receptor-channels and thus cannot induce LTP
What is a Hebbian Synapse?
Hebb suggested: “when an axon of cell A is near enough to excite cell B or repeatedly or consistently takes part in firing it, some growth or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased”
– Cells that fire together wire together
What is important about the NMDA receptor channel conduction?
The NMDA receptor channel conducts only when Pre and Post fire together
- Presynaptic activity releases glutamate
- Postsynaptic depol unblocks NMDAR (removes Mg++ block)
What is the cellular mechanism for Early-LTP?
NMDAR channel opens upon glutamate binding and Mg++ unblocking
Ca++ enters through the NMDAR and binds to Calmodulin to activated Cam Kinase II (CaMKII) - which autophosphorylates itself to maintain its own activity even in the absence of Ca++
results in AMPAR insertion at the synaptic membrane
↑AMPA = ↑LTP
What happens in spatial learning when a NMDA receptor antagonist (DL-AP5) is applied?
- In water maze learning, mice that received DL-AP5 showed no preference for any quadrant. This is impaired memory
- LTP in the hippocampus was blocked
CaMKII can ______ to maintain activation in absence of calcium
CaMKII can autophosphorylate itself to maintain activation in absence of calcium
Molecular memory
PKA activation involves release of _______
PKA activation involves release of catalytic subunits
- Four main subtypes of regulatory subunits
- C-alpha catalytic subunit shown
PKA mutant mice have revealed diverse functions for PKA:
- RIalpha knockout =
- RII-alpha knockout =
- C-alpha knockout
- RI-beta knockout =
- RII-beta knockout =
PKA mutant mice have revealed diverse functions for PKA:
- RI-alpha knockout = embryonic lethel, defective cardiogenesis
- RII-alpha knockout = no gross organ dysfunction; altered plasticity of ocular dominance
- C-alpha knockout = Neonatal lethality or growth retardation and defects in sperm motility
- RI-beta knockout = Defects in hippocampal function, pain nociception and plasticity of ocular dominance
- RII-beta knockout = lean phenotype
Total knockout of PKA is difficult and would be lethal
What is the pathway for early LTP?
increase Calcium → activation of CaMKII → protein phosphorylation → … → increase AMPAR (E-LTP)
Pathway for L-LTP
increase Calcium → activation of PKA → … → gene expression → structural changes + ↑AMPAR (L-LTP)
Mechanisms of long-term depression
small ↑ Ca++ → activation of phosphatase → protein dephosphorylation → ↓AMPAR
Fill in the chart of general LTP Mechanisms
See image
