NERVOUS SYSTEM: HEBBIAN AND SYNAPTIC PLASTICITY Flashcards
define: synaptic plasticity
Synaptic plasticity: synapses can be modified to strengthen or weaken their connections and communications between them
State Hebb’s rule
Hebb’s rule: neurons that fire together are wired together; Outlines the basic principle that learning and memory can occur due to changes in the strength of connections between neurons
State the 2 physiological mechanisms for Hebbian principles
2 physiological mechanisms for Hebbian principles:
1. Long-term potentiation (LTP)
2. Long-term depression (LTD)
Define: homeostatic plasticity
Homeostatic plasticity: moves neurons back to their original state (set point) after modification of input
Define: facilitation/potentiation
in the presynaptic neuron, if the # of stimulation/s increases, EPSPs size increases
Define: synaptic depression
reduction in size of stimulation/s and EPSP size
Describe the trisynaptic circuit in the hippocampus; what is the hippocampus important for?
Input from entorhinal cortex → granule cell → granule cell input → CA3 → CA3 input → CA1
Important for making new memories
Define: long term potentiation
repetitive activation of an afferent pathway to the hippocampus or an intrinsic connecting increases the response of pyramidal cells; this can last for hours, days, or weeks depending on the system
Involves the modification of presynaptic and postsynaptic events
When stimulated at low frequency, EPSPs amplitude stays constant.
- When stimulated at high frequency for a short period of time, EPSPs after the period of high stimulation has a higher amplitude but slowly returns to baseline.
can operate through intracellular Ca2+ signalling; often dependent on glutaminergic receptors (AMPA/NMDA) and indicates structural changes in the postsynaptic terminal
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What are 2 theories for why LTP occur?
What are some theories for why LTP occur?
- Presynaptic neuron is releasing more neurotransmitter
- Or; same neurotransmitter release but more post-synaptic receptors (the most favoured theory)
Describe postsynaptic events that lead to an Increase in AMPAR during LTP
LTP: With much stronger depolarization, you will get more release of glutamate and a large depolarization. Mg2+ is removed from NMDA which allows for Na+, K+ and Ca2+ flux. Ca2+ influx through NMDA activates intracellular CaMKII pathway which causes AMPAR phosphorylation and insertion of more AMPA receptors in postsynaptic membrane from vesicles
For AMPA
- give full name
- give receptor type
- what is it permeable to?
- describe what kind of current it has at negative mV and at positive mV
- a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid
- glutamate receptor
- Permeable to Na+ and K+
- Inward current at negative mV, positive current at positive mV
For NMDA
- give full name
- give receptor type
- what blocks it? how can it be unblocked
- what is it permeable to?
- describe what kind of current it has at negative mV and at positive mV
- N-methyl-D-aspartate
- glutamate receptor
- At resting membrane potential, NMDA receptor is blocked by Mg2+; Depolarization dispels Mg2+
- Permeable to Na+, K+ and Ca2+
- at negative mV, no current until Mg2+ is dispelled which occurs at -60 mV. inward current until at positive mV then it is an outward current
Describe postsynaptic events that lead to an decrease in AMPAR during LTD
LTD: With weak depolarization, you have short term decreases in EPSPS caused by inactivation of Cav channels or depletion of neurotransmitter-containing vesicles. This results in the
activation of phosphatases (protein phosphatase 1 - PP1 and calcineurin) that act on AMPA which results in the internalization of AMPA receptors
What will bilateral loss of hippocampi result in?
anterograde amnesia - inability to form new memories
Describe the 4 major structures that form the neural circuit inthe hippocampus
- CA1: major output goes to layer V of the entorhinal cortex (EC)
- CA3: receives input from the dentate gyrus (DG) and from the EC
- DG - dentate gyrus : projects to CA3 and receives input from the EC
- EC - entorhinal cortex (MTL): an interface between the hippocampus and the cortex