Module 3, lecture 1 Flashcards
what is synaptic plasticity and 2 types
synapses can undergo structural and functional changes that strengthen or weaken synaptic transmission
electrical and chemical synapses
Different types of plasticity are based on
- identity (and structure) of the synapse (are different)
-time course (how long changes in the synaptic strength last)
-underlying mechanism (how these synaptic mechanisms last)
-contributing factor - if activity - activity dependent plasticity (plasticity occurs as a result of experience, in terms of activity
2 facts about synpases
- Synaptic connections are dynamic! (flexible)
- Synapses can keep track of the history of activity (overtime)
Synaptic Plasticity (activity Dependent) - Forms:
Short Term
last few minutes or less, affect NT release
Depression (synaptic depression, decrease of NT release)
Facilitation (synaptic enhancement - eg.sensitization, enhancement of NT release)
Potentiation (synaptic enhancement - eg.sensitization, enhancement of NT release)
Augmentation (synaptic enhancement - eg.sensitization, enhancement of NT release)
Synaptic Plasticity (activity Dependent) - Forms:
Long Term
lasts 30 mins or longer, changes in NT Rs and/or synapse structure
- Long-Term potentiation
- Long-term depression
Heterogeneity of vesicles:
- Storage + recycling pool (RP)
- Readily releasable pool (RRP) : active zone, prime at membrane, replenished.
Synaptic Depression
-a decline in NT release during sustained synaptic activity
-inversely proportional to the amount of NT readily available for release (vesicle depletion H)
- decline occurs until readily available vesicle pool is replenished (RRP)
- Recovery can be accelerated by increasing presynaptic Ca2+
-duration ms or s
Ex: first AP, 10 vesicles fused, 7 out of 10 released. Replenishment is slow. Second AP: vesicle fusion occurs but only 3 vesicles are left to fuse and less NT is released.
- Changes happen in presynaptic neuron (before vesicle fusion), measure changes in postsynaptic neuron
- Most NT release with first AP = higher chance of depression w/2nd Nt release
Synaptic Facilitation
-repeated stimulation (2 or more APs) at short time intervals leads to transient increase in NT release probability
- increased NT release as a result of residual Ca2+ leftover in the presynaptic terminal
➔ enhancement of synaptic transmission - Lasts ms-s (same as depression)
- More Ca2+ causes more vesicle fusion, more NT release, higher post-synaptic response
Post-tetanus Potentiation (PTP)
- Sustained, high frequency activation -> increased Ca2+ entry -> increased vesicle fusion and NT release
- Lasts seconds-minutes
-May be mediated by activation of Ks and synapsin
-Inc in EPSP lasts long time
-Calcium influx, release machinery
Synaptic Augmentation
-Sustained, high frequency activation -> increased Ca2+ entry -> increased vesicle fusion and NT release
-Lasts 5-10 seconds
-May be mediated by regulation of Munc13
(SNARE-regulatory protein)
-Calcium influx, release machinery
Short-term Plasticity – Interaction at the NMJ
Interaction and contribution of each may vary at each synapse
E.g. At NMJ: repeated synaptic activity -> Ca2+ accumulation in the presynaptic terminal (sequences can happen any any given terminal)-> facilitation and then augmentation to enhance synaptic activity.
Non-associative learning
-A change in the strength of the response to a single stimulus that occurs with repeated exposure to the stimulus
-It occurs in all animals and involves sensory motor pathways
-The simplest form of learning
-Two types: Habituation, Sensitization
Plasticity of the Aplysia gill withdrawal reflex: Habituation
Decreased response with repeated (or prolonged) exposure to the same (non-harmful) stimulus. Happens overtime.
Plasticity of the Aplysia gill withdrawal reflex: Sensitization
Increased (generalized) response to stimuli after exposure to an intense (or noxious) stimulus. If you touch it again, it will respond as if it never habituated.
Synaptic mechanisms underlying plasticity of the Aplysia gill withdrawal reflex: Habituation
Depression of Glu release between sensory and motor neurons
Synaptic mechanisms underlying plasticity of the Aplysia gill withdrawal reflex
Sensitization
5-HT causes increase in cAMP (activates PKA) and PKA-dep enhancement of Glu release from sensory presynaptic terminals (K+ -P →↓K+ opening → prolonged AP → ↑pre- synaptic Ca2+)
more depol. More Ca2+ influx = more NT
Sensitization of the Aplysia gill withdrawal reflex:
Short-term/early-phase
– 5-HT causes cAMP and PKA-dep enhancement of Glu release from sensory terminals (↓K+ opening → prolonged AP → ↑pre- synaptic Ca2+)
- Can last 1 h.
No changes in protein synthesis, 1 shock
Sensitization of the Aplysia gill withdrawal reflex:
Long-term/late-phase
Long-lasting changes via:
- CREB-dependent and C-EBP- dependent gene expression
→ synthesis of proteins required to modify existing
Synapse. Changes in protein synthesis
- Can last days or weeks
Specific protocol of shocks (>1), inc in number of shocks
