synaptic plasticity Flashcards
synaptic plasticity
an increase or decrease in the ability of a presynaptic cell to influence the membrane potential of a post-synaptic cell
two classes of synaptic plasticity
short term (less than 30 mins) - usually mediated by the amount of neurotransmitters released presynaptically
long term - (45-60 mins) - mediated largely by receptor insertion and gene expression
synaptic facilitation
the increase in PSP amplitude that occurs when presynaptic action potentials occur within a short interval following previous action potentials
- occurs bc the calcium sequestering mechanisms have not fully reduced calcium levels evoked by the first action potential when the second action potential occurs; the result is an increase in calcium conc, which causes the release of more vesicles leading to increased postsynaptic receptor activation
synaptic depression
the decrease in PSP amplitude that occurs when many presynaptic action potentials occur within a short interval
- during repeated high-frequency stimulation, the pool of vesicles available for exocytosis is reduced, leading to reduced neurotransmitter release and reduced PSP amplitude
synaptic augmentation/potentiation
enhancement of PSP for a few seconds after tetanic (repetitive train of pulses) stimulation
- due to the enhanced ability of incoming calcium to cause vesicle fusion, but the molecular mechanism is poorly understood
habituation
subsequent light touches to the siphon tube cause a reduced withdraw
- brain mainly cares about differences
sensitization
electrical shock paired with light touch to the siphon tube causes increased gill retraction that lasts for many days
mechanism of short sensitization
- 5-HT is released by the interneuron and activates G-protein coupled receptors
- cAMP is produced
- PKA activated
- PKA catalytic subunits released causing phosphorylation of several proteins including K+ receptors (reducing opening time)
- allows additional ca2+ influx during action potential
- causes increased vesicle exocytosis
mechanism of long sensitization
- 5-HT is released by the interneuron and activates g-protein coupled receptors
- cAMP is produced
- PKA activated
- repeated stimulation causes PKA to activate CREB, which causes gene transcription
- ubiquitin hydroxylase degrades the regulatory proteins of PKA causing persistent presence of the catalytic subunits - PKA phosphorylates K+ channels
- increases Ca2+ influx during action potentials
- increased neurotransmitter release
long-term potentiation
long-term strengthening of synaptic transmission
important for info storage (memory)
1. input selectivity - only inputs that were previously active are potentiated
2. state dependence - on post-synaptic neuron activity (only occurs when postsynaptic neuron is depolarized)
3. associativity - btw simultaneously active inputs
why does the postsynaptic cell need to be depolarized for an LTP to occur?
- Ca2+ influx is critical for triggering mechanisms to induce LTP
- Ca2+ flows through NMDA channels
- NMDA channels do not conduct cations at hyperpolarized potentials bc of the Mg2+ blockade
- the postsynaptic membrane must be depolarized via AMPA receptors to remove the Mg2+ blockade and allow Ca2+ influx
- AMPA currents are very brief and therefore multiple presynaptic APs are needed to evoke EPSPs that temporally summate
molecular mechanisms involved in the initial phase of LTP
- large influxes of Ca2+ activate CaMKII and PKC
- new AMPA receptors are inserted into the postsynaptic density
- increased receptor density leads to increased evoked postsynaptic currents and potentials
how do we know it is Ca2+ dependent?
- blocking Ca2+ with chelators eliminates LTP
- enhancing Ca2+ enhances LTP
- activating NMDA directly induces LTP
silent synapses
some synapses do not generate a PSP when the postsynaptic cell is at rest, but do generate EPSPs at depolarized potentials
- this indicates that NMDA (but not AMPA) receptors are present at the synapse (Mg2+ is only removed at the depolarized potential)
late phase of LTP
depends of gene transcription
- inhibiting protein synthesis blocks LTP
Ca2+ -> cAMP -> PKA -> CREB -> proteins
- gene transcription can produce new dendritic spines
