Synaptic plasticity and Glia

Short vs long term plasticity

Short changes amount of NT released from the postsynaptic neuron, in response to stimulation from pre

Long causes changes in sensitivity to glutamate that last for days - molecular changes

Forms of short term plasticity

Facilitation - repeated stimulation causes Ca to accumulate, increasing NT release

Depression - NT stores are depleted throughout stimulation

Augmentation - if extracellular Ca is low, sensitivity to Ca will increase for seconds, to enhance NT release. Still less NT released, so decays slower than depression

Potentiation - following tetanic stimulation, sensitivity to Ca increases, so one stim causes more NT release

Long term plasticity

Sensitisation - increases response, and habituation - decreases response

Mechanism of sensitisation: changes pre-synaptic sensory neuron activity, to increase motor neuron response

Interneuron recieves input from other sensory neuron, synapses to sensory neuron, releases serotonin, activates G-protein coupled serotonin receptors, activates adenylyl cyclase, cAMP, protein kinase A, closes K+ channels. Greater depolarisation of sensory neuron.

How sensitisation leads to LTP

repeated activation of kinase A activates transcription factor CREB, synaptic growth, persistent increase in EPSP

Mechanism of LTP (long-term synaptic plasticity causing lasting increase in synaptic strength) in post-synaptic neuron

AMPA receptors receive glutamate, depolarise, NMDA receptors open, receive glutamate, influx of Ca, activates protein kinases, insert more AMPA receptors

Long-term LTP changes

Protein kinases activate cAMP, protein kinase A, activates CREB, synaptic growth, new dendritic spine heads

Process of LTD (due to prolonged low-intensity stim)

NMDA receptors open, slow increase in Ca activates calcium-dependent phosphatases, which inactive proteins inhibiting LTD, AMPA removed

Spike timing

Timing of presynaptic membrane depolarisation and stimulation of post-synaptic neuron

Passive vs active functions

passive in response to neuron activity, active regulates neuron activity

Potassium siphoning

Removes K after depolarisation efflux. Without potassium transporters, water diffuses into synapse, causing oedema

NT recycling

Converts glutamate and GABA to glutamine, returned to neurons for synthesis

Calcium waves

Increase in Ca conc in glia spreads across glia, causes release of glial transmitters (ATP - inhibits neurons). Occurs in response to injury

Astrocyte blood vessels

Calcium waves cause vasoconstriction: astrocytes wrap blood vessels and synapses, monitor activity

Microglia blood vessels

Neurons release fractalkine, microglia produce calcium wave and perform vasoconstriction