Therefore, the concentrations of extra-cellular glutamate (and other cations) and the quantity of post-synaptic AMPA receptors are directly correlated to a neurons' action potential firing rate.
Ibata and colleagues studied local AMPA receptor scaling mechanisms by imaging post-synaptic trans-membrane GluR2 subunits using pharmaceutical manipulations over a time period of 4 hours.
Intra-cellular electrophysiology recordings were conducted to verify whether increase in quantity of post-synaptic AMPA receptors equated to up-regulation of synaptic connection strength.
Intracellular recordings show robust increase in mEPSC amplitude (approximately 130% above control values) following 4–5 hours of TTX treatment.
This form of synaptic scaling takes place over a time period of days and has a more pronounced effect on the overall firing rate of neurons than local AMPA receptor trafficking.
A long-term, concurrent confocal microscopy and electrophysiology investigation conducted on cortical rat in-vitro neural networks (age > 3 weeks in-vitro) growing on Multi Electrode Arrays examined the correlation between network activity levels and changes in the sizes of individual synapses.
In the first set, synapse-morphology and spontaneous neural activity were monitored for about 90 hours (i.e. no external stimuli or pharmaceutical manipulations were used to perturb the neuronal networks).
[9]Presynaptic homeostatic plasticity involves: 1) Size and frequency of pre-synaptic neurotransmitter release (for example modulation of mEPSC).
Long-term potentiation (LTP) mechanisms are driven by related pre-synaptic and post-synaptic neuron firings; with the help of homeostatic plasticity, LTPs and LTDs create and maintain the precise synaptic weights in the neural network.
Persisting correlated neural activity—without a homeostatic feedback loop—causes LTP mechanisms to continually up regulate synaptic connection strengths.
Unspecified strengthening of synaptic weights causes neural activity to become unstable to the point that insignificant stimulatory perturbations can trigger chaotic, synchronous network-wide firing known as bursts.