Activity-dependent scaling of quantal amplitude in neocortical neurons

In the citing paper

“There is compelling evidence from experiments in neuronal cultures that central neurons are able to maintain average firing rates around a homeostatic set point.”

In the citing paper

“One such mechanism is synaptic scaling, which allows neurons to detect changes in their own firing rates through a set of calcium-dependent sensors that then regulate receptor trafficking to increase or decrease the accumulation of glutamate receptors at synaptic sites.”

In the citing paper

“When cortical or hippocampal neurons are induced to fire more than normal, over many hours firing returns to baseline levels, and similarly, if neuronal firing is reduced over time, neurons compensate and again firing is restored (Fig. 1A) (Turrigiano et al. 1998;Burrone et al. 2002).”

In the citing paper

“Synaptic scaling was first identified in cultured neocortical neurons, where it was observed that perturbing network activity generated compensatory changes in synaptic strength that were in the right direction to restore average firing rates to baseline values (Turrigiano et al. 1998).”

In the citing paper

“by measuring minis arising from many synapses onto the same neuron, it was observed that modulating network activity induced uniform increases or decreases in the entire mini amplitude distribution, in effect scaling postsynaptic strength up or down (Turrigiano et al. 1998;Desai et al. 2002;Gainey et al. 2009).”

In the citing paper

“Interestingly, the same manipulation (activity blockade using TTX or AMPAR antagonists) that only affects mini amplitude in young cultures (Turrigiano et al. 1998;Wierenga et al. 2005) can also induce changes in mini frequency and in presynaptic release probability in older neuronal cultures (Wierenga et al. 2006), through a process that involves postsynaptic hyperpolarization and a drop in”

In the citing paper

“Synaptic scaling has now been shown in a variety of central neurons both in vitro and in vivo, including neocortical and hippocampal pyramidal neurons and spinal neurons (O'Brien et al. 1998;Turrigiano et al. 1998;Desai et al. 2002;Stellwagen and Malenka 2006;Goel and Lee 2007;Kim and Tsien 2008;Knogler et al. 2010).”

In the citing paper

“Although in neocortical networks the net effects of changes in excitation and inhibition appear to be homeostatic (Rutherford et al. 1998;Turrigiano et al. 1998;Maffei et al. 2004), different classes of inhibitory synapse are regulated differently by lowered activity.”

In the citing paper

“In response to chronic hyperactivity or hypoactivity, neurons can engage homeostatic scaling-down or scaling-up respectively, in which the strength of excitatory synapses on a neuron is globally modified to maintain neuronal activity in a physiological range (O'Brien et al., 1998, Turrigiano et al., 1998, Turrigiano, 2008).”

In the citing paper

“Sample sizes were initially determined based on prior work using social interaction54,65 and intrinsic physiology62, no formal statistical methods were used to pre-determine sample sizes.”