Synaptic scaling mediated by glial TNF-α

In the citing paper

“This model is based on the observations that TNFa levels are elevated by prolonged (48 h) activity blockade, acute application of TNFa (or conditioned media from activity-blocked cultures) increases mEPSC amplitude, and scaling up in response to prolonged activity blockade is prevented by blocking TNFa signaling (Beattie et al. 2002;Stellwagen et al. 2005;Stellwagen and Malenka 2006).”

In the citing paper

“This model is based on the observations that TNFa levels are elevated by prolonged (48 h) activity blockade, acute application of TNFa (or conditioned media from activity-blocked cultures) increases mEPSC amplitude, and scaling up in response to prolonged activity blockade is prevented by blocking TNFa signaling (Beattie et al. 2002;Stellwagen et al. 2005;Stellwagen and Malenka 2006).”

In the citing paper

“It was recently proposed that prolonged activity blockade (with TTX) increases glial release of TNFa, which then acts on neurons to enhance AMPAR insertion and scale up mEPSC amplitude (Stellwagen and Malenka 2006).”

In the citing paper

“This model is based on the observations that TNFa levels are elevated by prolonged (48 h) activity blockade, acute application of TNFa (or conditioned media from activity-blocked cultures) increases mEPSC amplitude, and scaling up in response to prolonged activity blockade is prevented by blocking TNFa signaling (Beattie et al. 2002;Stellwagen et al. 2005;Stellwagen and Malenka 2006).”

In the citing paper

“Interestingly, the TNFa involved in scaling up synaptic strengths in response to TTX originates from glia rather than neurons, because wild-type neurons grown on TNFa 2/2 glia did not scale up synaptic strengths in response to 48 h of TTX treatment, whereas TNFa 2/2 neurons grown on wild-type glia did (Stellwagen and Malenka 2006).”

In the citing paper

“Inconsistent with the above model is the observation that scaling is a gradual and cumulative process evident after as little as 4-6 h of activity blockade (Sutton et al. 2006;Ibata et al. 2008), whereas TNFa-dependent scaling was only observed after prolonged activity block (48 h) (Stellwagen and Malenka 2006).”

In the citing paper

“Interestingly, the delayed potentiation in visual cortex following lid suture requires TNFa and Arc signaling (Kaneko et al. 2008;McCurry et al. 2011) as does synaptic scaling in vitro (Shepherd et al. 2006;Stellwagen and Malenka 2006;Steinmetz and Turrigiano 2010); however, both these manipulations likely affect many forms of plasticity, so it still remains to be seen if synaptic scaling”