Deprivation-Induced Strengthening of Presynaptic and Postsynaptic Inhibitory Transmission in Layer 4 of Visual Cortex during the Critical Period

Adult cortical plasticity following injury: Recapitulation of critical period mechanisms?

“…There is a reasonable consensus that the loss of cortical responsiveness to deprived eye stimulation after 2–3d MD involves some form of Hebbian-like long-term depression (LTD) (Rittenhouse et al, 1999, Heynen et al, 2008, Lambo and Turrigiano, 2013), as well as a coordinated strengthening of pre- and postsynaptic FS to pyramidal cell inhibition (Maffei et al, 2006, Maffei et al, 2010, Lefort et al, 2013, Nahmani and Turrigiano, 2014, Wang and Maffei, 2014). After 4–6d of MD, cells in V1 increase their responsiveness to both the open ipsilateral eye and the deprived contralateral eye (Frenkel and Bear, 2004, Mrsic-Flogel et al, 2007), and as mentioned above this synaptic depression followed by homeostatic potentiation are correlated with changes in firing measured in freely behaving rodents (Hengen et al, 2013).…”

“…the ability to reveal the normal shift in MD-induced ODP) relies heavily on the proper development of cortical inhibition (Hensch et al, 1998, Iwai et al, 2003, Fagiolini et al, 2004). Specifically, FS interneurons have been implicated as key regulators of CP initiation, because: (1) a precocious increase in FS interneuron morphological development via BDNF-overexpression results in an early CP for ODP (Huang et al, 1999, Chattopadhyaya et al, 2004), (2) cortical infusion of the transcription factor OTX2 is able to accelerate FS cell maturation, and OTX2 is necessary for CP initiation (Sugiyama et al, 2008), (3) degrading components of the extracellular matrix preferentially surrounding FS cell terminals results in increased ODP in adulthood (Pizzorusso et al, 2002), and (4) MD induces an increase in FS to pyramidal cell inhibitory synaptic strength during the CP in V1m, but not during the pre-critical period or in knock-out animals unable to express ODP (Maffei et al, 2004, Maffei et al, 2006, Nahmani and Turrigiano, 2014). Thus, something about the development of FS cell inhibition is necessary for either the induction or expression of ODP in V1.…”

“…Exactly how this maturation of inhibition triggers CP plasticity remains unclear. MD during the CP induces an initial decrease in FS cell firing after 1d, followed by increased FS cell firing (Hengen et al, 2013) and increased pre- and postsynaptic FS to pyramidal cell synaptic strength after 3d (Maffei et al, 2006, Maffei et al, 2010, Nahmani and Turrigiano, 2014, Wang and Maffei, 2014). The parallel drop in GABAergic firing and postsynaptic GABAARs beginning 1d after cortical injury in adult cortex (Imbrosci and Mittmann, 2011) suggests that cortical disinhibition is an initial step gating a suite of plasticity events that follow cortical pathology in both adult and CP brains.…”

Diffusion dynamics of synaptic molecules during inhibitory postsynaptic plasticity

“…At GABAergic synapses, postsynaptically-expressed potentiation of long-term potentiation inhibition (iLTP) depends on GABARAP-mediated increase of GABA A R exocytosis that in turn promotes receptors accumulation at the postsynaptic density (PSD), as observed in cultured neurons, in slices and in vivo (Nusser et al, 1998; Marsden et al, 2007; Kurotani et al, 2008; Nahmani and Turrigiano, 2014; Petrini et al, 2014). Conversely, inhibitory long-term depression (iLTD) has been correlated with reduced availability of GABA A Rs at synapses, although no consensus has been achieved yet whether this is due to altered GABA A R internalization or to receptor dispersal from the synapse (Kurotani et al, 2008; Bannai et al, 2009; Muir et al, 2010).…”

Circuits for active vision : parallel tectothalamocortical visual pathways in the mouse.

“…By comparing GAD65-GFP-labeled elements with GABA-stained elements, we conclude that, in contrast to thalamic interneurons which release GABA from dendritic terminals (Govindaiah and Cox, 2004;Bickford et al, 2010), cortical interneurons do not accumulate detectable levels of GABA within small diameter dendrites, presumably because they release GABA only from axon terminals (Nahmani and Turrigiano, 2014).…”