Synaptic Mechanisms for Plasticity in Neocortex

Department of Molecular and Cell Biology, and Helen Wills Neuroscience Institute, University of California, Berkeley, USA.
Annual Review of Neuroscience (Impact Factor: 19.32). 04/2009; 32(1):33-55. DOI: 10.1146/annurev.neuro.051508.135516
Source: PubMed


Sensory experience and learning alter sensory representations in cerebral cortex. The synaptic mechanisms underlying sensory cortical plasticity have long been sought. Recent work indicates that long-term cortical plasticity is a complex, multicomponent process involving multiple synaptic and cellular mechanisms. Sensory use, disuse, and training drive long-term potentiation and depression (LTP and LTD), homeostatic synaptic plasticity and plasticity of intrinsic excitability, and structural changes including formation, removal, and morphological remodeling of cortical synapses and dendritic spines. Both excitatory and inhibitory circuits are strongly regulated by experience. This review summarizes these findings and proposes that these mechanisms map onto specific functional components of plasticity, which occur in common across the primary somatosensory, visual, and auditory cortices.

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    • "For example, it is not clear which specific functional components of plasticity, if any, mediate which types or sites of rapid structural components of plasticity or whether chemical signaling is a proximal driver of structural plasticity (Feldman, 2009). Moreover, the relationship between functional changes and structural microscopic and then macroscopic changes – that is anatomical connectivity – is unknown (Feldman, 2009). Finally, the relationship between anatomical, functional, and effective connectivity in the cortex also represents a significant challenge (Tononi et al., 1994; Sporns et al., 2004 ). "
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    • "To determine how whisker deprivation affects development of L4 mIPSCs, we deprived the D-row whiskers by plucking beginning at P7. Deprivation was maintained continuously by re-plucking every 2–3 days until the date of recording (Fig 1D) . Whisker plucking reduces sensory-evoked activity in the corresponding S1 column [27] and drives robust plasticity of whisker-evoked spiking responses and synaptic properties in L2/3 of deprived columns282930. It has previously been shown that continuous whisker deprivation from P7 in GAD67-GFP mice causes weakened L4 inhibitory synapse efficacy measured at P28 [13]. "
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    ABSTRACT: Inhibitory synapse development in sensory neocortex is experience-dependent, with sustained sensory deprivation yielding fewer and weaker inhibitory synapses. Whether this represents arrest of synapse maturation, or a more complex set of processes, is unclear. To test this, we measured the dynamics of inhibitory synapse development in layer 4 of rat somatosensory cortex (S1) during continuous whisker deprivation from postnatal day 7, and in age-matched controls. In deprived columns, spontaneous miniature inhibitory postsynaptic currents (mIPSCs) and evoked IPSCs developed normally until P15, when IPSC amplitude transiently decreased, recovering by P16 despite ongoing deprivation. IPSCs remained normal until P22, when a second, sustained phase of weakening began. Delaying deprivation onset by 5 days prevented the P15 weakening. Both early and late phase weakening involved measurable reduction in IPSC amplitude relative to prior time points. Thus, deprivation appears to drive two distinct phases of active IPSC weakening, rather than simple arrest of synapse maturation.
    Full-text · Article · Feb 2016 · PLoS ONE
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    • "The cerebral cortex shows a remarkable capacity for functional plasticity (Feldman, 2009; Fox et al., 2000; Fox and Wong, 2005). Broadly, plasticity can take one of two forms: input-specific plasticity, which involves weakening of inactive inputs and strengthening (or weakening) of active inputs, and an inputagnostic form of plasticity, which involves both deprived and spared inputs and acts to maintain neuronal activity at some set point in a homeostatic fashion. "
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    ABSTRACT: Layer 5 contains the major projection neurons of the neocortex and is composed of two major cell types: regular spiking (RS) cells, which have cortico-cortical projections, and intrinsic bursting cells (IB), which have subcortical projections. Little is known about the plasticity processes and specifically the molecular mechanisms by which these two cell classes develop and maintain their unique integrative properties. In this study, we find that RS and IB cells show fundementally different experience-dependent plasticity processes and integrate Hebbian and homeostatic components of plasticity differently. Both RS and IB cells showed TNFα-dependent homeostatic plasticity in response to sensory deprivation, but IB cells were capable of a much faster synaptic depression and homeostatic rebound than RS cells. Only IB cells showed input-specific potentiation that depended on CaMKII autophosphorylation. Our findings demonstrate that plasticity mechanisms are not uniform within the neocortex, even within a cortical layer, but are specialized within subcircuits.
    Full-text · Article · Oct 2015 · Neuron
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