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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    • "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.
    Neuron 10/2015; DOI:10.1016/j.neuron.2015.09.025 · 15.05 Impact Factor
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    • "As modulation of cortical excitability as measured by e.g. motor evoked potentials (MEP) sustained after the electric current was switched off (Nitsche & Paulus, 2000), other mechanisms such as synaptic plasticity involving early gene expression and protein synthesis previously shown in animal studies (Gartside, 1968) influencing long-term depression (LTD) and potentiation (LTP) (Feldman, 2009) were postulated (Paulus, 2004). However, the exact mechanisms underlying the effects of tDCS are still incompletely understood, particularly how neurophysiological effects link to brain function and human behavior. "
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    ABSTRACT: Transcranial direct current stimulation (tDCS) can influence cognitive, affective or motor brain functions. Whereas previous imaging studies demonstrated widespread tDCS effects on brain metabolism, direct impact of tDCS on electric or magnetic source activity in task-related brain areas could not be confirmed due to the difficulty to record such activity simultaneously during tDCS. The aim of this proof-of-principal study was to demonstrate the feasibility of whole-head source localization and reconstruction of neuromagnetic brain activity during tDCS and to confirm the direct effect of tDCS on ongoing neuromagnetic activity in task-related brain areas. Here we show for the first time that tDCS has an immediate impact on slow cortical magnetic fields (SCF, 0-4Hz) of task-related areas that are identical with brain regions previously described in metabolic neuroimaging studies. 14 healthy volunteers performed a choice reaction time (RT) task while whole-head magnetoencephalography (MEG) was recorded. Task-related source-activity of SCFs was calculated using synthetic aperture magnetometry (SAM) in absence of stimulation and while anodal, cathodal or sham tDCS was delivered over the right primary motor cortex (M1). Source reconstruction revealed task-related SCF modulations in brain regions that precisely matched prior metabolic neuroimaging studies. Anodal and cathodal tDCS had a polarity-dependent impact on RT and SCF in primary sensorimotor and medial centro-parietal cortices. Combining tDCS and whole-head MEG is a powerful approach to investigate the direct effects of transcranial electric currents on ongoing neuromagnetic source activity, brain function and behavior.
    NeuroImage 10/2015; DOI:10.1016/j.neuroimage.2015.09.068 · 6.36 Impact Factor
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    • ", 1975 ; Thompson et al . , 1983 ; Feldman , 2009 ) , but it is at least two orders of magnitude slower than the timescale of associative plasticity , which changes synaptic weights within minutes or even tens of seconds . Runaway dynamics of synaptic weights and activity can be induced by Hebbian - type learning rules within seconds or minutes ( e . "
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    ABSTRACT: Homosynaptic Hebbian-type plasticity provides a cellular mechanism of learning and refinement of connectivity during development in a variety of biological systems. In this review we argue that a complimentary form of plasticity-heterosynaptic plasticity-represents a necessary cellular component for homeostatic regulation of synaptic weights and neuronal activity. The required properties of a homeostatic mechanism which acutely constrains the runaway dynamics imposed by Hebbian associative plasticity have been well-articulated by theoretical and modeling studies. Such mechanism(s) should robustly support the stability of operation of neuronal networks and synaptic competition, include changes at non-active synapses, and operate on a similar time scale to Hebbian-type plasticity. The experimentally observed properties of heterosynaptic plasticity have introduced it as a strong candidate to fulfill this homeostatic role. Subsequent modeling studies which incorporate heterosynaptic plasticity into model neurons with Hebbian synapses (utilizing an STDP learning rule) have confirmed its ability to robustly provide stability and competition. In contrast, properties of homeostatic synaptic scaling, which is triggered by extreme and long lasting (hours and days) changes of neuronal activity, do not fit two crucial requirements for a hypothetical homeostatic mechanism needed to provide stability of operation in the face of on-going synaptic changes driven by Hebbian-type learning rules. Both the trigger and the time scale of homeostatic synaptic scaling are fundamentally different from those of the Hebbian-type plasticity. We conclude that heterosynaptic plasticity, which is triggered by the same episodes of strong postsynaptic activity and operates on the same time scale as Hebbian-type associative plasticity, is ideally suited to serve a homeostatic role during on-going synaptic plasticity.
    Frontiers in Computational Neuroscience 07/2015; 9:89. DOI:10.3389/fncom.2015.00089 · 2.20 Impact Factor
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