LTD Induction Causes Morphological Changes of Presynaptic Boutons and Reduces Their Contacts with Spines

Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 München-Martinsried, Germany.
Neuron (Impact Factor: 15.05). 12/2008; 60(4):590-7. DOI: 10.1016/j.neuron.2008.09.018
Source: PubMed


Activity-dependent changes in the synaptic connections of the brain are thought to be important for learning and memory. Imaging techniques have enabled the examination of structural rearrangements during activity-dependent processes at the synapse. While many studies have examined structural changes of dendritic spines, little is known about structural plasticity of presynaptic boutons. We therefore examined how axonal boutons are affected during long-term depression (LTD). We used time lapse two-photon laser scanning microscopy and extracellular field recordings to monitor simultaneously synaptic morphology and activity for up to five hours in mouse organotypic hippocampal slice cultures. LTD induction dramatically increased the turnover of presynaptic boutons, while decreasing the number of putative synaptic contacts between Schaffer collateral boutons and spines of CA1 pyramidal cells. Our data indicate a substantial presynaptic contribution to activity-dependent morphological plasticity and provide opportunities for studying the molecular mechanisms of the structural remodeling of synaptic circuits.

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Available from: Corette J Wierenga, Jul 01, 2014
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    • "However, given that MEPs were still significantly suppressed at 60 min following simultaneous so-tDCS and cTBS, it is possible that this combined stimulation induced a longer lasting form of LTD. Whereas earlyphase LTD is characterized by functional changes such as the internalization of [2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl) propanoic acid] receptors in the post-synaptic cell (Snyder et al., 2001; Brown et al., 2005), late-phase LTD is additionally dependent on changes in gene transcription and protein synthesis, which ultimately lead to more persistent morphological changes (Zhou et al., 2003; Becker et al., 2008). It is possible that the application of a slowly oscillating current and concurrent modulation of N-methyl-d-aspartate receptor activation by cTBS may have facilitated the molecular mechanisms responsible for late-phase LTD, expressed as longer lasting inhibition of MEP amplitude. "
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    ABSTRACT: The objective of this study was to assess whether the simultaneous application of slow-oscillation transcranial direct current stimulation enhances the neuroplastic response to transcranial magnetic theta burst stimulation. Motor evoked potential amplitude was assessed at baseline and at regular intervals up to 60 min following continuous theta burst stimulation, slow-oscillation transcranial direct current stimulation, and the simultaneous application of these paradigms. In addition, the electroencephalographic power spectra of slow and fast delta, and theta frequency bands recorded over the motor cortex were analyzed prior to and up to 5 min following each intervention. There was longer-lasting motor evoked potential suppression following the simultaneous application of continuous theta burst stimulation and slow-oscillation transcranial direct current stimulation compared with when continuous theta burst stimulation was applied alone. Slow-oscillation transcranial direct current stimulation applied alone did not modulate the motor evoked potential amplitude. No significant changes in spectral power were observed following slow-oscillation transcranial direct current stimulation. Simultaneous application of continuous theta burst stimulation and slow-oscillation transcranial direct current stimulation may provide an approach to prolong the induction of neuroplastic changes in motor cortical circuits by repetitive transcranial magnetic brain stimulation.
    European Journal of Neuroscience 06/2012; 36(5):2661-8. DOI:10.1111/j.1460-9568.2012.08181.x · 3.18 Impact Factor
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    • "). The elimination likely involves a complex series of events but activity-dependent synaptic depression such as long-term depression (LTD) may be an initial step for elimination (Bastrikova et al., 2008; Becker et al., 2008). It has been suggested that activity-dependent synaptic plasticity described in the more mature brain as involved in learning and memory can be seen as a model for synaptic plasticity also in the developing brain (Kandel and O'Dell, 1992). "
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    ABSTRACT: In the developing brain synaptogenesis is accompanied by elimination of synapses possibly initiated by activity-dependent synaptic plasticity such as long-term depression (LTD). Experiments using 2nd postnatal week hippocampal CA3-CA1 synapses have previously shown that these synapses, in contrast to those in the more adult brain, are easily depressed even during very low frequency (0.05-0.2 Hz) activity. We have now addressed the question whether such stimulation actually results in LTD, and if so, under which conditions this occurs. By introducing 30-60 min of stimulus interruption following 900 stimuli at 0.2 Hz and 0.05 Hz we found this stimulation to result in an LTD of -37% and -24%, respectively. The LTD following 0.2 Hz stimulation did not differ significantly from that resulting from 900 stimuli using the common LTD-inducing frequency of 1 Hz. When 0.2 Hz and 1 Hz stimulations were applied in the presence of a combined N-methyl-d-aspartate receptor (NMDAR)/mGluR blockade the LTDs were only marginally smaller. However, the LTD observed under this latter condition was labile in that it reversed (de-depressed) by spontaneous and/or ambient NMDAR activity (labile LTD). 0.2 and 1 Hz-evoked NMDAR activity resulted in LTD not de-depressed by spontaneous and/or ambient NMDAR activity (stable LTD) and in little or no labile LTD. The stable LTD was fully de-depressed by high frequency-evoked NMDAR activity. 0.2 and 1 Hz-evoked mGluR activity impaired the labile LTD but did not result in stable LTD. In conclusion, in 2nd postnatal week CA3-CA1 synapses LTD is induced at frequencies well below one Hz as well as in the absence of NMDAR activity. Very low/low frequency-evoked NMDAR activity stabilizes LTD by raising its threshold for NMDAR-dependent de-depression. LTD at these developing synapses thus seems adapted for ease of induction as well as of de-depression.
    Neuroscience 07/2011; 192:54-66. DOI:10.1016/j.neuroscience.2011.06.081 · 3.36 Impact Factor
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    • "Activity-dependent structural remodeling of dendritic spines and adjacent glial processes has been suggested to play a significant role in the induction of LTP, plasticity and memory [8], [9], [10], [36], [37]. Support for this hypothesis comes from post-mortem histological or invasive in-vivo animal studies. "
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    ABSTRACT: Activity-induced structural remodeling of dendritic spines and glial cells was recently proposed as an important factor in neuroplasticity and suggested to accompany the induction of long-term potentiation (LTP). Although T1 and diffusion MRI have been used to study structural changes resulting from long-term training, the cellular basis of the findings obtained and their relationship to neuroplasticity are poorly understood. Here we used diffusion tensor imaging (DTI) to examine the microstructural manifestations of neuroplasticity in rats that performed a spatial navigation task. We found that DTI can be used to define the selective localization of neuroplasticity induced by different tasks and that this process is age-dependent in cingulate cortex and corpus callosum and age-independent in the dentate gyrus. We relate the observed DTI changes to the structural plasticity that occurs in astrocytes and discuss the potential of MRI for probing structural neuroplasticity and hence indirectly localizing LTP.
    PLoS ONE 06/2011; 6(6):e20678. DOI:10.1371/journal.pone.0020678 · 3.23 Impact Factor
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