Chapter 11 Spine dynamics and synapse remodeling during LTP and memory processes

Department of Neuroscience, Centre Médical Universitaire, 1211 Geneva 4, Switzerland.
Progress in brain research (Impact Factor: 2.83). 02/2008; 169:199-207. DOI: 10.1016/S0079-6123(07)00011-8
Source: PubMed


While changes in the efficacy of synaptic transmission are believed to represent the physiological bases of learning mechanisms, other recent studies have started to highlight the possibility that a structural reorganization of synaptic networks could also be involved. Morphological changes of the shape or size of dendritic spines or of the organization of postsynaptic densities have been described in several studies, as well as the growth and formation following stimulation of new protrusions. Confocal in vivo imaging experiments have further revealed that dendritic spines undergo a continuous turnover and replacement process that may vary as a function of development, but can be markedly enhanced by sensory activation or following brain damage. The implications of these new aspects of plasticity for learning and memory mechanisms are discussed.

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Available from: Paul Klauser, Oct 01, 2015
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    • "During brain ontogenesis, overproduction of synapses and their subsequent elimination through activity-dependent processes are critical for correct refinement and normal functioning of neural circuits.36,37 Moreover, dynamic processes of assembly and disassembly of synapses persist into adulthood;38,39 in rodent hippocampus, including CA1, synapse density has been shown to increase into adult age,40,41 nearly doubling between postnatal day 15 and 48,42 thus pointing to a highly protracted period of synapse formation and refinement. The increase of axo-spinous synapses observed in CA1 stratum radiatum of adult rats maternally exposed to excess of α-T may reflect an aberrant gauging of synapse production/elimination balance during hippocampal maturation. "
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    ABSTRACT: An increased intake of the antioxidant α-Tocopherol (vitamin E) is recommended in complicated pregnancies, to prevent free radical damage to mother and fetus. However, the anti-PKC and antimitotic activity of α-Tocopherol raises concerns about its potential effects on brain development. Recently, we found that maternal dietary loads of α-Tocopherol through pregnancy and lactation cause developmental deficit in hippocampal synaptic plasticity in rat offspring. The defect persisted into adulthood, with behavioral alterations in hippocampus-dependent learning. Here, using the same rat model of maternal supplementation, ultrastructural morphometric studies were carried out to provide mechanistic interpretation to such a functional impairment in adult offspring by the occurrence of long-term changes in density and morphological features of hippocampal synapses. Higher density of axo-spinous synapses was found in CA1 stratum radiatum of α-Tocopherol-exposed rats compared to controls, pointing to a reduced synapse pruning. No morphometric changes were found in synaptic ultrastructural features, i.e., perimeter of axon terminals, length of synaptic specializations, extension of bouton-spine contact. Gliasynapse anatomical relationship was also affected. Heavier astrocytic coverage of synapses was observed in Tocopherol-treated offspring, notably surrounding axon terminals; moreover, the percentage of synapses contacted by astrocytic endfeet at bouton-spine interface (tripartite synapses) was increased. These findings indicate that gestational and neonatal exposure to supranutritional Tocopherol intake can result in anatomical changes of offspring hippocampus that last through adulthood. These include a surplus of axo-spinous synapses and an aberrant gliasynapse relationship, which may represent the morphological signature of previously described alterations in synaptic plasticity and hippocampus-dependent learning.
    European journal of histochemistry: EJH 04/2014; 58(2):2355. DOI:10.4081/ejh.2014.2355 · 2.04 Impact Factor
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    • "NMDAR-mediated influx of Ca+2 contributes to the long term potentiation, thereby controlling the behavioral learning, fear response and extinction [66], [69], [74]. Related observation of elevated mGluR2 (GRM2) in FD-fed mice was rather counterintuitive. "
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    ABSTRACT: The health benefits of fish oil enriched with high omega-3 polyunsaturated fatty acids (n-3 PUFA) are widely documented. Fish oil as dietary supplements, however, show moderate clinical efficacy, highlighting an immediate scope of systematic in vitro feedback. Our transcriptomic study was designed to investigate the genomic shift of murine brains fed on fish oil enriched diets. A customized fish oil enriched diet (FD) and standard lab diet (SD) were separately administered to two randomly chosen populations of C57BL/6J mice from their weaning age until late adolescence. Statistical analysis mined 1,142 genes of interest (GOI) differentially altered in the hemibrains collected from the FD- and SD-fed mice at the age of five months. The majority of identified GOI (∼40%) encodes proteins located in the plasma membrane, suggesting that fish oil primarily facilitated the membrane-oriented biofunctions. FD potentially augmented the nervous system's development and functions by selectively stimulating the Src-mediated calcium-induced growth cascade and the downstream PI3K-AKT-PKC pathways. FD reduced the amyloidal burden, attenuated oxidative stress, and assisted in somatostatin activation-the signatures of attenuation of Alzheimer's disease, Parkinson's disease, and affective disorder. FD induced elevation of FKBP5 and suppression of BDNF, which are often linked with the improvement of anxiety disorder, depression, and post-traumatic stress disorder. Hence we anticipate efficacy of FD in treating illnesses such as depression that are typically triggered by the hypoactivities of dopaminergic, adrenergic, cholinergic, and GABAergic networks. Contrastingly, FD's efficacy could be compromised in treating illnesses such as bipolar disorder and schizophrenia, which are triggered by hyperactivities of the same set of neuromodulators. A more comprehensive investigation is recommended to elucidate the implications of fish oil on disease pathomechanisms, and the result-driven repositioning of fish oil utilization may revitalize its therapeutic efficacy.
    PLoS ONE 03/2014; 9(3):e90425. DOI:10.1371/journal.pone.0090425 · 3.23 Impact Factor
    • "elation between the intensity of cocaine seeking and both morphological and electrophysiological measures of synaptic potentiation . Changes in spine density and / or head diameter ( d h ) are a struc - tural substrate for synaptic plasticity , with larger d h being asso - ciated with LTP and reduced d h with LTD ( Carlisle and Kennedy , 2005 ; De Roo et al . , 2008 ; Yang and Zhou , 2009 ) . Consistent with previous reports ( Kourrich et al . , 2007 ; Moussawi et al . , 2011 ; Shen et al . , 2009 ) , withdrawal from investigator - or self - adminis - tered cocaine increased d h and A / N compared to yoked - saline rats . The d h and A / N were further increased 15 min after initiating cue - induce"
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    ABSTRACT: Cocaine addiction is characterized by long-lasting vulnerability to relapse arising because neutral environmental stimuli become associated with drug use and then act as cues that induce relapse. It is not known how cues elicit cocaine seeking, and why cocaine seeking is more difficult to regulate than seeking a natural reward. We found that cocaine-associated cues initiate cocaine seeking by inducing a rapid, transient increase in dendritic spine size and synaptic strength in the nucleus accumbens. These changes required neural activity in the prefrontal cortex. This is not the case when identical cues were associated with obtaining sucrose, which did not elicit changes in spine size or synaptic strength. The marked cue-induced synaptic changes in the accumbens were correlated with the intensity of cocaine, but not sucrose seeking, and may explain the difficulty addicts experience in managing relapse to cocaine use.
    Neuron 03/2013; 77(5):867-72. DOI:10.1016/j.neuron.2013.01.005 · 15.05 Impact Factor
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