Synaptic structural plasticity: Role of synaptic shape

Markus, Etan J.; Petit, Ted L.

doi:10.1002/syn.890030102

Cited by 75 publications

(32 citation statements)

References 53 publications

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“…Similar to the findings from 1 h, concave-shaped synapses were larger in the MML of the LTP animals at 5 days postinduction. Irregular-shaped synapses were also larger, which indicates that synapses from both of the curvature subgroups thought to have increased efficacy are larger in these animals (Markus and Petit, 1989). Interestingly, these same concave synapses were smaller at 24 h post-LTP induction, which suggests that this subgroup is particularly involved in the structural plasticity associated with LTP (Weeks et al, 1999).…”

Section: Length Of Synapsesmentioning

confidence: 76%

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Sequential changes in the synaptic structural profile following long-term potentiation in the rat dentate gyrus: III. Long-term maintenance phase

Weeks

Ivanco

LeBoutillier

et al. 2001

Synapse

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Section: Length Of Synapsesmentioning

confidence: 76%

“…Synaptic curvature may alter synaptic efficacy by changing the proximity of receptor channels to the dendritic shaft or by increasing the amount of synaptic contact area (see Markus and Petit, 1989;Petit, 1988Petit, , 1995. Presynaptically, curvature may affect calcium concentrations leading to altered probability of transmitter release.…”

Section: Discussionmentioning

confidence: 99%

Sequential changes in the synaptic structural profile following long-term potentiation in the rat dentate gyrus: III. Long-term maintenance phase

Weeks

Ivanco

LeBoutillier

et al. 2001

Synapse

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“…Synaptic curvature is a plastic feature of the synapse that changes during development and after activity (Markus and Petit, 1989;Marrone and Petit, 2002). Formation of synaptic curvature has been proposed to be related to synaptic efficacy and hypothesized to reflect synaptic membrane enlargement as a result of neurotransmitter release and SV insertion.…”

Section: Discussionmentioning

confidence: 99%

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

et al. 2006

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Relatively mild ischemic episode can initiate a chain of events resulting in delayed cell death and significant lesions in the affected brain regions. We studied early synaptic modifications after brief ischemia modeled in rats by transient vessels' occlusion in vivo or oxygen-glucose deprivation in vitro and resulting in delayed death of hippocampal CA1 pyramidal cells. Electron microscopic analysis of excitatory spine synapses in CA1 stratum radiatum revealed a rapid increase of the postsynaptic density (PSD) thickness and length, as well as formation of concave synapses with perforated PSD during the first 24 h after ischemic episode, followed at the long term by degeneration of 80% of synaptic contacts. In presynaptic terminals, ischemia induced a depletion of synaptic vesicles and changes in their spatial arrangement: they became more distant from active zones and had larger intervesicle spacing compared to controls. These rapid structural synaptic changes could be implicated in the mechanisms of cell death or adaptive plasticity. Comparison of the in vivo and in vitro model systems used in the study demonstrated a general similarity of these early morphological changes, confirming the validity of the in vitro model for studying synaptic structural plasticity.

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“…It was reported that Al deposited in the brain could impair the configuration of synapse, postsynaptic membrane and PSD which reflected the synaptic organization and metabolism (Jing, 2004). Especially, the thickness of the PSD represented synaptic efficacy (Jing, 2004); synaptic curvature reflected a morphological index of synaptic plasticity representing the different function of synapses such as the neuron transmitter release signs and the configuration changes in postsynaptic receptors (Markus and Petit, 1989). Subtle changes in synaptic structure can alter biophysical properties of synapses (Tang et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats

et al. 2013

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-Epidemiological investigations have indicated that aluminum (Al), as an important environmental neurotoxicant, could cause damage to the cognitive function which was closely related with neurodegenerative diseases. Long-term potentiation (LTP) is one form of synaptic plasticity in association with cognitive function. Previous studies have demonstrated that Al impaired early phase long-term potentiation (E-LTP) in vivo and in vitro. However, Al-induced damage to late phase long-term potentiation (L-LTP) has poorly been studied. The present study was designed to observe the effects of subchronic Al exposure on the spatial memory, hippocampus ultrastructure and L-LTP in rats. Pregnant Wistar rats were assigned to four groups. Neonatal rats were exposed to Al by parental lactation from parturition to weaning for 3 weeks and then fed with the distilled water containing 0, 0.2%, 0.4% and 0.6% aluminum chloride (AlCl 3 ) respectively from weaning to postnatal 3 months. The levels of Al in blood and hippocampus were quantitated by atomic absorption spectrophotometer. Morris water maze test was performed to study spatial memory. The induction and maintenance of L-LTP in area of Schaffer collateral-CA1 synapse was recorded by extracellular microelectrode recording technology in hippocampus of experimental rats. Hippocampus was collected for transmission electron microscopy observation. The results showed that the Al concentrations in blood and hippocampus of Al-exposed rats were higher than those of the control rats. Al could impair spatial memory ability of rats. Neuronal and synaptic ultrastructure from Al-exposed rats presented pathological changes; the incidence of L-LTP has a decrease trend while population spike (PS) amplitude was much smaller significantly stimulated by high-frequency stimulation (HFS) in Al-exposed rats. Our findings showed that Al exposure caused spatial memory damage, under which the neuronal and synaptic ultrastructure changes maybe were their morphological basis and the impaired L-LTP of hippocampus could be their electrophysiological basis.

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Synaptic structural plasticity: Role of synaptic shape

Cited by 75 publications

References 53 publications

Sequential changes in the synaptic structural profile following long-term potentiation in the rat dentate gyrus: III. Long-term maintenance phase

Sequential changes in the synaptic structural profile following long-term potentiation in the rat dentate gyrus: III. Long-term maintenance phase

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats

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