Structure–stability–function relationships of dendritic spines

Kasai, Hideaki; Matsuzaki, Masunori; Noguchi, Junjirō; Yasumatsu, Nobuaki; Nakahara, Hiroyuki

doi:10.1016/s0166-2236(03)00162-0

Cited by 771 publications

(731 citation statements)

References 94 publications

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“…These larger spines with wider necks are thought to represent spines that acquired AMPA receptors immediately after the induction of long-term potentiation (Matsuzaki et al, 2001;Kasai et al, 2003), and thus enhance spine-dendrite coupling leading to widespread dendritic Ca 2+ signaling during excitatory synaptic transmission (Noguchi et al, 2005). Together with the morphological effects of BDNF on presynaptic terminals (Tyler et al, 2002b) and postsynaptic spine growth and form Pozzo-Miller, 2001, 2003;Alonso et al, 2004), we propose that the larger Ca 2+ signals in spiny dendrites during coincident pre-and postsynaptic activation represent a physiological consequence of the structural BDNF actions at hippocampal synapses.…”

Section: Discussionmentioning

confidence: 99%

BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

Pozzo-Miller

2006

Brain Research

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BDNF, a member of the neurotrophin family, is emerging as a key modulator of synaptic structure and function in the CNS. Due to the critical role of postsynaptic Ca 2+ signals in dendritic development and synaptic plasticity, we tested whether long-term exposure to BDNF affects Ca 2+ elevations evoked by coincident excitatory postsynaptic potentials (EPSPs) and back-propagating action potentials (bAPs) in spiny dendrites of CA1 pyramidal neurons within hippocampal slice cultures. In control neurons, a train of 5 coincident EPSPs and bAPs evoked Ca 2+ elevations in oblique radial branches of the main apical dendrite that were of similar amplitude than those evoked by a train of 5 bAPs alone. On the other hand, dendritic Ca 2+ signals evoked by coincident EPSPs and bAPs were always larger than those triggered by bAPs in CA1 neurons exposed to BDNF for 48 h. This difference was not observed after blockade of NMDA receptors (NMDARs) with D,L-APV, but only in BDNFtreated neurons, suggesting that Ca 2+ signals in oblique radial dendrites include a synaptic NMDARdependent component. Co-treatment with the receptor tyrosine kinase inhibitor k-252a prevented the effect of BDNF on coincident dendritic Ca 2+ signals, suggesting the involvement of neurotrophin Trk receptors. These results indicate that long-term exposure to BDNF enhances Ca 2+ signaling during coincident pre-and postsynaptic activity in small spiny dendrites of CA1 pyramidal neurons, representing a potential functional consequence of neurotrophin-mediated dendritic remodeling in developing neurons.

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Section: Discussionmentioning

confidence: 99%

BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

Pozzo-Miller

2006

Brain Research

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“…In fact, the average size of these thin spines showed the tightest correlation with DNMS acquisition (Dumitriu et al 2010). Thus, in area 46, the class of spines selectively vulnerable to aging and essential for acquiring the nonmatching rule of the task appears to be the smallest of the thin spines, characterized by high motility, plasticity, and turnover rate (Kasai et al 2003;Hao et al 2007;Dumitriu et al 2010).…”

Section: Pfc Synapsesmentioning

confidence: 97%

Neuronal and morphological bases of cognitive decline in aged rhesus monkeys

Hara

Rapp

Morrison

2011

AGE

114

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Rhesus monkeys provide a valuable model for studying the basis of cognitive aging because they are vulnerable to age-related decline in executive function and memory in a manner similar to humans. Some of the behavioral tasks sensitive to the effects of aging are the delayed response working memory test, recognition memory tests including the delayed nonmatching-to-sample and the delayed recognition span task, and tests of executive function including reversal learning and conceptual set-shifting task. Much effort has been directed toward discovering the neurobiological parameters that are coupled to individual differences in age-related cognitive decline. Area 46 of the dorsolateral prefrontal cortex (dlPFC) has been extensively studied for its critical role in executive function while the hippocampus and related cortical regions have been a major target of research for memory function. Some of the key age-related changes in area 46 include decreases in volume, microcolumn strength, synapse density, and α1-and α2-adrenergic receptor binding densities. All of these measures significantly correlate with cognitive scores. Interestingly, the critical synaptic subtypes associated with cognitive function appear to be different between the dlPFC and the hippocampus. For example, the dendritic spine subtype most critical to task acquisition and vulnerable to aging in area 46 is the thin spine, whereas in the dentate gyrus, the density of AGE (2012) large mushroom spines with perforated synapses correlates with memory performance. This review summarizes age-related changes in anatomical, neuronal, and synaptic parameters within brain areas implicated in cognition and whether these changes are associated with cognitive decline.

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“…Spines change shape as they mature, most noticeably by developing a head at the end of the spine (Kasai et al, 2003). Large, more mature spines express high numbers of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepro-prionic acid receptors, greater glutamate sensitivity, and are associated with long-term potentiation (LTP), which is thought to reflect greater synaptic activity and memory function (Matsuzaki et al, 2001;Kasai et al, 2003).…”

Section: Effects Of Chronic Stress On Hippocampal Morphologymentioning

confidence: 99%

Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: Possible involvement of CA1 neurons

et al. 2005

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Emerging data report sex differences in how the brain responds to chronic stress. Here, we investigated the effects of chronic restraint stress (6 h/day/21 days) on hippocampal morphology and function in ovariectomized female rats. Chronic restraint stress caused CA3 apical dendritic retraction in short-and long-shafted neurons, while it reduced basal dendritic arbors in long-shafted neurons only. Chronic restraint did not affect CA1 dendritic arborization, although it increased the proportion of CA1 spine heads compared with controls. Both stressed and control animals performed well on the Y-maze, a spatial memory task. However, chronic stress enhanced Y-maze performance compared with controls, which may reflect facilitated spatial memory or reduced habituation. Ymaze performance correlated with CA1 spine head proportion. This relationship suggests that spatial ability in females may be more tightly coupled with CA1 morphology, which may override the influence of CA3 dendritic retraction. Thus, this research provides additional evidence that CA3 morphology does not always parallel spatial memory.

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Structure–stability–function relationships of dendritic spines

Cited by 771 publications

References 94 publications

BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

Neuronal and morphological bases of cognitive decline in aged rhesus monkeys

Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: Possible involvement of CA1 neurons

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