High frequency stimulation-induced dendritic calcium waves in rat hippocampal neurons

Jäger, Tino; Behnisch, Thomas; Reymann, Klaus G.

doi:10.1016/s0304-3940(02)01165-5

Cited by 6 publications

(4 citation statements)

References 16 publications

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“…A local stimulation of the Schaffer collaterals not only triggers a rise in [Ca ++ ] i in the activated dendritic spines (Sabatini et al 2002) but also elicits an intradendritic [Ca ++ ] i rise that propagates as a wave along the dendrites of CA1 neurons, but only at short distance (not exceeding 70 µm) (Jäger et al 2002). This propagation of Ca ++ waves occurs along the dendritic endoplasmic reticulum using IP3 receptors (Nishiyama et al 2000).…”

Section: Learning and Memory 187mentioning

confidence: 99%

Synapse specificity of long-term potentiation breaks down with aging

Ris¹,

Godaux²

2007

Learn. Mem.

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Memory shows age-related decline. According to the current prevailing theoretical model, encoding of memories relies on modifications in the strength of the synapses connecting the different cells within a neuronal network. The selective increases in synaptic weight are thought to be biologically implemented by long-term potentiation (LTP). Here, we report that tetanic stimulation of afferent fibers in slices from 12-mo-old mice triggers an LTP not restricted to the activated synapses. This phenomenon, which can be anticipated to hinder memory encoding, is suppressed by blocking either L-type Ca ++ channels or Ca ++ -induced Ca ++ release, both well known to become disregulated with aging.During the normal aging process, humans and animals experience age-related memory decline (Bach et al. 1999;Rosenzweig and Barnes 2003). Historically, it was thought that the primary contribution to the etiology of this decline was a massive loss of neurons in all the cortical layers and in the hippocampus (Brody 1955;Scheibel et al. 1976;Scheibel 1979). However, when it became possible to eliminate many of the confounding factors of the previous studies, this was proved to be a misconception (Burke and Barnes 2006). Nowadays, a great number of studies have identified multiple changes in Ca ++ -related electrophysiological processes as consistent biomarkers of aging (Landfield and Pitler 1984;Thibault and Landfield 1996;Norris et al. 1998;Thibault et al. 2001;Gant et al. 2006). One of the current prevailing hypotheses is that those Ca ++ dysregulations underlie many aspects of aging. However, the potential link between agerelated Ca ++ dysregulations and memory decline is still missing.For neurocomputing theorists, every memory is encoded in a neuronal network thanks to a change in the distribution of its synaptic weights (Zipser and Andersen 1988). Among the possible biological mechanisms, long-term potentiation (LTP) is the favored candidate to be at the basis of memory storage because this activity-induced increase in synaptic strength is (1) durable and (2) input-selective (restricted to the activated synapses). In the hippocampal synapses between Schaffer collaterals and CA1 pyramidal neurons, a single train of tetanic stimulation triggers a short-lasting LTP (S-LTP), which lasts 1-2 h, whereas multiple trains induce a long-lasting LTP (L-LTP) lasting >4 h (Huang and Kandel 1994;Abel et al. 1997). Potential age-related LTP defects have been sought out in the past. It has been reported that S-LTP in area CA1 from aged animals was normal when supra-threshold stimulation parameters were used (Moore et al. 1993;Burke and Barnes 2006) and showed deficits only when peri-threshold stimulation was applied (Barnes et al. 1992;Burke and Barnes 2006). The L-LTP triggered by multiple trains has been reported to be decreased in aged mice (18 mo) (Bach et al. 1999). In contrast, a brief 1-Hz paired-pulse stimulation has been found to induce an L-LTP in old mice but not in young animals (Huang and Kandel 2006). In our work, we focused on...

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Section: Learning and Memory 187mentioning

confidence: 99%

Synapse specificity of long-term potentiation breaks down with aging

Ris¹,

Godaux²

2007

Learn. Mem.

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“…In addition, there is widening support that the HFS stimulation protocol is also physiologically relevant. First, increases in postsynaptic intracellular Ca 2ϩ concentrations have been associated with high-frequency patterns of stimulation (Jager et al 2002). Second, gamma oscillations (30 -100 Hz) are known to be evoked by bursts of LTP inducing bursts of HFS (100 Hz) (Poschel et al 2003) and by sensory stimulation (Poschel et al 2002).…”

Section: Mechanisms Of Age-related Ltp Deficitsmentioning

confidence: 99%

Reduced Synaptic Plasticity in the Lateral Perforant Path Input to the Dentate Gyrus of Aged C57BL/6 Mice

Froc

Eadie

et al. 2003

Journal of Neurophysiology

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Hippocampal slices obtained from C57BL/6 mice (3-25 mo) were used to investigate the effects of aging on excitatory postsynaptic potentials (EPSPs) elicited in dentate gyrus with lateral perforant path stimulation. The maximal amplitude of the EPSP, as well as the degree of paired-pulse facilitation, was significantly reduced in animals aged 12 mo or more compared with younger animals (<12 mo). Although all animals showed equivalent short-term potentiation (STP) in response to high-frequency stimulation, this did not translate into a long-lasting increase in synaptic efficacy in the older animals. A significant degree of long-term potentiation (LTP) of synaptic efficacy was only observed in animals <12 mo of age when measured 30 min after induction. Blocking GABAA-mediated inhibition significantly enhanced STP in younger and older animals; however, a significant degree of LTP was again only observed in slices taken from younger animals. These data indicate that the lateral perforant path input to the dentate gyrus is altered by the aging process, and that this results in a reduction in the capacity of this input to exhibit long-lasting synaptic plasticity.

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“…The tip of the stimulation electrodes was positioned in close proximity to clearly visible fluorescent dendrites (Fig. 2A1) (Jager et al,2002). The fESPSs were recorded using ACSF filled pipettes and amplified by an AxonClamp 200B amplifier (Molecular Devices, Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

“…Dendrites were chosen that are clearly visible and localized at the same horizontal and vertical positions as the stimulation electrode (Fig. 2A1) (Jager et al, 1998,2002; Karpova et al,2006). Fluorescence intensities were background corrected and expressed as percentage changes from baseline.…”

Section: Methodsmentioning

confidence: 99%

Hippocampal LTP triggers proteasome‐mediated SPAR degradation in CA1 neurons

Chen

Yuanxiang

Knöpfel

et al. 2011

Synapse

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Activity-dependent synaptic plasticity is associated with synaptic protein turnover involving the ubiquitin proteasome system (UPS) for protein degradation. In primary hippocampal cell culture, it has been shown that increased or decreased activity of synaptic transmission can regulate the amount of postsynaptic density (PSD) proteins via UPS. However, the specific spatio-temporal dynamic of PSD protein degradation after LTP induction and its downstream signaling pathways remains to be clarify. We used confocal microscopy to monitor levels of eGFP-tagged SPAR (spine-associated Rap GTPase activating protein) expressed in acute hippocampal slices and found that LTP induction triggered a UPS-dependent decay of eGFP-SPAR fluorescence. SPAR degradation was reduced upon inhibition of cyclin-dependent kinase 5 (CDK5) as well as by a protein synthesis inhibitor. Comparison of eGFP-tagged SPAR levels with those obtained in control experiments with eGFP revealed a protein synthesis-independent component of LTP-associated SPAR degradation. This second component required UPS and NMDA receptor activation but not CDK5. We conclude that LTP triggers a down regulation of SPAR by two complementary mechanisms, one of which has previously been described to mediate homeostatic plasticity.

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High frequency stimulation-induced dendritic calcium waves in rat hippocampal neurons

Cited by 6 publications

References 16 publications

Synapse specificity of long-term potentiation breaks down with aging

Synapse specificity of long-term potentiation breaks down with aging

Reduced Synaptic Plasticity in the Lateral Perforant Path Input to the Dentate Gyrus of Aged C57BL/6 Mice

Hippocampal LTP triggers proteasome‐mediated SPAR degradation in CA1 neurons

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