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Hippocampal ischemia causes deficits in local field potential and synaptic plasticity.

Wang S, Zhang J, Sheng T, Lu W, Miao D - J Biomed Res (2015)

Bottom Line: We found that LTP of fEPSPs, induced by high-frequency stimulation, displayed a progressive impairment at 12 and 24 hours after ischemia.Moreover, using in vivo multi-channel recording, we found that the local field potential, which represents electrical property of cell ensembles in more restricted regions, was also dampened at these two time points.These results suggest that i-LTP elevates the induction threshold of subsequent synaptic plasticity.

View Article: PubMed Central - PubMed

Affiliation: The Research Center for Bone and Stem Cells, Department of Human Anatomy.

ABSTRACT
The long-term enhancement in glutamate receptor mediated excitatory responses has been observed in stroke model. This pathological form of plasticity, termed post-ischemic long-term potentiation (i-LTP), points to functional reorganization after stroke. Little is known, however, about whether and how this i-LTP would affect subsequent induction of synaptic plasticity. Here, we first directly confirmed that i-LTP was induced in the endothelin-1-induced ischemia model as in other in vitro models. We also demonstrated increased expression of NR2B, CaMKII and p-CaMKII, which are reminiscent of i-LTP. We further induced LTP of field excitatory postsynaptic potentials (fEPSPs) on CA1 hippocampal neurons in peri-infarct regions of the endothelin-1-induced mini-stroke model. We found that LTP of fEPSPs, induced by high-frequency stimulation, displayed a progressive impairment at 12 and 24 hours after ischemia. Moreover, using in vivo multi-channel recording, we found that the local field potential, which represents electrical property of cell ensembles in more restricted regions, was also dampened at these two time points. These results suggest that i-LTP elevates the induction threshold of subsequent synaptic plasticity. Our data helps to deepen the knowledge of meta-synaptic regulation of plasticity after focal ischemia.

No MeSH data available.


Related in: MedlinePlus

Ischemia impairs LFP in dorsal hippocampus.A: Schematic diagram showing position of rejection and 8-channel recording electrodes. Recording electrodes are surrounded with the injection point. B: Schematic pictures of 8-channel recording electrodes. C: Sample traces showing LFP recorded in 3 of 8 channels. Scale bar: 200 ms, 0.5 mV. LTP was significantly suppressed at 12 hours and 24 hours time-points after ischemia. D: Power spectral density (PSD) of LFP in A. Note the decrease in the peaks at low frequency rhythm in the PSD of LFP(At the first peak marked with red asterisk: Control: −29.54±0.24, n = 8; 12 hours: −44.01±0.48, n = 8, P<0.001 compared with control; 24 hours: −43.86±1.08, n = 8, P<0.001 compared with control; At the sencond peak marked with green asterisk: Contol: −42.08±0.33, n = 8; 12 hours: −58.95±0.96, n = 8, P<0.001 compared with control; 24 hours: −60.55±1.01, n = 8, P<0.001 compared with control). Statistic differences were compared using one-way ANOVA.
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f05: Ischemia impairs LFP in dorsal hippocampus.A: Schematic diagram showing position of rejection and 8-channel recording electrodes. Recording electrodes are surrounded with the injection point. B: Schematic pictures of 8-channel recording electrodes. C: Sample traces showing LFP recorded in 3 of 8 channels. Scale bar: 200 ms, 0.5 mV. LTP was significantly suppressed at 12 hours and 24 hours time-points after ischemia. D: Power spectral density (PSD) of LFP in A. Note the decrease in the peaks at low frequency rhythm in the PSD of LFP(At the first peak marked with red asterisk: Control: −29.54±0.24, n = 8; 12 hours: −44.01±0.48, n = 8, P<0.001 compared with control; 24 hours: −43.86±1.08, n = 8, P<0.001 compared with control; At the sencond peak marked with green asterisk: Contol: −42.08±0.33, n = 8; 12 hours: −58.95±0.96, n = 8, P<0.001 compared with control; 24 hours: −60.55±1.01, n = 8, P<0.001 compared with control). Statistic differences were compared using one-way ANOVA.

Mentions: Compared to conventional fEPSPs, LFP reflects electrical property of cell ensembles in more restricted regions. To examine possible alterations in LFP, we employed in vivo multi-channel recording to study the effect of ischemia on LFP in hippocampal CA1 pyramidal neurons. We continuously recorded LFP signals with 8-channel electrodes at different time-points after ischemia on anesthesized rats. We found that the amplitude of the LFP decreased dramatically at both 12 and 24 hours after ischemia (Fig. 5A). The power spectral density (PSD) analysis of LFP showed that the low frequency rhythms were also impaired significantly at these time points after ischemia (At the first peak: Control: −29.54±0.24; 12 hours: −44.01±0.48, P<0.001 compared with controls; 24 hours: −43.86±1.08, P<0.001 compared with controls; At the second peak: Control: −42.08±0.33; 12 hours: −58.95±0.96, P<0.001 compared with control; 24 hours: −60.55±1.01, P<0.001 compared with controls, Fig. 5B).


Hippocampal ischemia causes deficits in local field potential and synaptic plasticity.

Wang S, Zhang J, Sheng T, Lu W, Miao D - J Biomed Res (2015)

Ischemia impairs LFP in dorsal hippocampus.A: Schematic diagram showing position of rejection and 8-channel recording electrodes. Recording electrodes are surrounded with the injection point. B: Schematic pictures of 8-channel recording electrodes. C: Sample traces showing LFP recorded in 3 of 8 channels. Scale bar: 200 ms, 0.5 mV. LTP was significantly suppressed at 12 hours and 24 hours time-points after ischemia. D: Power spectral density (PSD) of LFP in A. Note the decrease in the peaks at low frequency rhythm in the PSD of LFP(At the first peak marked with red asterisk: Control: −29.54±0.24, n = 8; 12 hours: −44.01±0.48, n = 8, P<0.001 compared with control; 24 hours: −43.86±1.08, n = 8, P<0.001 compared with control; At the sencond peak marked with green asterisk: Contol: −42.08±0.33, n = 8; 12 hours: −58.95±0.96, n = 8, P<0.001 compared with control; 24 hours: −60.55±1.01, n = 8, P<0.001 compared with control). Statistic differences were compared using one-way ANOVA.
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Related In: Results  -  Collection

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f05: Ischemia impairs LFP in dorsal hippocampus.A: Schematic diagram showing position of rejection and 8-channel recording electrodes. Recording electrodes are surrounded with the injection point. B: Schematic pictures of 8-channel recording electrodes. C: Sample traces showing LFP recorded in 3 of 8 channels. Scale bar: 200 ms, 0.5 mV. LTP was significantly suppressed at 12 hours and 24 hours time-points after ischemia. D: Power spectral density (PSD) of LFP in A. Note the decrease in the peaks at low frequency rhythm in the PSD of LFP(At the first peak marked with red asterisk: Control: −29.54±0.24, n = 8; 12 hours: −44.01±0.48, n = 8, P<0.001 compared with control; 24 hours: −43.86±1.08, n = 8, P<0.001 compared with control; At the sencond peak marked with green asterisk: Contol: −42.08±0.33, n = 8; 12 hours: −58.95±0.96, n = 8, P<0.001 compared with control; 24 hours: −60.55±1.01, n = 8, P<0.001 compared with control). Statistic differences were compared using one-way ANOVA.
Mentions: Compared to conventional fEPSPs, LFP reflects electrical property of cell ensembles in more restricted regions. To examine possible alterations in LFP, we employed in vivo multi-channel recording to study the effect of ischemia on LFP in hippocampal CA1 pyramidal neurons. We continuously recorded LFP signals with 8-channel electrodes at different time-points after ischemia on anesthesized rats. We found that the amplitude of the LFP decreased dramatically at both 12 and 24 hours after ischemia (Fig. 5A). The power spectral density (PSD) analysis of LFP showed that the low frequency rhythms were also impaired significantly at these time points after ischemia (At the first peak: Control: −29.54±0.24; 12 hours: −44.01±0.48, P<0.001 compared with controls; 24 hours: −43.86±1.08, P<0.001 compared with controls; At the second peak: Control: −42.08±0.33; 12 hours: −58.95±0.96, P<0.001 compared with control; 24 hours: −60.55±1.01, P<0.001 compared with controls, Fig. 5B).

Bottom Line: We found that LTP of fEPSPs, induced by high-frequency stimulation, displayed a progressive impairment at 12 and 24 hours after ischemia.Moreover, using in vivo multi-channel recording, we found that the local field potential, which represents electrical property of cell ensembles in more restricted regions, was also dampened at these two time points.These results suggest that i-LTP elevates the induction threshold of subsequent synaptic plasticity.

View Article: PubMed Central - PubMed

Affiliation: The Research Center for Bone and Stem Cells, Department of Human Anatomy.

ABSTRACT
The long-term enhancement in glutamate receptor mediated excitatory responses has been observed in stroke model. This pathological form of plasticity, termed post-ischemic long-term potentiation (i-LTP), points to functional reorganization after stroke. Little is known, however, about whether and how this i-LTP would affect subsequent induction of synaptic plasticity. Here, we first directly confirmed that i-LTP was induced in the endothelin-1-induced ischemia model as in other in vitro models. We also demonstrated increased expression of NR2B, CaMKII and p-CaMKII, which are reminiscent of i-LTP. We further induced LTP of field excitatory postsynaptic potentials (fEPSPs) on CA1 hippocampal neurons in peri-infarct regions of the endothelin-1-induced mini-stroke model. We found that LTP of fEPSPs, induced by high-frequency stimulation, displayed a progressive impairment at 12 and 24 hours after ischemia. Moreover, using in vivo multi-channel recording, we found that the local field potential, which represents electrical property of cell ensembles in more restricted regions, was also dampened at these two time points. These results suggest that i-LTP elevates the induction threshold of subsequent synaptic plasticity. Our data helps to deepen the knowledge of meta-synaptic regulation of plasticity after focal ischemia.

No MeSH data available.


Related in: MedlinePlus