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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 LTP induction in CA1 hippocampal neuorns.A: ET-1 injection sites. B: Schematic diagram showing position of stimulating and recording electrodes. Recording and stimulation sites are at a distance of 150-200 μm from the injection point. C: Sample traces showing LFP recorded in 3 of 8 channels. Scale bar: 200 ms, 0.5 mV. LTP was slightly but significantly decreased at 12 hours after ischemia (Control: 1.82±0.02 at 61-75 minutes, n = 5; 12 hours: 1.46±0.03, n = 5; P<0.001). D: LTP was completely abolished at 24 hours after ischemia (Control: 1.82±0.02 at 61-75 minutes, n = 5; 24 hours: 0.92±0.01, n = 5; P<0.001). Data represents mean±SEM. C and D share the same data of control group. Statistic differences were compared using independent-sample t-test.
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f04: Ischemia impairs LTP induction in CA1 hippocampal neuorns.A: ET-1 injection sites. B: Schematic diagram showing position of stimulating and recording electrodes. Recording and stimulation sites are at a distance of 150-200 μm from the injection point. C: Sample traces showing LFP recorded in 3 of 8 channels. Scale bar: 200 ms, 0.5 mV. LTP was slightly but significantly decreased at 12 hours after ischemia (Control: 1.82±0.02 at 61-75 minutes, n = 5; 12 hours: 1.46±0.03, n = 5; P<0.001). D: LTP was completely abolished at 24 hours after ischemia (Control: 1.82±0.02 at 61-75 minutes, n = 5; 24 hours: 0.92±0.01, n = 5; P<0.001). Data represents mean±SEM. C and D share the same data of control group. Statistic differences were compared using independent-sample t-test.

Mentions: To examine whether LTP induction, after i-LTP, upon ischemic attack is altered, we induced LTP of fEPSPs in CA1 neurons of the peri-infarct regions on acute hippocampal slices. The hippocampal slices were prepared at 12 and 24 hours after ischemia (Fig. 4A). We only selected the slices containing injection sites and set the recording and stimulation electrode at a distance of 150-200 μm from the injection point (Fig. 4B). We found that LTP induced by HFS decreased slightly, but significantly in CA1 hippocampal neurons at 12 hours after ischemia (Control: 1.82± 0.02 at 61-75 min; 12 hours: 1.46±0.03; P<0.001, Fig. 4C). At 24 hours after ischemia, LTP was totally reversed (Control: 1.82±0.02 at 61-75 min; 24 hours: 0.92±0.01; P<0.001, Fig. 4D). In addition, we also found that the maximal amplitude of excitatory postsynaptic potentials that could be achieved gradually decreased (data not shown). Further studies are necessary to examine whether it is a general phenomenon.


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 LTP induction in CA1 hippocampal neuorns.A: ET-1 injection sites. B: Schematic diagram showing position of stimulating and recording electrodes. Recording and stimulation sites are at a distance of 150-200 μm from the injection point. C: Sample traces showing LFP recorded in 3 of 8 channels. Scale bar: 200 ms, 0.5 mV. LTP was slightly but significantly decreased at 12 hours after ischemia (Control: 1.82±0.02 at 61-75 minutes, n = 5; 12 hours: 1.46±0.03, n = 5; P<0.001). D: LTP was completely abolished at 24 hours after ischemia (Control: 1.82±0.02 at 61-75 minutes, n = 5; 24 hours: 0.92±0.01, n = 5; P<0.001). Data represents mean±SEM. C and D share the same data of control group. Statistic differences were compared using independent-sample t-test.
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Related In: Results  -  Collection

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f04: Ischemia impairs LTP induction in CA1 hippocampal neuorns.A: ET-1 injection sites. B: Schematic diagram showing position of stimulating and recording electrodes. Recording and stimulation sites are at a distance of 150-200 μm from the injection point. C: Sample traces showing LFP recorded in 3 of 8 channels. Scale bar: 200 ms, 0.5 mV. LTP was slightly but significantly decreased at 12 hours after ischemia (Control: 1.82±0.02 at 61-75 minutes, n = 5; 12 hours: 1.46±0.03, n = 5; P<0.001). D: LTP was completely abolished at 24 hours after ischemia (Control: 1.82±0.02 at 61-75 minutes, n = 5; 24 hours: 0.92±0.01, n = 5; P<0.001). Data represents mean±SEM. C and D share the same data of control group. Statistic differences were compared using independent-sample t-test.
Mentions: To examine whether LTP induction, after i-LTP, upon ischemic attack is altered, we induced LTP of fEPSPs in CA1 neurons of the peri-infarct regions on acute hippocampal slices. The hippocampal slices were prepared at 12 and 24 hours after ischemia (Fig. 4A). We only selected the slices containing injection sites and set the recording and stimulation electrode at a distance of 150-200 μm from the injection point (Fig. 4B). We found that LTP induced by HFS decreased slightly, but significantly in CA1 hippocampal neurons at 12 hours after ischemia (Control: 1.82± 0.02 at 61-75 min; 12 hours: 1.46±0.03; P<0.001, Fig. 4C). At 24 hours after ischemia, LTP was totally reversed (Control: 1.82±0.02 at 61-75 min; 24 hours: 0.92±0.01; P<0.001, Fig. 4D). In addition, we also found that the maximal amplitude of excitatory postsynaptic potentials that could be achieved gradually decreased (data not shown). Further studies are necessary to examine whether it is a general phenomenon.

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