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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

The occurrence of i-LTP in ET-1-induced mini-stroke model.A: Weak high-frequency stimulation (HFS) induced i-LTP at 3 hours after ischemia. When a weak HFS (wHFS, 1 train, consisting of 10 bursts in 100 Hz) was delivered to Schaffer fibers in control slices, no LTP was induced. In contrast, a persistenpotentiation was induced upon stimulation with wHFS in slices obtained from ET-1-treated animals (A2, Control: 1.11±0.04, P<0.001, n = 5 at 61-75 minutes; 3 hours: 1.97±0.08, P<0.001, n = 8). B: HFS faciliates LTP in ET-1-induced stroke model. Compared with normal LTP in control brain slices, LTP in ET-1-treated slices displayed LTP with enhanced potentiation magnitude (B2, Control: 1.63±0.06, P<0.001, n = 5 at 61-75 minutes; 3 hours: 2.75±0.08, P<0.001, n = 5). Data represents mean±SEM. Data represents mean±s.e.m. Statistic differences were compared using independent-sample t-test.
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f02: The occurrence of i-LTP in ET-1-induced mini-stroke model.A: Weak high-frequency stimulation (HFS) induced i-LTP at 3 hours after ischemia. When a weak HFS (wHFS, 1 train, consisting of 10 bursts in 100 Hz) was delivered to Schaffer fibers in control slices, no LTP was induced. In contrast, a persistenpotentiation was induced upon stimulation with wHFS in slices obtained from ET-1-treated animals (A2, Control: 1.11±0.04, P<0.001, n = 5 at 61-75 minutes; 3 hours: 1.97±0.08, P<0.001, n = 8). B: HFS faciliates LTP in ET-1-induced stroke model. Compared with normal LTP in control brain slices, LTP in ET-1-treated slices displayed LTP with enhanced potentiation magnitude (B2, Control: 1.63±0.06, P<0.001, n = 5 at 61-75 minutes; 3 hours: 2.75±0.08, P<0.001, n = 5). Data represents mean±SEM. Data represents mean±s.e.m. Statistic differences were compared using independent-sample t-test.

Mentions: We then examined, in the ET-1-induced ischemia model, whether i-LTP can be induced as in other in vitro models[16-17]. Three hours after ET treatment, acute hippocampal brain slices were obtained. When a weak HFS (wHFS, 1 train, consisting of 10 bursts in 100 Hz) was delivered to Schaffer fibers in control slices, no LTP was induced. In contrast, a persistent potentiation was induced upon stimulation with wHFS in slices obtained from ET-1-treated animals (Control: 1.11±0.04, P<0.001, n = 5, at 61-75 minutes; 3 hours: 1.97±0.08, P<0.001, n = 8; Fig. 2A). Consistently, compared with normal LTP in control brain slices, LTP in ET-1-treated slices displayed LTP with enhanced potentiation magnitude (Control: 1.63±0.06, P<0.001, n = 5, at 61-75 minutes; 3 hours: 2.75±0.08, P<0.001, n = 5; Fig. 2B), suggesting that LTP was facilitated in ET-1-treated stroke model. Taken together, these results confirm the occurrence of i-LTP in the ET-1-induced stroke model.


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)

The occurrence of i-LTP in ET-1-induced mini-stroke model.A: Weak high-frequency stimulation (HFS) induced i-LTP at 3 hours after ischemia. When a weak HFS (wHFS, 1 train, consisting of 10 bursts in 100 Hz) was delivered to Schaffer fibers in control slices, no LTP was induced. In contrast, a persistenpotentiation was induced upon stimulation with wHFS in slices obtained from ET-1-treated animals (A2, Control: 1.11±0.04, P<0.001, n = 5 at 61-75 minutes; 3 hours: 1.97±0.08, P<0.001, n = 8). B: HFS faciliates LTP in ET-1-induced stroke model. Compared with normal LTP in control brain slices, LTP in ET-1-treated slices displayed LTP with enhanced potentiation magnitude (B2, Control: 1.63±0.06, P<0.001, n = 5 at 61-75 minutes; 3 hours: 2.75±0.08, P<0.001, n = 5). Data represents mean±SEM. Data represents mean±s.e.m. Statistic differences were compared using independent-sample t-test.
© Copyright Policy
Related In: Results  -  Collection

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f02: The occurrence of i-LTP in ET-1-induced mini-stroke model.A: Weak high-frequency stimulation (HFS) induced i-LTP at 3 hours after ischemia. When a weak HFS (wHFS, 1 train, consisting of 10 bursts in 100 Hz) was delivered to Schaffer fibers in control slices, no LTP was induced. In contrast, a persistenpotentiation was induced upon stimulation with wHFS in slices obtained from ET-1-treated animals (A2, Control: 1.11±0.04, P<0.001, n = 5 at 61-75 minutes; 3 hours: 1.97±0.08, P<0.001, n = 8). B: HFS faciliates LTP in ET-1-induced stroke model. Compared with normal LTP in control brain slices, LTP in ET-1-treated slices displayed LTP with enhanced potentiation magnitude (B2, Control: 1.63±0.06, P<0.001, n = 5 at 61-75 minutes; 3 hours: 2.75±0.08, P<0.001, n = 5). Data represents mean±SEM. Data represents mean±s.e.m. Statistic differences were compared using independent-sample t-test.
Mentions: We then examined, in the ET-1-induced ischemia model, whether i-LTP can be induced as in other in vitro models[16-17]. Three hours after ET treatment, acute hippocampal brain slices were obtained. When a weak HFS (wHFS, 1 train, consisting of 10 bursts in 100 Hz) was delivered to Schaffer fibers in control slices, no LTP was induced. In contrast, a persistent potentiation was induced upon stimulation with wHFS in slices obtained from ET-1-treated animals (Control: 1.11±0.04, P<0.001, n = 5, at 61-75 minutes; 3 hours: 1.97±0.08, P<0.001, n = 8; Fig. 2A). Consistently, compared with normal LTP in control brain slices, LTP in ET-1-treated slices displayed LTP with enhanced potentiation magnitude (Control: 1.63±0.06, P<0.001, n = 5, at 61-75 minutes; 3 hours: 2.75±0.08, P<0.001, n = 5; Fig. 2B), suggesting that LTP was facilitated in ET-1-treated stroke model. Taken together, these results confirm the occurrence of i-LTP in the ET-1-induced stroke model.

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