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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

MRI and 2,3,5-triphenyltetrazolium chloride (TTC) staining confirms the ischemic region after local endothelin-1 (ET-1) injection.A: Schematic diagram shows the site of injection. B: Methylthionine chloride solution is applied to display the accuracy of the injection site. Left, the area in the red box is the methylthionine chloride solution diffusion region, showing accurate localization of the dorsal hippocampus CA1 region; Right: another sample showing injection sites in magnified image. The line indicates the pyramidal cell layer in CA1 region. C: Sequential brain T2-w MRI in rats with ischemic lesion. The image in the red box and the magnified image shown underneath indicate the infarct regions. D: A series of brain slices stained with TTC after ischemic lesion. Pale staining in the black box and the magnified image shown underneath indicates the infarct region. C and D also show progressive increase of the infarct regions.
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f01: MRI and 2,3,5-triphenyltetrazolium chloride (TTC) staining confirms the ischemic region after local endothelin-1 (ET-1) injection.A: Schematic diagram shows the site of injection. B: Methylthionine chloride solution is applied to display the accuracy of the injection site. Left, the area in the red box is the methylthionine chloride solution diffusion region, showing accurate localization of the dorsal hippocampus CA1 region; Right: another sample showing injection sites in magnified image. The line indicates the pyramidal cell layer in CA1 region. C: Sequential brain T2-w MRI in rats with ischemic lesion. The image in the red box and the magnified image shown underneath indicate the infarct regions. D: A series of brain slices stained with TTC after ischemic lesion. Pale staining in the black box and the magnified image shown underneath indicates the infarct region. C and D also show progressive increase of the infarct regions.

Mentions: We first stereotaxically infused ET-1 with middle concentration and volume (15 pmol, 0.8 µL dissolved in sterile saline) into the CA1 region of the dorsal hippocampus to establish mini-stroke model (Fig. 1A)[12]. The location of ET-1 injection sites was then confirmed (Fig. 1B) by application of methylthionine chloride solution. We also used the MRI and TTC to examine and confirm the establishment of the mini-stroke model. We found that the region subjecting to ischemic attack was progressively enlarging. At 6 hours post-ischemia, the ischemic region was just around the injection site; 12 hours post-ischemia, the infarct region was slightly increased as indicated by MRI and TTC staining. At 24 hours post-ischemia, the infarct region significantly increased in both MRI and TTC staining experiments (Figs. 1C, 1D).


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)

MRI and 2,3,5-triphenyltetrazolium chloride (TTC) staining confirms the ischemic region after local endothelin-1 (ET-1) injection.A: Schematic diagram shows the site of injection. B: Methylthionine chloride solution is applied to display the accuracy of the injection site. Left, the area in the red box is the methylthionine chloride solution diffusion region, showing accurate localization of the dorsal hippocampus CA1 region; Right: another sample showing injection sites in magnified image. The line indicates the pyramidal cell layer in CA1 region. C: Sequential brain T2-w MRI in rats with ischemic lesion. The image in the red box and the magnified image shown underneath indicate the infarct regions. D: A series of brain slices stained with TTC after ischemic lesion. Pale staining in the black box and the magnified image shown underneath indicates the infarct region. C and D also show progressive increase of the infarct regions.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4585431&req=5

f01: MRI and 2,3,5-triphenyltetrazolium chloride (TTC) staining confirms the ischemic region after local endothelin-1 (ET-1) injection.A: Schematic diagram shows the site of injection. B: Methylthionine chloride solution is applied to display the accuracy of the injection site. Left, the area in the red box is the methylthionine chloride solution diffusion region, showing accurate localization of the dorsal hippocampus CA1 region; Right: another sample showing injection sites in magnified image. The line indicates the pyramidal cell layer in CA1 region. C: Sequential brain T2-w MRI in rats with ischemic lesion. The image in the red box and the magnified image shown underneath indicate the infarct regions. D: A series of brain slices stained with TTC after ischemic lesion. Pale staining in the black box and the magnified image shown underneath indicates the infarct region. C and D also show progressive increase of the infarct regions.
Mentions: We first stereotaxically infused ET-1 with middle concentration and volume (15 pmol, 0.8 µL dissolved in sterile saline) into the CA1 region of the dorsal hippocampus to establish mini-stroke model (Fig. 1A)[12]. The location of ET-1 injection sites was then confirmed (Fig. 1B) by application of methylthionine chloride solution. We also used the MRI and TTC to examine and confirm the establishment of the mini-stroke model. We found that the region subjecting to ischemic attack was progressively enlarging. At 6 hours post-ischemia, the ischemic region was just around the injection site; 12 hours post-ischemia, the infarct region was slightly increased as indicated by MRI and TTC staining. At 24 hours post-ischemia, the infarct region significantly increased in both MRI and TTC staining experiments (Figs. 1C, 1D).

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