Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons

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Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons. / Kang, J.; Kang, N.; Yu, Y.; Zhang, J.; Petersen, Nicolas Caesar; Tian, G. F.; Nedergaard, M.

In: Neuroscience, Vol. 169, No. 4, 2010, p. 1601-1609.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Kang, J, Kang, N, Yu, Y, Zhang, J, Petersen, NC, Tian, GF & Nedergaard, M 2010, 'Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons', Neuroscience, vol. 169, no. 4, pp. 1601-1609. https://doi.org/10.1016/j.neuroscience.2010.06.020

APA

Kang, J., Kang, N., Yu, Y., Zhang, J., Petersen, N. C., Tian, G. F., & Nedergaard, M. (2010). Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons. Neuroscience, 169(4), 1601-1609. https://doi.org/10.1016/j.neuroscience.2010.06.020

Vancouver

Kang J, Kang N, Yu Y, Zhang J, Petersen NC, Tian GF et al. Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons. Neuroscience. 2010;169(4):1601-1609. https://doi.org/10.1016/j.neuroscience.2010.06.020

Author

Kang, J. ; Kang, N. ; Yu, Y. ; Zhang, J. ; Petersen, Nicolas Caesar ; Tian, G. F. ; Nedergaard, M. / Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons. In: Neuroscience. 2010 ; Vol. 169, No. 4. pp. 1601-1609.

Bibtex

@article{61d41550d95911df825b000ea68e967b,
title = "Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons",
abstract = "Sulforhodamine 101 (SR101) has been extensively used for investigation as a specific marker for astroglia in vivo and activity-dependent dye for monitoring regulated exocytosis. Here, we report that SR101 has bioactive effects on neuronal activity. Perfusion of slices with SR101 (1 microM) for 10 min induced long-term potentiation of intrinsic neuronal excitability (LTP-IE) and a long-lasting increase in evoked EPSCs (eEPSCs) in CA1 pyramidal neurons in hippocampal slices. The increase in intrinsic neuronal excitability was a result of negative shifts in the action potential (AP) threshold. The N-methyl D-aspartate receptor (NMDAR) antagonist, AP-5 (50 microM), blocked SR101-induced LTP-IE, but glutamate receptor blockers, AP-5 (50 microM), MCPG (200 microM), and MSOP (100 microM), only partially blocked SR101-induced potentiation of eEPSCs. SR101 induced an enhancement of evoked synaptic NMDAR currents, suggesting that SR101 enhances activation of synaptic NMDARs. SR101-induced LTP-IE and potentiation of synaptic transmission triggered spontaneous neuronal firing in slices and in vivo epileptic seizures. Our results suggest that SR101 is an epileptogenic agent that long-lastingly lowers the AP threshold to increase intrinsic neuronal excitability and enhances the synaptic efficacy to increase synaptic inputs. As such, SR101 can be used as an experimental tool to induce epileptic seizures.",
author = "J. Kang and N. Kang and Y. Yu and J. Zhang and Petersen, {Nicolas Caesar} and Tian, {G. F.} and M. Nedergaard",
note = "(c) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.",
year = "2010",
doi = "10.1016/j.neuroscience.2010.06.020",
language = "English",
volume = "169",
pages = "1601--1609",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Pergamon Press",
number = "4",

}

RIS

TY - JOUR

T1 - Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons

AU - Kang, J.

AU - Kang, N.

AU - Yu, Y.

AU - Zhang, J.

AU - Petersen, Nicolas Caesar

AU - Tian, G. F.

AU - Nedergaard, M.

N1 - (c) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.

PY - 2010

Y1 - 2010

N2 - Sulforhodamine 101 (SR101) has been extensively used for investigation as a specific marker for astroglia in vivo and activity-dependent dye for monitoring regulated exocytosis. Here, we report that SR101 has bioactive effects on neuronal activity. Perfusion of slices with SR101 (1 microM) for 10 min induced long-term potentiation of intrinsic neuronal excitability (LTP-IE) and a long-lasting increase in evoked EPSCs (eEPSCs) in CA1 pyramidal neurons in hippocampal slices. The increase in intrinsic neuronal excitability was a result of negative shifts in the action potential (AP) threshold. The N-methyl D-aspartate receptor (NMDAR) antagonist, AP-5 (50 microM), blocked SR101-induced LTP-IE, but glutamate receptor blockers, AP-5 (50 microM), MCPG (200 microM), and MSOP (100 microM), only partially blocked SR101-induced potentiation of eEPSCs. SR101 induced an enhancement of evoked synaptic NMDAR currents, suggesting that SR101 enhances activation of synaptic NMDARs. SR101-induced LTP-IE and potentiation of synaptic transmission triggered spontaneous neuronal firing in slices and in vivo epileptic seizures. Our results suggest that SR101 is an epileptogenic agent that long-lastingly lowers the AP threshold to increase intrinsic neuronal excitability and enhances the synaptic efficacy to increase synaptic inputs. As such, SR101 can be used as an experimental tool to induce epileptic seizures.

AB - Sulforhodamine 101 (SR101) has been extensively used for investigation as a specific marker for astroglia in vivo and activity-dependent dye for monitoring regulated exocytosis. Here, we report that SR101 has bioactive effects on neuronal activity. Perfusion of slices with SR101 (1 microM) for 10 min induced long-term potentiation of intrinsic neuronal excitability (LTP-IE) and a long-lasting increase in evoked EPSCs (eEPSCs) in CA1 pyramidal neurons in hippocampal slices. The increase in intrinsic neuronal excitability was a result of negative shifts in the action potential (AP) threshold. The N-methyl D-aspartate receptor (NMDAR) antagonist, AP-5 (50 microM), blocked SR101-induced LTP-IE, but glutamate receptor blockers, AP-5 (50 microM), MCPG (200 microM), and MSOP (100 microM), only partially blocked SR101-induced potentiation of eEPSCs. SR101 induced an enhancement of evoked synaptic NMDAR currents, suggesting that SR101 enhances activation of synaptic NMDARs. SR101-induced LTP-IE and potentiation of synaptic transmission triggered spontaneous neuronal firing in slices and in vivo epileptic seizures. Our results suggest that SR101 is an epileptogenic agent that long-lastingly lowers the AP threshold to increase intrinsic neuronal excitability and enhances the synaptic efficacy to increase synaptic inputs. As such, SR101 can be used as an experimental tool to induce epileptic seizures.

U2 - 10.1016/j.neuroscience.2010.06.020

DO - 10.1016/j.neuroscience.2010.06.020

M3 - Journal article

C2 - 20600669

VL - 169

SP - 1601

EP - 1609

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 4

ER -

ID: 22546968