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 journal › Journal article › Research › peer-review
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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