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ATP-mediated synaptic transmission and the relationship with glutamatergic neurons in hippocampus
We have reported that ATP mediates synaptic transmission in rat cultured hippocampal neurons (Jap.J.Pharmacol.,61, 67p, 1993). Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics...
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Published in: | Japanese Journal of Pharmacology 1994, Vol.64 (suppl.1), p.143-143 |
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Language: | Japanese |
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container_end_page | 143 |
container_issue | suppl.1 |
container_start_page | 143 |
container_title | Japanese Journal of Pharmacology |
container_volume | 64 |
creator | Kazuhide Inoue Ken Nakazawa Shuichi Koizumi Akira Takanaka |
description | We have reported that ATP mediates synaptic transmission in rat cultured hippocampal neurons (Jap.J.Pharmacol.,61, 67p, 1993). Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics (namely fast and slow currents). Slow currents were reversibly blocked by suramin (100μM), reactive blue 2 (100μM) and α,β-methylene ATP(100μM), all ATP receptor antagonists. Fast currents were reversibly blocked by CNQX(30μM), a non-NMDA receptor blocker. An increase of internal Ca (「Ca」i) was evoked by the application of ATP(100μM) or glutamate (10μM), and blocked by suramin or CNQX. The cells which had only ATP receptors showed great increases in 「Ca」i by the stimulation of glutamate in the absence of tetrodotoxin (TTX, 3μM). The response was blocked by suramin (100μM). These data suggest that glutamatergic neurons connect with purinergic neurons. |
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Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics (namely fast and slow currents). Slow currents were reversibly blocked by suramin (100μM), reactive blue 2 (100μM) and α,β-methylene ATP(100μM), all ATP receptor antagonists. Fast currents were reversibly blocked by CNQX(30μM), a non-NMDA receptor blocker. An increase of internal Ca (「Ca」i) was evoked by the application of ATP(100μM) or glutamate (10μM), and blocked by suramin or CNQX. The cells which had only ATP receptors showed great increases in 「Ca」i by the stimulation of glutamate in the absence of tetrodotoxin (TTX, 3μM). The response was blocked by suramin (100μM). 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Here we demonstrate two-type synaptic currents, glutamatergic and purinergic synaptic currents in the neurons, which could be distinguished by differences of decay kinetics (namely fast and slow currents). Slow currents were reversibly blocked by suramin (100μM), reactive blue 2 (100μM) and α,β-methylene ATP(100μM), all ATP receptor antagonists. Fast currents were reversibly blocked by CNQX(30μM), a non-NMDA receptor blocker. An increase of internal Ca (「Ca」i) was evoked by the application of ATP(100μM) or glutamate (10μM), and blocked by suramin or CNQX. The cells which had only ATP receptors showed great increases in 「Ca」i by the stimulation of glutamate in the absence of tetrodotoxin (TTX, 3μM). The response was blocked by suramin (100μM). These data suggest that glutamatergic neurons connect with purinergic neurons.</abstract><pub>The Japanese Pharmacological Society</pub></addata></record> |
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title | ATP-mediated synaptic transmission and the relationship with glutamatergic neurons in hippocampus |
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