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Research paper thumbnail of L-PGlu-(2-propyl)-L-His-L-ProNH 2 attenuates 4-aminopyridine-induced epileptiform activity and sodium current: a possible action of new thyrotropin-releasing hormone analog for its anticonvulsant potential

Neuroscience

In the present study, mechanism of action for protective effect of NP-647 was explored by studyin... more In the present study, mechanism of action for protective effect of NP-647 was explored by studying role of NP-647 on epileptiform activity and sodium channels by using patchclamp methods. Epileptiform activity was induced in subicular pyramidal neurons of hippocampal slice of rat by perfusing 4-aminopyridine (4-AP) containing Mg ؉2 -free normal artificial cerebrospinal fluid (nACSF). Increase in mean firing frequency was observed after perfusion of 4-AP and zero Mg ؉2 (2.10؎0.47 Hz) as compared with nACSF (0.12؎0.08 Hz). A significant decrease in mean firing frequency (0.61؎0.22 Hz), mean frequency of epileptiform events (0.03؎0.02 Hz vs. 0.22؎0.05 Hz of 4-AP؉0 Mg), and average number of action potentials in paroxysmal depolarization shift-burst (2.54؎1.21 Hz vs. 8.16؎0.88 Hz of 4-AP؉0 Mg) was observed. A significant reduction in peak dV/dt (246؎19 mV ms ؊1 vs. 297؎18 mV ms ؊1 of 4-AP؉0 Mg) and increase (1.332؎0.018 ms vs. 1.292؎0.019 ms of 4-AP؉0 Mg) in time required to reach maximum depolarization were observed indicating role of sodium channels. Concentration-dependent depression of sodium current was observed after exposure to dorsal root ganglion neurons to NP-647. NP-647 at different concentrations (1, 3, and 10 M) depressed sodium current (15؎0.5%, 50؎2.6%, and 75؎0.7%, respectively). However, NP-647 did not show change in the peak sodium current in CNa18 cells. Results of present study demonstrated potential of NP-647 in the inhibition of epileptiform activity by inhibiting sodium channels indirectly.

Research paper thumbnail of L-PGlu-(2-propyl)-L-His-L-ProNH 2 attenuates 4-aminopyridine-induced epileptiform activity and sodium current: a possible action of new thyrotropin-releasing hormone analog for its anticonvulsant potential

Neuroscience

In the present study, mechanism of action for protective effect of NP-647 was explored by studyin... more In the present study, mechanism of action for protective effect of NP-647 was explored by studying role of NP-647 on epileptiform activity and sodium channels by using patchclamp methods. Epileptiform activity was induced in subicular pyramidal neurons of hippocampal slice of rat by perfusing 4-aminopyridine (4-AP) containing Mg ؉2 -free normal artificial cerebrospinal fluid (nACSF). Increase in mean firing frequency was observed after perfusion of 4-AP and zero Mg ؉2 (2.10؎0.47 Hz) as compared with nACSF (0.12؎0.08 Hz). A significant decrease in mean firing frequency (0.61؎0.22 Hz), mean frequency of epileptiform events (0.03؎0.02 Hz vs. 0.22؎0.05 Hz of 4-AP؉0 Mg), and average number of action potentials in paroxysmal depolarization shift-burst (2.54؎1.21 Hz vs. 8.16؎0.88 Hz of 4-AP؉0 Mg) was observed. A significant reduction in peak dV/dt (246؎19 mV ms ؊1 vs. 297؎18 mV ms ؊1 of 4-AP؉0 Mg) and increase (1.332؎0.018 ms vs. 1.292؎0.019 ms of 4-AP؉0 Mg) in time required to reach maximum depolarization were observed indicating role of sodium channels. Concentration-dependent depression of sodium current was observed after exposure to dorsal root ganglion neurons to NP-647. NP-647 at different concentrations (1, 3, and 10 M) depressed sodium current (15؎0.5%, 50؎2.6%, and 75؎0.7%, respectively). However, NP-647 did not show change in the peak sodium current in CNa18 cells. Results of present study demonstrated potential of NP-647 in the inhibition of epileptiform activity by inhibiting sodium channels indirectly.

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