The effect of cysteamine on long-term potentiation and paired-pulse stimulation in the CA1 region of hippocampal slices in rat

The effect of cysteamine, a somatostatin depletor, on synaptic plasticity induced by tetanic and paired-pulse stimulation was investigated in rat hippocampal CA1. For this purpose, hippocampal slices from saline (1 ml/kg, s.c.) and cysteamine (200 fig/kg, s.c.)-treated and intact rats were used. Population spikes were recorded following Schaffer collateral stimulation. To induce LTP, primed burst tetanic stimulation was used. Paired-pulse stimulation at IPIs of 10, 20, 60, 120, 240, 360, and 480 ms were used and then EPI and PPI of CA1 were calculated. The results showed that the amplitude of population spike (PSA) increased 5, 15, 30, and 60 min after tetanic stimulation and 60 min after primed bursts, PSA increased at all stimulus intensities for all groups. In cysteamine-treated group, the magnitude of LTP was decreased as compared to intact and saline-treated groups. In the latter group, the magnitude of LTP Increased as compared to Intact and cysteamme- treated group. At IPI of 10 ms, mean value of EPI was greater than 1 for intact group and less than 1 for saline- and cysteamine-treated groups. In cysteamine-treated group, the mean value of EPI was significantly less than intact group. At IPIs from 20 to 480 ms, mean value of EPI was greater than or equal to I for all of the groups and no significant difference was observed among them. At IPI of 10 ms, mean value of PPI was greater than I in intact group and less than I in saline- and cysteamine-treated groups. In these groups, mean value of PPI was significantly less than intact group. At IPI of 20 ms, mean value of PPI was greater than I in intact and saline-treated group and less than I in cysteamine-treated group. In the latter group, the mean value of PPI was significantly less than saline-treated and intact groups. At IPIs of 60-680 ms, mean value of PPI was greater than I in all of the groups with no significant difference among them. It is concluded that cysteamine can alter susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanic and paired-pulse paradigms.