Hippocampal LTP shifts from NMDAR dependence to mGluR/VGCC-supported mechanisms following juvenile status epilepticus in rats.
Hippocampal long-term potentiation (LTP) can persist in the chronic epileptic state, but the mechanisms supporting this residual plasticity remain poorly understood. In particular, it is unclear whether LTP retains canonical N-methyl-D-aspartate receptor (NMDAR) dependence or shifts to alternative induction mechanisms....