Here we address the effects of cyclothiazide (CTZ), an allosteric inhibitor of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor desensitization, on low-[Mg²⁺]-induced seizure-like events (SLEs) recorded from the CA3 pyramidal layer of juvenile rat hippocampal slices. CTZ (100 µM) made the period of tonic-like discharges (161 ± 18 % of control) and the whole SLE (151 ± 15 % of control) longer (in 7 out of 9 slices), or induced endless SLE by stabilizing clonic-like bursting (in 2 out of 9 slices). 30 µM CTZ had no significant effects on SLE dynamics (N=4), while 300 µM CTZ induced endless SLEs in 4 out of 8 slices. Co-application of CTZ (100 µM) with 100 µM GYKI 52466, the allosteric inhibitor of AMPA receptor function restrained the effects of CTZ and shortened SLEs and their tonic phases to 37 ± 4.2 % and 47 ± 4.2 % of the control, respectively. Effects of GYKI-52466 and GYKI-52466 with CTZ on SLE dynamics were indistinguishable. 50 µM 4-aminopyridine (4-AP) alone (N=5) or in combination with CTZ (N=6) transformed recurrent SLE pattern into incessant epileptiform activity with patterns distinguishable from those under 100 µM CTZ application. The effect of 4-AP may suggest a role for facilitated presynaptic glutamate release in disrupting recurrent dynamics. In contrast, the self-similar slow-down of low-[Mg²⁺]-induced SLE dynamics by CTZ indicate AMPA receptor desensitization as a parameter shaping SLEs.