Low-voltage　fast　(LVF)　seizure-onset　is　one　of　the　two　frequently　observed　temporal　lobe　seizure-onset　patterns.　Depth　electroencephalogram　profile　analysis　illustrated　that　the　peak　amplitude　of　LVF　onset　was　deep　temporal　areas,　e.g.,　hippocampus.　However,　the　specific　dynamic　transition　mechanisms　between　normal　hippocampal　rhythmic　activity　and　LVF　seizure-onset　remain　unclear.　Recently,　the　optogenetic　approach　to　gain　control　over　epileptic　hyper-excitability　both　in　vitro　and　in　vivo　has　become　a　novel　noninvasive　modulation　strategy.　Here,　we　combined　biophysical　modeling　to　study　LVF　dynamics　following　changes　in　crucial　physiological　parameters,　and　investigated　the　potential　optogenetic　intervention　mechanism　for　both　excitatory　and　inhibitory　control.　In　an　Ammon＇s　horn　3　(CA3)　biophysical　model　with　light-sensitive　protein　channelrhodopsin　2　(ChR2),　we　found　that　the　cooperative　effects　of　excessive　extracellular　potassium　concentration　of　parvalbumin-positive　(PV+)　inhibitory　interneurons　and　synaptic　links　could　induce　abundant　types　of　discharges　of　the　hippocampus,　and　lead　to　transitions　from　gamma　oscillations　to　LVF　seizure-onset.　Simulations　of　optogenetic　stimulation　revealed　that　the　LVF　seizure-onset　and　morbid　fast　spiking　could　not　be　eliminated　by　targeting　PV+　neurons,　whereas　the　epileptic　network　was　more　sensitive　to　the　excitatory　control　of　principal　neurons　with　strong　optogenetic　currents.　We　illustrate　that　in　the　epileptic　hippocampal　network,　the　trajectories　of　the　normal　and　the　seizure　state　are　in　close　vicinity　and　optogenetic　perturbations　therefore　may　result　in　transitions.　The　network　model　system　developed　in　this　study　represents　a　scientific　instrument　to　disclose　the　underlying　principles　of　LVF,　to　characterize　the　effects　of　optogenetic　neuromodulation,　and　to　guide　future　treatment　for　specific　types　of　seizures.