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Introduction. Epilepsy is a disease characterized by an enduring predisposition to generate epileptic seizures and by the neurobiological, cognitive, psychological, and social consequences of this condition. Temporal lobe epilepsy (TLE) is the most common and often drug-resistant type of epilepsies in the adult and aging populations and has greatly diverse in etiologies and electro-clinical manifestations. Kindling through repeated brief stimulation of limbic structures has long been used as a model of TLE. While classic kindling in a few weeks does not induce spontaneous recurrent seizures (SRS), extended kindling is able to induce SRS in several animal species. The SRS induction by extended kindling is generally not associated with gross brain injury, but rather a loss of subgroups of GABAergic interneurons in the hippocampal hilar region. The lack of observed gross brain injury in extended kindled animals is different from post status epilepticus models in which SRS emergence is accompanied with pronounced brain damage. As such the extended kindling model may help explore epileptogenesis in the absence of major brain pathology as is seen in many patients with TLE. To data, there is limited insight about EEG characteristics of SRS in rodent models of extended kindling. We therefore attempted to provide more information in this area using a mouse model of extended hippocampal kindling (Song et al., 2018; Liu et al., 2019; Frontier Pharmacology). Methods. Male C57 black mice ages 11–13 months were operated to implant intracranial electrodes. Each mouse was implanted with two pairs of bipolar electrodes, one in the hippocampal CA3 for kindling stimulation and local recordings and another in contralateral/ipsilateral hippocampal CA3, dorsomedial thalamus, parietal cortex or entorhinal cortex. Hippocampal kindling (60 Hz for 2 sec) was applied twice daily, and SRS were detected by 24-hour EEG-video monitoring. Age-match mice that received similar electrode implantation and twice daily handling manipulation but not kindling were used as controls. Brain histological examinations were performed in a subset of mice to verify the location of implanted electrodes and to examine potential gross brain lesion. Results. (1) SRS were observed from 47 mice following 80–140 kindling stimulation; no spontaneous seizure was detected in 12 control mice. (2) SRS remained detectable in individual mice up to 4 months after termination of the kindling stimulation. SRS incidences varied in a range of 2–14 events per day but inter-SRS intervals were ≤2 hours for about 65% of SRS events. (3) Most of SRS were featured with EEG ictal discharges and concurrent motor seizures at the Racine scale 3–5. SRS that presented EEG ictal discharges without or with concurrent motor behaviors at the Racine scale 1–2 were also noticeable, particularly in mice with implanted electrode in the dorsomedial thalamus. (4) In ≥1500 SRS events examined, nearly all EEG ictal discharges presented low-voltage signals at onset and such ictal onset appeared to concur in the kindled CA3 and unkindled site despite the latter targeted to different brain structures. (5) CA3 and cortical EEG ictal discharges were not substantially affected by intra-peritoneal injection of lorazepam (a benzodiazepine positive GABAa receptor modulator) but concurrent severe motor seizures were greatly suppressed. Summary. We suggest that epileptogenic network activity encompassing multiple forebrain areas may be responsible for SRS initiation in the mouse model of extended hippocampal kindling. Subcortical structures involving the dorsomedial thalamic circuitry may play an important role in manifestation and/or control of severe motor seizures in this model. Support. EpLink – The Epilepsy Research Program of the Ontario Brain Institute and Natural Sciences and Engineering Research Council of Canada.