Study objective was to evaluate whether seizure-inducing chemoconvulsants could induce dysregulation of non-coding RNAs (ncRNAs), similar to epileptogenic brain insults and seizures observed in-vivo.Rat primary cortical cultures were exposed to 11 chemoconvulsants (4-aminopyridine, amoxapine, bicuculline, chlorpromazine, donepezil, kainic acid, pentylenetetrazol, picrotoxin, pilocarpine HCl, SNC80, strychnine HCl) for 24 h, followed by extraction of RNA for sequencing. Salmon tool quantified ncRNAs. DESeq2 analyzed differential expressions. qPCR validations for samples exposed to amoxapine, chlorpromazine, and SNC80 were conducted on lncRNA-ENSRNOT00000076663.2 and Snora31-ENSRNOT00000080370.2. RNA-seq data from SnoRA31 mutated cortical neurons (SRA dataset: PRJNA580002) was utilized to delineate SnoRA31 dysregulation. GSEA followed by DAVID functional annotation analyzed SnoRA31 knockout genes' regulation.Altogether 4,648 different ncRNAs were dysregulated in at least one sample and the number was chemoconvulsant dependent (0 to 814; FDR<0.05). LncRNAs and snoRNAs were most dysregulated. QPCR confirmed upregulation of lncRNA-ENSRNOT00000076663.2 with amoxapine (FC=1.9, p=0.016) and chlorpromazine-treatment (FC=1.5, p=0.016). Upregulation of Snora31-ENSRNOT00000080370.2 with amoxapine (FC=3.9, p=0.016), SNC80 (FC=2.2, p=0.016) and chlorpromazine (FC=2.0, p=0.016) treatment was observed. GSEA demonstrated a reciprocal pattern where genes downregulated following Snora31 knockout displayed upregulation in our dataset coinciding with increased Snora31 expression. Snora31 co-expressed genes impact exosomes, extracellular vesicles and extracellular matrix organization.To conclude, chemoconvulsant-induced ncRNA dysregulation is compound specific. Dysregulation of snoRNAs and lncRNAs was consistent with previous studies in experimental and human epilepsy. Our findings reinforce prior research associating extracellular matrix and vesicles with epileptogenesis. Snora31 dysregulation might selectively target these pathways, suggesting its potential as a treatment target for epileptogenesis and seizures.