<p>We previously identified a set of genes with hypermethylated promoter regions that expressed reduced levels of mRNAs by next-generation sequencing in the hippocampal dentate gyrus (DG) of weaned rats [postnatal day (PND) 21] after maternal exposure to valproic acid, propylthiouracil (PTU), or glycidol, compounds that induce persistent disruption of hippocampal neurogenesis until adulthood at PND 77. The current study was performed to identify immunohistochemically available epigenetic markers of developmental neurotoxicity, focusing on neurite outgrowth and synaptic plasticity-related genes from those identified previously. After maternal PTU exposure, hypermethylation of <i>Jph3</i>, <i>Kcnj6</i>, and <i>Scn1b</i> at weaning and their persistent reduced expression until adulthood were confirmed by methylation-sensitive high-resolution melting and real-time reverse transcription PCR, respectively. Among the translated products of candidate genes, immunohistochemistry revealed decreased numbers of sodium voltage-gated channel β subunit 1 (SCN1B)⁺ DG granule cells both at weaning and in adulthood after maternal PTU exposure. Maternal or postpubertal exposure to human developmental neurotoxicants (aluminum chloride, ethanol, and lead acetate) revealed that maternal lead acetate exposure also decreased numbers of SCN1B⁺ cells at weaning. Double immunohistochemistry with granule cell lineage markers revealed that immature and mature granule cells were SCN1B⁺. In addition, expression of sodium voltage-gated channel α-subunit genes, <i>Scn1a</i> and <i>Scn8a</i>, was reduced at weaning after maternal PTU exposure. These results indicate that SCN1B levels were suppressed in postmitotic granule cells in accordance with promoter-region hypermethylation of <i>Scn1b</i>. The resulting suppressed formation of intact voltage-gated sodium channels might be related to neurotoxicant-impaired neurogenesis and suppressed synaptic plasticity of granule cells.</p>