Using a model of CPI‐induced IUGR in the fetal guinea pig, we have shown that IUGR results in a reduction in the density of SST‐IR interneurons in the cerebral cortex and hilus of the DG, but not the hippocampal SO or the striatum, without impacting CR‐IR interneurons or Ctip2‐IR excitatory pyramidal neurons; these data highlight that there is a developmental window of vulnerability for different neuronal subtypes relative to the timing of the IUGR insult. The gene discussed is CALB2; the disease is fetal growth restriction.