Animal studies have shown that prenatal stress is able to induce long-lasting neurobiological and behavioral alterations in adult offspring. In spite of the facts that hippocampus is sensitive to early developmental influences and its known functional importance in learning and memory, few data are available on the effect of prenatal stress on the structure of hippocampus. Therefore, this study was carried out to evaluate the effect of repeated restraint stress during prenatal period on the total number and individual volume of neurons in granular and pyramidal layers in male adult rat. For this purpose, pregnant Wistar rats were randomly divided into two groups, stressed (n= 9) and non-stressed (n = 8). Pregnant dams in the stress group were placed in a Plexiglas restraint tube for 1 h/day from days 15-21 of gestation. Control rats were left undisturbed in their home cages. Then, 2-months old male offspring were anesthetized and transcardially perfused. The brains were removed and divided into hemispheres. One hemisphere was selected at random for estimating number of neurons and the other for estimating volume of individual neurons. The total number of granular and pyramidal cells (area CA1,3) in the hippocampus was analyzed using optical fractionator. The Rotator method was applied to estimate individual volume of neurons. Prenatally stressed rats showed a decrease in the size of granular and pyramidal neurons (CA1 and CA3) as compared to their non-prenatally stressed counterparts. This study also showed that there are no significant differences in the total number of granular layer neurons, CA1 pyramidal and CA3 pyramidal neurons of prenatally stressed and control animals. These data provide a neuroanatomical basis that may be relevant to the reported disturbances in behavior and learning in prenatally stressed offspring. In this respect, previous studies demonstrated that prolonged stress reduces mRNA levels for neurotrophins in the hippocampus. It is well known that a reduction in neurotrophin level can lead to neuronal atrophy without necessarily being accompanied by neuronal loss.