In the hippocampus, short-term exposure to ethanol (EtOH) has been shown to inhibit some functions, and nitric oxide (NO) is an important modulator of physiologic processes. In this study, investigators explored the effects of EtOH on the total number of neurons in rat CA regions and the possible neuroprotective role of NO. The role of NO in rats given EtOH was examined with the use of a nonselective inhibitor of NOS (N[G]-nitro-L-arginine methyl ester [L-NAME], D[G]-nitro-L-arginine methyl ester [D-NAME]), a central selective inhibitor of NOS (7-NI), and a donor of NO (L-arginine). Toward this end, rats were randomly divided into 6 groups: control (saline 3 g/kg intraperitoneal [ip]), ethanol (ethanol 3 g/kg ip), L-NAME (ethanol 3 g/kg ip + L-NAME 60 mg/kg ip), L-arginine (ethanol 3 g/kg ip + L-arginine 1 g/kg ip), D-NAME (ethanol 3 g/kg ip + D-NAME 60 mg/kg ip), and 7-NI (ethanol 3 g/kg ip + 7-NI 40 mg/kg ip). Blood ethanol concentrations were measured 90 min after EtOH administration. Means (value±standard deviation) of total pyramidal neuronal numbers in the right hippocampus were estimated using the optical fractionator counting method. Values were as follows: 446,558±6207, 483,517±20,311, 464,588±30,637, 479,688±10,780, 458,294±17,770, and 477,281 ±7641 in the control, ethanol, L-arginine, 7-NI, L-NAME, and D-NAME groups, respectively. No significant differences were observed between groups (P > .05). The results of the present study imply that short-term administration of EtOH does not affect total pyramidal neuronal number in the right hippocampus of the rat. Furthermore, NO does not change the effects of short-term EtOH on total pyramidal neuronal number in the right hippocampal CA regions of the rat. Additional studies are needed to clarify the role of NO and NOS inhibition in the effects associated with EtOH given on a short-term basis.