Zinc (Zn²⁺) is a metal found at high concentration in the central nervous system (CNS), especially in hippocampus. In the CNS cells Zn²⁺ might produces neurotoxic or neuroprotective responses. Zn²⁺ has been implicated in the modulation of mitogen-activated protein kinases (MAPKs) and AKT pathways in models of cultured cells. MAPKs (ERK1/2, p38^MAPK and JNK) are activated by phosphorylation and may regulate gene expression, cell proliferation, apoptosis, neurotransmission and neuroplasticity. In the present work we analyzed the effects of zinc chloride (ZnCl) administered in vivo on the phosphorylation state of ERK1/2, p38^MAPK and JNK as well as on the cell viability in the hippocampus of immature rats. Rats were treated with zinc chloride (1, 2 or 4 mg/kg, i.p) or saline (NaCl 0.9%, control group) over de 8^th to 12^th postnatal day. Hippocampal slices were prepared on the 14^th day for the neurochemical analysis. Slice viability was measured by MTT reduction and MAPKs phosphorylation was measured by western blotting. All data were normalized as a percent relative to the control (considered 100%). The results showed that the zinc treatment did not modify the viability of cells, the phosphorylation of JNK and the level of all MAPKs in hippocampal slices. However, phosphorylation of ERK1, ERK2 and p38^MAPK was significantly increased at 115%, 85% and 35%, respectively, by ZnCl (4 mg/Kg) treatment. The results suggest that hippocampal ERK1/2, involved in plasticity and spatial memory, and p38^MAPK involved in stress responses, may be important molecular targets for Zn²⁺ in the CNS of immature rats in a period of rapid postnatal brain growth. Supported by CNPq and PROCAD/CAPES.