Synaptic zinc (Zn), a co-factor in some glutamatergic synapses, has been implicated in plasticity effects, as well as in several excitotoxic and other pathophysiological conditions. In this study, we provide information about the distribution of Zn in inferotemporal cortex, a region at the interface of the visual and hippocampal networks. In brief, we found a lateral to medial increase in Zn, where TEad, a unimodal visual area, showed low levels of Zn; TEav, intermediate levels; and perirhinal cortex, a multimodal limbic area, high levels. The distribution of parvalbumin, a calcium binding protein, showed a reverse gradient to that of Zn. The neurons of origin of the Zn+ termination were identified by making intracortical injections sodium selenite (Na2SeO3). This substance interacts with Zn to form precipitates of ZnSe and in this form is transported retrogradely to the soma. A mixed population of labeled neurons was visualized, which included Zn+ neurons in CA1 of the hippocampus and in several amygdala subnuclei. In CA1, Zn+ neurons were restricted to the upper part of stratum pyramidale. Zn is thought to contribute to activity-dependent synaptic plasticity. The specifically high level in perirhinal cortex, and its origin from neurons in CA1 and the amygdala, may relate to cellular events involved in visual long-term memory formation.