The N-methyl-D-aspartate (NMDA)-type glutamate receptor in the basolateral amygdala (BLA) has been implicated in activity-dependent plasticity important for cortically evoked acquisition of fear-potentiated startle response. We examined the ultrastructural immunoperoxidase labeling of the R1 subunit of the NMDA receptor in the BLA of adult rats to determine the potential cellular and subcellular sites mediating the effects generated by NMDA activation. The localization was compared with that seen in the bed nucleus of the stria terminalis (BNST), the major efferent pathway from the central nucleus of the amygdala, which has a more pronounced involvement in autonomic function. Electron microscopy established that in the BLA, 68.4% (n = 177) of the profiles showing NMDAR1-like immunoreactivity (NMDAR1-LI) were dendrites, and 19.8% were distal tips of astrocytic processes. In contrast, profiles containing NMDAR1-LI (n = 262) in the BNST were more equally distributed between dendrites (37.4%) and axons (38.2%). The subcellular localization of NMDAR1 immunoreactivity was, however, similar in both regions. Our findings provide the first ultrastructural evidence that glutamate may prominently act through NMDAR1 receptors to elicit postsynaptic actions on intrinsic neurons in the BLA and BNST. The results also indicate that, in the BLA, the NMDAR1 receptor plays an important role in astrocytic function, whereas the receptor is more preferentially a presynaptic modulator in axons which terminate in or pass through the BNST.