To localize neurotrophin binding sites within the rat dentate gyrus, the distribution of low‐affinity p75 neurotrophin receptor (p75^NTR) immunoreactivity (IR) was examined by using antiserum raised against the cytoplasmic domain of the receptor. Semiquantitative electron microscopic examination of p75^NTR‐labeled sections showed that most p75^NTR‐labeled profiles were axons and axon terminals (72% from a total of 3,975); p75^NTR‐IR was observed throughout the extent of these structures and was not limited to the plasmalemmal surface. Axons and axon terminals containing p75^NTR‐IR were distributed in approximately equal proportions across the hilus, infragranular zone, and the inner, middle, and outer molecular layers; significantly fewer p75^NTR‐labeled profiles were observed in the granule cell layer. Axon terminals containing p75^NTR‐IR, which made synapses (296 of 552), formed equal proportions of symmetric and asymmetric synapses, primarily with the shafts and spines of dendrites. The remainder of the p75^NTR‐labeled terminals apposed unlabeled somata and dendrites without forming synapses in the single sections analyzed. In addition, p75^NTR‐IR was contained within some astrocytes (17.5% of 3,975) and dendritic shafts (3%) and spines (5%). Within dendritic spines, p75^NTR‐IR was most often associated with the plasmalemmal surface near postsynaptic densities; in dendritic shafts, p75^NTR labeling was associated with microfilaments distant from the plasmalemma. Most p75^NTR‐labeled dendritic profiles were located in the molecular layer, and some originated from granule cells. Moreover, in some granule cell somata (<1% of 3,975), p75^NTR‐IR was associated with endosomes. The primary localization of p75^NTR‐IR to presynaptic structures in the dentate gyrus, presumably arising from medial septal/diagonal band neurons, agrees with previous reports. However, p75^NTR‐IR within some astrocytes, somata, and dendritic structures suggests that this receptor may also be involved in controlling local neurotrophin levels and possibly modulating the viability of local hippocampal cell populations. J. Comp. Neurol. 407:77–91, 1999. © 1999 Wiley‐Liss, Inc.