Adult neurogenesis in the dentate gyrus of the hippocampal formation occurs throughout adult life (1) and our aim was to determine whether alpha7 nicotinic receptors (α7*nAChRs) might play a role in this process. The immunocytochemical localisation of α7*nAChR subunits in the dentate gyrus was examined in conjunction with markers for immature granule cells (GCs) in Wistar rats (21 d, n=10) and heterozygous GAD67-GFP mice (21-30 d, n=5), anaesthetised with sodium pentobarbitone (100 mg kg-1, i.p.) and perfused with fixative. To label adult-born GCs, BrdU injections (100mg kg-1, i.p) were made in GAD67-GFP mice (2-10 w), which were perfused-fixed after 3 d (n=4) or 3 w (n=3) survival. A higher intensity of α7*nAChR subunit immunofluorescence was found around GCs adjacent to the germinal subgranular zone (inner GCs) than those next to the molecular layer (outer GCs), including GCs that expressed immunofluorescence for markers for immature GCs such as doublecortin and BrdU. GABAergic neurons expressed α7*nAChR subunit immunofluorescence but did not label for immature markers. To determine whether immature GCs express functional α7*nAChRs, whole cell patch clamp recordings were made from rodent hippocampal slices in conjunction with ACh puff in the presence of atropine and biocytin labelling. Wistar rats (n=24, 14-21 d), GAD67-GFP mice (n=55, 14-62 d) and wild-type mice (n=13, 21-37 d) were anaesthetized with sodium pentobarbitone (100mg kg-1, i.p.) and perfused with sucrose-rich saline prior to preparation of the slices. Most interneurons showed robust responses to ACh, and outer GCs showed no responses to ACh (n=36). A proportion (9-19%) of inner GCs expressed small responses to ACh (n=108), the proportion being higher (19%) in younger animals (2-5 w) than older animals (9%, 5-10 w, GAD67-GFP mice). ACh-responsive inner GC cells had actions potentials but displayed immature electrophysiological properties; e.g., the input resistance of these cells (970±150 MΩ) was significantly higher than that of non-responding inner GC cells (725±60 MΩ) and outer GC cells (460±60 MΩ; ANOVA, p<0.001). The responses to ACh (including those of most interneurons) were blocked by 4 nM of the α7*nAChR antagonist methyllycaconitine and potentiated by the α7*nAChR modulator PNU120596, which was ineffective on outer GCs. The responses to ACh were not blocked by NBQX (AMPA receptor antagonist), D-AP5 (NMDA receptor antagonist), or bicuculline (GABAA receptor antagonist). Although previous work had failed to find GCs with nAChRs (2), our studies suggest that certain immature GCs express α7*nAChRs, and that this fraction declines with age, in keeping with the known decrease in the rate of adult neurogenesis with age (3).