Though it was previously thought that the birth of new neurons stopped after development, we now know that neurogenesis continues throughout life in some areas of the brain (i.e. the olfactory bulb and the dentate gyrus of the hippocampus). Learning, in particular, has been shown to facilitate the survival of newborn neurons in the dentate gyrus. The endocannabinoid system, famous for its activation by the illicit drug cannabis (marijuana), is known to play a role in learning as well as both developmental and normal adult hippocampal neurogenesis. This study aimed to test whether the role of the endocannabinoid system extends to the specific neuronal survival that is induced by learning. Fifteen male Long-Evans rats were injected with bromodeoxyuridine (a marker for newborn cells; BrdU), implanted with hippocampal injection cannulae, and trained on a hippocampal-dependent odor discrimination learning task while being infused with either rimonabant, which effectively blocks the endocannabinoid system, vehicle (DMSO), or saline control. After the rats were sacrificed, brains were removed and newborn cells were visualized using immunohistochemical labeling of BrdU. Our behavioral results show that rimonabant rats tend to learn slower than saline control rats but no slower than the DMSO vehicle controls. This may imply that our vehicle impairs learning such that any effect of the CB1 antagonist cannot be distinguished. Though there were not enough subjects for formal statistical tests, preliminary histology data shows that vehicle, rimonabant, and saline rats have the most to least new cells numerically. It turns out that DMSO can cause neural damage and therefore may have led to gliosis and resulted in inflated cell counts. Future studies should continue to explore the questions of this study using a different vehicle, a larger sample size, and fluorescent double-labelling for neurons.