Abstract:
The purpose of this research study was (1) to verify whether nicotine results in the same dendritic remodeling in the dorsal striatum that has been shown to occur in the nucleus accumbens (NAcc) (Ehlinger et al., 2014) and (2) whether the use of D1-class receptor (D1DR) antagonists prior to the injection of nicotine would prevent the hypothesized dendritic remodeling. Rats were divided into four groups, each having been injected with either a D1DR antagonist (SCH23390 hydrocholride) or saline solution 20 minutes prior to the injection of either nicotine or saline solution. This treatment occurred every other day over a period of fourteen days (P28-P42). After a Golgi-Cox staining, neurons were reconstructed and three morphological parameters (length, intersections, and bifurcations) were analyzed. While neither hypothesis was supported, significant differences within the dorsal striatum were found between the neurons of the dorsomedial (DMS) and dorsolateral (DLS) regions, with neurons in the DLS having greater dendritic length. In addition, an interaction between location and nicotine treatment was found, suggesting nicotine differentially affected neurons in the DLS and DMS. Specifically, there was a tendency for nicotine to decrease dendritic length in the DMS, but increase dendritic length in the DLS. These findings suggest that the DLS and DMS act antagonistically, and that nicotine exposure could promote inflexible habit learning (e.g. addiction), which is mediated by the DLS, at the expense of DMS-mediated goal-oriented learning.
