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Abstract
The tremendous public health problem created by substance use disorders (SUDs) presents a major opportunity for mouse genetics. Inbred mouse strains exhibit substantial and heritable differences in their responses to drugs of abuse (DOA) and in many of the behaviors associated with susceptibility to SUD. Therefore, genetic discoveries emerging from analysis of murine genetic models can provide critically needed insight into the neurobiological effects of DOA, and they can reveal how genetic factors affect susceptibility drug addiction. There are already indications, emerging from our prior analyses of murine genetic models of responses related to SUDs that mouse genetic models of SUD can provide actionable information, which can lead to new approaches for alleviating SUDs. Lastly, we consider the features of murine genetic models that enable causative genetic factors to be successfully identified; and the methodologies that facilitate genetic discovery.
Highlights
There are already indications, emerging from our prior analyses of murine genetic models of responses related to substance use disorder (SUD) that mouse genetic models of SUD can provide actionable information, which can lead to new approaches for alleviating SUDs
When a murine genetic model of opioidinduced hyperalgesia (OIH) was analyzed, we discovered that genetic variation within the P-glycoprotein transporter (Abcb1b) contributed to inter-strain differences in this opiate response [8]
We found that genetic variation within genes encoding the Netrin-1 receptor (Dcc) [42] and multi-PDZ-domain protein (Mpdz that encodes MUPP1) [20] contributed to inter-strain differences in the extent of tolerance, dependence and OIH that develops after repeated opiate exposure
Summary
We believe that the relationship between murine models and human diseases (or biomedical traits) resembles that between a small Cessna airplane and a large 787 jet plane. Murine Models of SUD socioeconomic and psychosocial factors have on triggering relapse This is an important limitation since human drug addiction proceeds through a three-stage cycle whose intensity increases over time, and each stage results from DOAinduced changes in brain circuits [1,2,3]. Mice provide a less optimal model for analyzing 3rd stage phenomena, which involves responses to environmental triggers and far more complex DOA-induced changes that impact a wider range of neural circuits. To fly the jet plane (i.e., develop effective prevention or treatment methods for SUDs) we must use murine genetic models of SUD to understand the underlying principles of aviation (i.e., the mechanisms mediating SUDs). We consider the features of murine models that enable causative genetic factors to be successfully identified; and the methodologies that can facilitate genetic discovery
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