The gastrointestinal (GI) tract is a diverse habitat for multiple microorganisms. Disturbances in the microbiome of the GI tract have been associated with psychiatric disorders including autism spectrum disorder (ASD). Individuals with ASD, when compared to neurotypical individuals, have demonstrated differing gut species. Also, it has been shown that microbial transplant therapies impact ASD symptoms in patients. Animal models of behaviors associated with ASD might offer insight for the actual role these microbial differences may occupy regarding symptoms. Unfortunately, ASD does not have an accepted animal model where the GI alterations have been thoroughly explored. In this study, we sought to determine if the microbiome and other GI alterations were observed in two potential mouse models of social behavior deficits, the genetic BTBR T+Itpr3tf/J (BTBR) mouse strain and an environmental mouse strain consisting of offspring of valproic acid (VA) treated pregnant controls. Both mouse models have been shown to exhibit social and repetitive behaviors that are found in human ASD. Using the Illumina MiSeq, we were able to identify taxonomy associated with 16S ribosomal DNA sequences extracted from fecal matter. We were able to compare the sequencing results from the two affected strains and a control C5BL/6J mouse strain for both female and male animals using the Qiagen CLC Genomics Workbench software. Overall, microbiome composition was found to be significantly different between the male control animals (N=6) when compared to the VA (N=5; p-value=.00216; F-score 11.20904) or the BTBR (N=7; p-value=.00216; F-score 18.47839) males using a PERMANOVA analysis. This was replicated in female groups where composition significantly differed between the control (N=14) and VA (N=14; p-value=.00001; F-score 3.53307) or BTBR (N=14; p-value=.00001; F-score 11.23443) females. Additionally, short-chain fatty acid analysis using gas capillary-based chromatography was used to examine acetate, butyrate, propionate, and valerate levels in feces. Only valerate levels were significantly lower (p

TOPIC. Despite substantive advances in understanding of genetic and biochemical basis of substance abuse and addiction in the last decade, little information has been translated into alternative treatment models for the addicted patient. Rapid detox, an alternative form of detox treatment, is gaining in both acceptance and popularity. PURPOSE. To increase readers' understanding of the neurobiology of addiction and the mode of action of new detox approaches for patients addicted to opiate drugs. SOURCES. A review of the current literature pertaining to rapid detox. CONCLUSIONS. Rapid detox is a viable alternative for selected patients attempting to detox from opiate agents of abuse. Increasing knowledge of new treatment approaches allows nurses working to assist addicted patients in planning and receiving treatment based on new awareness of the neurobiology of addiction.

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A period of cell death during a critical period early in life is responsible for causing permanent structural changes to many brain areas, but it is not known whether cell death plays a role in brain organization outside of early postnatal life. Puberty is considered a second sensitive period because the brain is the target organ of gonadal hormones. This study looked at global and regional patterns of cell death during pre-puberty and puberty in the mouse brain. My findings show there is more cell death happening during pre-puberty than during puberty. Cell death does happen during puberty but at adult levels. Furthermore females at P20 have more dying cells than males globally and in the hippocampus, but no other sex differences were observed. Knocking out the Bax gene, which is important for neuronal death, had only a modest effect on cell death during pre-puberty and puberty compared to what has been shown in younger ages. My findings demonstrate that prepubertal animals have more cell death than pubertal animals. Also, since Bax gene deletion only had a modest effect on cell death, cell populations other than neurons may be dying during these periods.