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Paternal nicotine enhances fear memory, reduces nicotine administration and alters hippocampal genetic and neural function in offspring

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series

INSTRUMENT(S): Illumina HiSeq 2500 (Mus musculus)

SUBMITTER: Lisa Goldberg

PROVIDER: GSE140905 | GEO | 2019-11-25

REPOSITORIES: GEO

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Paternal nicotine enhances fear memory, reduces nicotine administration and alters hippocampal genetic and neural function in offspring [Bisulfite-seq]

Project description:We tested the effects of chronic paternal nicotine exposure in C57BL6/J mice on hippocampal DNA methylation in F1 offspring. Overall design: Examination of differential DNA methylation in the hippocampus of offspring from males treated chronically with nicotine or males treated chronically with saline.

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Paternal nicotine enhances fear memory, reduces nicotine administration and alters hippocampal genetic and neural function in offspring [RNA-seq]

Project description:We tested the effects of chronic paternal nicotine exposure in C57BL6/J mice on hippocampal RNA expression in F1 offspring. Overall design: Examination of differential gene expression in the hippocampus of offspring from males treated chronically with nicotine or males treated chronically with saline.

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Paternal nicotine enhances fear memory, reduces nicotine administration and alters hippocampal genetic and neural function in offspring

Project description:Paternal nicotine enhances fear memory, reduces nicotine administration and alters hippocampal genetic and neural function in offspring

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Paternal nicotine enhances fear memory, reduces nicotine administration and alters hippocampal genetic and neural function in offspring [RNA-seq]

Project description:Paternal nicotine enhances fear memory, reduces nicotine administration and alters hippocampal genetic and neural function in offspring [RNA-seq]

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Paternal nicotine enhances fear memory, reduces nicotine administration and alters hippocampal genetic and neural function in offspring [Bisulfite-seq]

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Paternal nicotine exposure alters hepatic xenobiotic metabolism in offspring.

Project description:Paternal environmental conditions can influence phenotypes in future generations, but it is unclear whether offspring phenotypes represent specific responses to particular aspects of the paternal exposure history, or a generic response to paternal 'quality of life'. Here, we establish a paternal effect model based on nicotine exposure in mice, enabling pharmacological interrogation of the specificity of the offspring response. Paternal exposure to nicotine prior to reproduction induced a broad protective response to multiple xenobiotics in male offspring. This effect manifested as increased survival following injection of toxic levels of either nicotine or cocaine, accompanied by hepatic upregulation of xenobiotic processing genes, and enhanced drug clearance. Surprisingly, this protective effect could also be induced by a nicotinic receptor antagonist, suggesting that xenobiotic exposure, rather than nicotinic receptor signaling, is responsible for programming offspring drug resistance. Thus, paternal drug exposure induces a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotics.

2017-01-01 | S-EPMC5340528 | BioStudies

Paternal nicotine exposure alters hepatic xenobiotic metabolism in offspring

Project description:Although it is increasingly accepted that some paternal environmental conditions can influence phenotypes in future generations, it remains unclear whether phenotypes induced in offspring represent specific responses to particular aspects of the paternal exposure history, or whether they represent a more generic response to paternal “quality of life”. To establish a paternal effect model based on a specific ligand-receptor interaction and thereby enable pharmacological interrogation of the offspring phenotype, we explored the effects of paternal nicotine administration on offspring phenotype in mouse. We show that paternal exposure to chronic nicotine induced a broad protective response to xenobiotic exposure in the next generation. This effect manifested as increased survival following an injection of toxic levels of nicotine, was specific to male offspring, and was only observed after these offspring were first acclimated to low levels of nicotine for a week. Importantly, offspring xenobiotic resistance was documented not only for toxic nicotine challenge, but also for toxic cocaine challenge, indicating that paternal nicotine exposure reprograms offspring to become broadly resistant to environmental toxins. Mechanistically, the reprogrammed state was characterized by enhanced clearance of nicotine in drug-acclimated animals, and we found that isolated hepatocytes displayed upregulation of enzymes that metabolize xenobiotics. Taken together, our data show that paternal nicotine exposure induces a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotics in the environment. Overall design: Hepatocytes were isolated from eight week-old male F1 animals from control (TA) and nicotine-exposed fathers, 4 biological replicates each.

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Hippocampal Processing of Ambiguity Enhances Fear Memory.

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Hippocampal Administration of Levothyroxine Impairs Contextual Fear Memory Consolidation in Rats.

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2017-01-01 | S-EPMC5534464 | BioStudies

Paternal Age Alters Social Development in Offspring.

Project description:Advanced paternal age (APA) at conception has been linked with autism and schizophrenia in offspring, neurodevelopmental disorders that affect social functioning. The current study explored the effects of paternal age on social development in the general population.We used multilevel growth modeling to investigate APA effects on socioemotional development from early childhood until adolescence, as measured by the Strengths and Difficulties Questionnaire (SDQ) in the Twins Early Development Study (TEDS) sample. We also investigated genetic and environmental underpinnings of the paternal age effects on development, using the Additive genetics, Common environment, unique Environment (ACE) and gene-environment (GxE) models.In the general population, both very young and advanced paternal ages were associated with altered trajectory of social development (intercept: p = .01; slope: p = .03). No other behavioral domain was affected by either young or advanced age at fatherhood, suggesting specificity of paternal age effects. Increased importance of genetic factors in social development was recorded in the offspring of older but not very young fathers, suggesting distinct underpinnings of the paternal age effects at these two extremes.Our findings highlight that the APA-related deficits that lead to autism and schizophrenia are likely continuously distributed in the population.

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