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Bergin, P.

Publications and source records attributed to Bergin, P..

3 recordsLinked to original sources

Acquisition and extinction of drug-context memories are linked to distinct epigenetic and transcriptional mechanisms in the mouse dentate gyrus

Acquisition and extinction of drug-context associations both involve learning, yet whether extinction erases the original drug memory remains unresolved. As learning is associated with epigenetically mediated transcriptional plasticity, we asked whether acquisition-induced DNA methylation and gene expression changes are reversed by extinction, or whether extinction induces its own distinct methylation and transcriptional changes. Here, we show that both acquisition and extinction of cocaine conditioned place preference (CPP) preferentially hypomethylated cis-regulatory elements and upregulated transcription, but at largely non-overlapping genomic regions and genes in the dorsal dentate gyrus, a key region in contextual learning. In both learning paradigms, the number of differentially expressed genes was an order of magnitude smaller than those differentially methylated, highlighting the robustness of the transcriptional network to epigenetic modifications, and implicating a non-linear relationship between regulatory elements and transcription characteristic for gene regulatory networks (GRNs). Notably, animals that failed to extinguish cocaine CPP displayed attenuated DNA methylation changes and minimal transcriptional response, consistent with the stochastic output of GRNs to produce alternative outcomes across individuals. Acquisition-upregulated genes were enriched in neuronal cilium functions, consistent with the known role of primary cilia in hippocampal learning and the persistence of drug-context memories through stable axo-ciliary signaling. In contrast, extinction-upregulated genes were overrepresented in mitochondrial energy homeostasis functions, suggesting their role in meeting rapid energy demands during learning. Overall, acquisition and extinction engage fundamentally distinct molecular mechanisms, providing a potential mechanistic explanation for why drug-context memories are suppressed but not erased by extinction.

animal behavior and cognition↗

Females with epilepsy show abnormal changes to perimenstrual sensory induced long-term potentiation

IntroductionCatamenial epilepsy refers to a cyclical exacerbation of seizure frequency and/or severity linked to stages of the menstrual cycle. To investigate the contribution of underlying excitatory and inhibitory mechanisms of this exacerbation we induced and measured long-term potentiation (LTP). Oestradiol modulates primarily NMDA receptor driven excitation and would enhance visual LTP. Allopregnanolone modulates GABA receptor mediated inhibition and would suppress visual LTP. MethodA control cohort (n = 25) and a cohort with epilepsy (n = 20) were recruited. Participants took part in a visual LTP task while EEG was recorded. Three study visits were timed to capture the mid-follicular (days +5 to +8), mid-luteal (days -9 to -5) phases, as well as the hormone withdrawal in the perimenstrual phase (days -3 to +2). Blood samples confirmed session timing. Generative computational modelling of thalamocortical changes in the EEG was paired with standard evoked potential analysis. Result17 (age 26 {+/-} 9.40) participants with epilepsy, and a control cohort of 25 (age 30 {+/-} 7.06) without epilepsy completed the study. The P2 visually evoked potential (a positive-going component of the visual event related potential waveform) was significantly more enhanced by LTP induction in the mid-follicular phase than the mid-luteal or perimenstrual phases in the control cohort (F(2, 144) =11.54, p = 0.004 corrected). In contrast, in the epilepsy cohort the P2 was significantly more potentiated in the perimenstrual phase than the mid-follicular or mid-luteal phases (F(2,108) = 12.21, p = 0.005 corrected). The effect of cycle on visual LTP was robust, with only 3/17 participants with epilepsy showing highest P2 modulation in the mid-follicular phase (which is the pattern the healthy cohort showed). The computational modelling showed that in epilepsy, the perimenstrual phase was associated with a decrease in superficial pyramidal grain control as well as decreased LTP driven modulation of feed-forward superficial connections to layer 5 and layer 6 to thalamus. DiscussionOur finding of enhanced visual LTP in the luteal phase and perimenstrual phase of females with epilepsy indicates a breakthrough of glutamatergic excitation. Given the relationship between oestrogen and n-methyl-D-aspartate (NMDA) receptor dependent LTP this is plausibly NMDA receptor driven. Several thalamocortical model parameter changes observed warrant further investigation in studies stratifying participants by catamenial epilepsy type. Overall, while research into allopregnanolone and its inhibitory effects dominate perimenstrual catamenial epilepsy research, this study justifies consideration of the role of seizure exacerbating oestradiol.

neuroscience↗

A transposase-derived gene required for human brain development

DNA transposable elements and transposase-derived genes are present in most living organisms, including vertebrates, but their function is largely unknown. PiggyBac Transposable Element Derived 5 (PGBD5) is an evolutionarily conserved vertebrate DNA transposase-derived gene with retained nuclease activity in human cells. Vertebrate brain development is known to be associated with prominent neuronal cell death and DNA breaks, but their causes and functions are not well understood. Here, we show that PGBD5 contributes to normal brain development in mice and humans, where its deficiency causes disorder of intellectual disability, movement, and seizures. In mice, Pgbd5 is required for the developmental induction of post-mitotic DNA breaks and recurrent somatic genome rearrangements. In the brain cortex, loss of Pgbd5 leads to aberrant differentiation and gene expression of distinct neuronal populations, including specific types of glutamatergic neurons, which explains the features of PGBD5 deficiency in humans. Thus, PGBD5 might be a transposase-derived enzyme required for brain development in mammals. One-Sentence SummaryPiggyBac Transposable Element Derived 5 (PGBD5) is required for brain development in humans and mice through genetic and epigenetic mechanisms.

neuroscience↗