Biology subjects

Chouhan, N. S.

Publications and source records attributed to Chouhan, N. S..

4 recordsLinked to original sources

bioRxiv2025

A paradoxical impact of alcohol on sleep-memory coupling

Sleep serves a fundamental role in memory consolidation, and yet it must adapt to the organisms physiological state. The latter is impacted profoundly by acute ethanol consumption, but whether intoxication affects the role of sleep in memory consolidation remains unexplored. Here, we demonstrate that acute ethanol inverts the canonical link between sleep and memory in Drosophila. Typically, satiated flies require sleep for appetitive memory consolidation, but starved flies that must forage for food switch to sleep-independent memory. Ethanol selectively impairs memory consolidation in satiated flies by causing a switch to sleep-independent memory, which then cant be supported because of ethanol-induced sedation. Under these conditions, sleep deprivation rescues memory and requires the upregulation of neuropeptide F, which signals through NPF receptors on PPL1 dopaminergic neurons. We suggest that reward-seeking behaviors, induced by starvation or ethanol, invoke sleep-independent memory. However, ethanol has a paradoxical impact, wherein it induces a switch in memory pathways but concurrently suppresses consolidation through the preferred pathway, thereby causing sleep to become detrimental for memory consolidation.

neuroscience↗

bioRxiv2023

Neuronal correlates of time integration into memories

The circadian clock affects a wide range of physiological processes. Of particular interest is the influence of the clock on memory performance, as circadian dysfunction is associated with age- and disease-related decline in memory. In various species it has been shown that memory performance is regulated by the circadian clock. However, the anatomical and functional connection of the circadian clock and memory neurons has not been described in detail so far. This study now identifies that Diuretic hormone 31 (DH31)-positive clock neurons of the DN1p cluster regulate memory performance. DH31, a functional homolog of the mammalian calcitonin gene-related peptide, plays a crucial role in this process as a clock communication signal. DH31 facilitates memory performance during the night via indirect signalling, while DH31 signals directly to the mushroom bodies restricting memory performance specifically in the evening. This pleiotropic action of DH31 suggests that the circadian clock confines memory performance to a physiological dynamic range.

neuroscience↗

bioRxiv2023

Sleep and memory consolidation are linked by RNA processing genes in the Drosophila mushroom body

Memory consolidation in Drosophila can be sleep-dependent or sleep-independent, depending on the availability of food. The anterior posterior (ap) alpha'/beta' ('/{beta}') neurons of the mushroom body (MB) are required for sleep-dependent memory consolidation in flies fed after training. These neurons are also involved in the increase of sleep after training, suggesting a coupling of sleep and memory. To better understand the mechanisms underlying sleep and memory consolidation initiation, we analyzed the transcriptome of ap '/{beta}' neurons one hour after appetitive memory conditioning. A small number of genes, enriched in RNA processing functions, were differentially expressed in flies fed after training relative to trained and starved flies or untrained flies. Knockdown of each of these differentially expressed genes in the ap '/{beta}' neurons revealed notable sleep phenotypes for Polr1F and Regnase-1, both of which decrease in expression after conditioning. Knockdown of Polr1F, a regulator of ribosome RNA transcription, in adult flies promotes sleep and increases pre-ribosome RNA expression as well as overall translation, supporting a function for Polr1F downregulation in sleep-dependent memory. Conversely, while constitutive knockdown of Regnase-1, an mRNA decay protein localized to the ribosome, reduces sleep, adult specific knockdown suggests that effects of Regnase-1 on sleep are developmental in nature. We further tested the role of each gene in memory consolidation. Knockdown of Polr1F does not affect memory, which may be expected from its downregulation during memory consolidation. Regnase-1 knockdown in ap '/{beta}' neurons impairs all memory, including short-term, implicating Regnase-1 in memory, but leaving open the question of why it is downregulated during sleep-dependent memory. Overall, our findings demonstrate that the expression of RNA processing genes is modulated during sleep-dependent memory and, in the case of Polr1F, this modulation likely contributes to increased sleep.

neuroscience↗

bioRxiv2016

Distinct cAMP signaling modalities mediate behavioral flexibility and consolidation of social status in Drosophila aggression.

Social rituals, like male-male aggression in Drosophila, are often stereotyped and the component behavioral patterns modular. The likelihood of transition from one behavioral pattern to another is malleable by experience and confers flexibility to the behavioral repertoire. Experience-dependent modification of innate aggressive behavior in flies alters fighting strategies during fights and establishes dominant-subordinate relationships. Dominance hierarchies resulting from agonistic encounters are consolidated to longer lasting social status-dependent behavioral modifications resulting in a robust loser effect.\n\nWe show that cyclic adenosine monophosphate (cAMP) dynamics regulated by the calcium/calmodulin-dependent adenylyl cyclase, Rut and the cAMP phosphodiesterase, Dnc but not the Amn gene product, in specific neuronal groups of the mushroom body and central complex, mediate behavioral plasticity necessary to establish dominant- subordinate relationships. rut and dnc mutant flies are unable to alter fighting strategies and establish dominance relationships during agonistic interactions. This real-time flexibility during a fight is independent of changes in aggression levels. Longer-term consolidation of social status in the form of a loser effect, however, requires additional Amn-dependent inputs to cAMP signaling and involves a circuit-level association between the /{beta} and {gamma} neurons of the mushroom body.\n\nOur findings implicate cAMP signaling in mediating plasticity of behavioral patterns in aggressive behavior and in the generation of a temporally stable memory trace that manifests as a loser effect.\n\nSUMMARY STATEMENTPhasic recruitment of different cAMP signaling modalities in specific neuronal groups lead to the formation of temporally distinct components of learning and memory in fly aggression.

neuroscience↗