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Mahishi, D.

Publications and source records attributed to Mahishi, D..

3 recordsLinked to original sources

Molecular architecture of excitatory and inhibitory neurons in the first gustatory relay

Taste perception is a major determinant of food intake and is dynamically modulated by hunger and satiety signals across species. While the peripheral and cortical representations of taste sensory stimuli are well characterized, far less is known about how metabolic state shapes taste processing in subcortical structures such as the brainstem. The rostral nucleus of the solitary tract (rNTS) is the first central relay for gustatory input, yet how fasting remodels transcriptional programs in rNTS neurons remains poorly defined. To address this gap, we performed cell-type-specific bulk nuclear RNA sequencing of molecularly defined excitatory (Vglut2+) and inhibitory (Vgat+) rNTS neurons. We combined Cre-dependent Sun1-sfGFP nuclear tagging with fluorescence-activated nuclear sorting to profile each population in ad libitum-fed and 24-hour-fasted mice. The two populations were transcriptionally distinct and differed in their baseline complement of hunger- and metabolic-sensing genes. Fasting elicited a transcriptional response that was largely restricted to excitatory, Vglut2+, rNTS neurons, while the inhibitory population was minimally affected. In excitatory neurons, fasting reduced the expression of Gabrd, the {delta} subunit of the GABAA receptor that mediates extrasynaptic tonic inhibition, while leaving synaptic GABAA subunits and the glutamatergic or GABAergic neurotransmission machinery unchanged. RNAscope in situ hybridization confirmed Gabrd expression in Vglut2+ rNTS neurons and showed that Gabrd is also expressed in the non-Vglut2+ population; the cell-type specificity of the fasting response therefore reflects differential regulation of a shared gene rather than its restricted expression. Our results identify a cell-type-specific, state-dependent transcriptional signature in which fasting downregulates a mediator of tonic GABAergic inhibition in excitatory rNTS neurons, providing a candidate substrate for the metabolic modulation of taste processing within the brainstem. HighlightsO_LIExcitatory and inhibitory rNTS neurons are intermingled, not spatially segregated, in rNTS C_LIO_LIVglut2+ and Vgat+ rNTS nuclear transcriptomes are distinct at baseline C_LIO_LIFasting reshapes the Vglut2+ transcriptome but leaves Vgat+ neurons largely unchanged C_LIO_LIFasting downregulates Gabrd, a mediator of tonic inhibition, in Vglut2+ neurons C_LI

neuroscience↗

Long-lasting impact of starvation experience on fly activity and place preference

Animal behaviours are demonstrably governed by sensory stimulation, previous experience and internal states like hunger. With increasing hunger, priorities shift towards foraging and feeding. During foraging, flies are known to employ efficient path integration strategies. However, general long-term activity patterns for both hungry and satiated flies in conditions of foraging remain to be better understood. Similarly, little is known about how chronic contact chemosensory stimulation affects locomotion. To address these questions, we have developed a novel, simplistic fly activity tracking setup - the Panopticon. Using a 3D-printed Petri dish inset, our assay allows recording of walking behaviour, of several flies in parallel, with all arena surfaces covered by a uniform substrate layer. We tested two constellations of providing food: i) in single patches, and ii) omnipresent within the substrate layer. Fly tracking is done with FIJI, further assessment, analysis and presentation is done with a custom-built MATLAB analysis framework. We find that starvation history leads to a long-lasting reduction in locomotion, as well as a delayed place preference for food patches not driven by immediate hunger motivation.

animal behavior and cognition↗

Placental epigenetics for evaluation of fetal congenital heart defects: Ventricular septal defect (VSD)

Ventricular Septal Defect (VSD), the most common congenital heart defect, is characterized by a hole in the septum between the right and left ventricles. The pathogenesis of VSD is unknown in most clinical cases. There is a paucity of data relevant to epigenetic changes in VSD. The placenta is a fetal tissue and is a potentially useful surrogate for the evaluation of fetal organ development. To understand epigenetic mechanisms that may play a role in the development of VSD, a genome-wide DNA methylation assay of the placentas of 8 term subjects with isolated VSD and no known or suspected genetic syndromes and 10 normal controls was performed using the Illumina HumanMethylation450 BeadChip assay. The study identified a total of 80 highly accurate potential epigenomic markers in 80 genes for the detection of VSD; area under the receiver operating characteristic curve (AUC ROC) = 1.0 with significant 95% CI (FDR) p-values < 0.05. The biological processes and functions for these differentially methylated genes are known to be associated with heart development or heart disease, including cardiac ventricle development (HEY2, ISL1), heart looping (SRF), cardiac muscle cell differentiation (ACTC1, HEY2), cardiac septum development (ISL1), heart morphogenesis (SRF, HEY2, ISL1, HEYL), Notch signaling pathway (HEY2, HEYL), cardiac chamber development (ISL1), and cardiac muscle tissue development (ACTC1, ISL1). The study also identified eight microRNA genes that have the potential to be biomarkers for the early detection of VSD including miR-191, miR-548F1, miR-148A, miR-423, miR-92B, miR-611, miR-2110, and miR-548H4. To our knowledge this is the first report in which placental analysis has been used for determining the pathogenesis of and predicting CHD.

genomics↗