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Pattnaik, T.

Publications and source records attributed to Pattnaik, T..

3 recordsLinked to original sources

Mesolimbic dopamine signaling mediates increased hedonic feeding and food seeking in lactating mice

Lactation dramatically increases energy intake to support milk production and care for the offspring. However, the behavioral and neural circuit mechanisms driving heightened feeding during lactation remain unclear. Here, we reveal that lactation increases food-seeking behavior and enhances palatable food intake in mice. Fiber photometry recordings demonstrate increased dopamine release in the nucleus accumbens in lactating animals during feeding tasks. This elevated dopamine signaling is ultimately required for promoting both food seeking and palatable food intake during lactation as pharmacological inhibition of dopamine receptors or chemogenetic inhibition of VTA dopamine neurons both reduce food seeking and palatable food intake in lactating mice to non-lactating levels. Further, selective inhibition of dopamine receptors in the nucleus accumbens produces similar results. Together, these findings provide a circuit basis mediating elevated food seeking and palatable food intake during lactation, providing novel insights into the regulation of maternal energy balance and feeding behavior. HighlightsLactation increases food seeking and hedonic feeding in mice Mesolimbic dopamine levels are enhanced during feeding in lactating mice VTA dopamine neurons mediate increased palatable food intake and food seeking during lactation VTA-NAc dopamine transmission mediates increased food seeking and palatable food intake during lactation

neuroscience↗

Elevated activity of the mesolimbic dopamine system promotes feeding during pregnancy in mice

The pregnancy period is accompanied by increased feeding behavior to accommodate the elevated energy demands associated with fetal growth and development. However, the underlying neural circuitry and molecular mechanisms mediating increased feeding during pregnancy are largely unknown. Here, we utilize a combination of fiber photometry, chemogenetics, and mouse behavioral assays to characterize altered feeding behavior during pregnancy in mice. We uncover that pregnancy increases the activity of the mesolimbic dopamine system during both homeostatic and hedonic feeding behavior in mice. VTA dopamine neurons are ultimately required for promoting increased hedonic feeding during pregnancy as inhibition of these cells selectively reduces acute high fat diet intake in pregnant mice. Further, pregnant mice exhibit increased sensitivity to food deprivation, an effect which requires activity of the mesolimbic dopamine system. Together, these findings provide a circuit basis mediating altered hedonic feeding behavior and sensitivity to negative energy balance during pregnancy in mice. HighlightsO_LIVTA dopamine neurons show enhanced responsivity to palatable food during pregnancy C_LIO_LIVTA dopamine neurons show enhanced responsivity to negative energy balance during pregnancy C_LIO_LINucleus accumbens dopamine is increased during homeostatic and hedonic feeding in pregnant mice C_LIO_LIVTA dopamine neuron activity regulates hedonic eating and fast-induced refeeding in pregnant mice C_LI

neuroscience↗

Reduced melanocortin tone mediates increased feeding during pregnancy in mice

During pregnancy mammals increase their food intake to accommodate the elevated metabolic demands associated with fetal growth and development. However, the molecular and neural circuit mechanisms mediating increased feeding during pregnancy are largely unknown. Here, we demonstrate that arcuate nucleus agouti-related peptide (AgRP) neurons are activated and pro-opiomelanocortin (POMC) neurons are inhibited during pregnancy in mice. These changes are required for promoting hyperphagia during pregnancy as chemogenetic inhibition of AgRP neurons or activation of POMC neurons both reduced the feeding of pregnant mice to non-pregnant levels. Finally, we utilized single cell resolution spatial transcriptomics in the arcuate nucleus of non-pregnant and pregnant mice to characterize pregnancy-induced changes in the transcriptomic state of arcuate nucleus neurons, including significant changes in both AgRP and POMC neurons. Together, these findings outline a circuit mechanism mediating increased feeding during pregnancy, providing important mechanistic insights related to conditions at the intersection of reproduction and metabolism. HighlightsO_LIAgRP neuron activity is increased and POMC neuron activity is decreased in pregnant mice C_LIO_LIIncreased AgRP neuron activity and reduced POMC neuron activity is required for increased feeding during pregnancy C_LIO_LIPregnancy enhances responsivity of AgRP neurons to palatable food C_LIO_LIPregnancy drastically alters the transcriptional state of both AgRP and POMC neurons towards positive energy balance C_LI

neuroscience↗