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Doan, T. P.

Publications and source records attributed to Doan, T. P..

2 recordsLinked to original sources

Long-range inhibitory axons from medial entorhinal cortex target lateral entorhinal neurons projecting to the hippocampus

The functionally different lateral entorhinal cortex (LEC) and medial entorhinal cortex (MEC) are strongly interconnected. The role of this interconnectivity in view of their functional differences is not known. Here we provide details on a circuit that directly connects MEC to neurons in the superficial layers of LEC. Using a combination of anatomical tracing experiments and in vitro electrophysiological recordings in the mouse, we report that axons from MEC somatostatin-expressing GABAergic neurons densely distribute in layer I of LEC, where they drive strong and near selective inhibition of principal neurons in layer IIa. This inhibitory pathway is accompanied by MEC glutamatergic axons that innervate multiple layers of LEC and preferentially synapse onto principal neurons in layers IIb and III rather than principal neurons in layer IIa. These findings indicate that excitatory and inhibitory projections from MEC may separately regulate the activity of different populations of hippocampal-projecting principal neurons in LEC.

neuroscience↗

Leptin-receptor neurons in the dorsomedial hypothalamus regulate the timing of circadian rhythms in feeding and metabolism in mice

Animal behavior and metabolism are tightly coordinated with sleep-wake cycles governed by the brain in harmony with environmental light:dark cycles. Within the brain, the dorsomedial hypothalamic nucleus (DMH) has been implicated in the integrative control of feeding, energy homeostasis, and circadian rhythms [1], but the underlying cell types are unknown. Here, we identify a role for DMH leptin receptor-expressing neurons (DMHLepR) in these effects. Using a viral approach, we show that silencing DMHLepR neurons in adult mice not only increases body weight and adiposity, but also shifts circadian rhythms in feeding and metabolism into the light-cycle. Moreover, DMHLepR silencing abolishes the normal increase in dark-cycle locomotor activity characteristic of nocturnal rodents. Furthermore, DMHLepR-silenced mice fail to entrain to a restrictive change in food availability. Together, these findings identify DMHLepR neurons as critical determinants of the daily time of feeding and associated metabolic rhythms.

neuroscience↗