@article{20972,
  abstract     = {Small amounts of stress are thought to have beneficial effects. A new study reports a mechanism by which the psychedelic drug, psilocybin, causes acute release of stress hormones, despite its known long-term anti-anxiety effects.},
  author       = {Kücükdereli, Hakan and Douglass, Amelia May Barnett},
  issn         = {1879-0445},
  journal      = {Current Biology},
  number       = {1},
  pages        = {R27--R29},
  publisher    = {Elsevier},
  title        = {{Neuroscience: What doesn’t kill you makes you stronger}},
  doi          = {10.1016/j.cub.2025.11.056},
  volume       = {36},
  year         = {2026},
}

@article{21744,
  abstract     = {The paraventricular hypothalamus (PVH) controls behavioral and physiologic processes, including appetite, social behavior, autonomic outflow, and pituitary hormone secretion. However, molecular markers for centrally projecting PVH neuron populations remain largely undefined, and a complete census of PVH cell types has not been established. Therefore, we performed extensive single-cell/nucleus RNA sequencing to catalog PVH neuron subtypes and multiplexed error-robust fluorescence in situ hybridization (MERFISH) to map them spatially. Our spatial transcriptomic atlas resolves 26 Sim1+ and 29 GABAergic neuron populations from the PVH and surrounding areas. Additionally, projection-based profiling identified neurons that project to the parabrachial region (PB) and spinal cord, helping to determine PVH populations that regulate satiety and sympathetic nervous system activity, respectively. Notably, activation of PB-projecting PVH neurons expressing Brs3 reduces food intake, and silencing them causes obesity. Together, this atlas contributes high-resolution PVH spatial and circuit-based gene expression profiles, representing a valuable resource for the field of homeostasis.},
  author       = {Li, Yuxi and Butler, Trevor C. and Nardone, Stefano and Jacobs, Christopher L. and Douglass, Amelia May Barnett and Madara, Joseph C. and McDonough, Miriam C. and Tao, Jenkang and Lowenstein, Elijah D. and Wang, Luhong and Pant, Deepti and Walker, Samuel J. and Wang, Annette and Srinivasan, Harini and Yang, Zongfang and Campbell, John N. and Tsai, Linus T. and Lowell, Bradford B. and Resch, Jon M.},
  issn         = {2211-1247},
  journal      = {Cell Reports},
  number       = {2},
  publisher    = {Elsevier},
  title        = {{A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic cell types}},
  doi          = {10.1016/j.celrep.2025.116904},
  volume       = {45},
  year         = {2026},
}

@article{21955,
  abstract     = {AgRP neurons cause hunger, the drive to seek and consume food. Their activation by fasting is key for survival and is thought to be triggered by feedback when energy stores are low. However, we know that environmental cues can also regulate AgRP neurons since cues that predict future food intake rapidly inhibit AgRP neurons, but is the converse true: can the prediction of future fasting rapidly activate AgRP neurons? Here, we show in mice that such rapid fasting activation of AgRP neurons does occur. This rapid activation is driven by excitatory input from paraventricular hypothalamic (PVH) neurons expressing Sim2, which are bidirectionally sensitive to predictions of future energy state. Thus, cognitively processed contextual information conveyed by PVHSim2 neurons strongly activates AgRP neurons. Lastly, chronic silencing of PVHSim2 neurons causes persistent hypophagia. This PVHSim2-to-AgRP-neuron circuit, by anticipating and preventing negative energy balance, provides an important new dimension of hunger regulation.},
  author       = {Walker, Samuel J. and Lowenstein, Elijah D. and Douglass, Amelia May Barnett and Thomas, Callum M.P. and Madara, Joseph C. and Kucukdereli, Hakan and Barbosa-Meillon, Eunice A. and Tao, Jenkang and Resch, Jon M. and Lowell, Bradford B.},
  issn         = { 1097-4199},
  journal      = {Neuron},
  keywords     = {hunger, hypothalamus, AGRP neurons, neuroscience, metabolism, homeostasis, feeding, food intake, energy balance, appetite},
  publisher    = {Elsevier},
  title        = {{A hypothalamic circuit for anticipating future changes in energy balance}},
  doi          = {10.1016/j.neuron.2026.05.010},
  year         = {2026},
}

@article{19470,
  abstract     = {When food is freely available, eating occurs without energy deficit. While agouti-related peptide (AgRP) neurons are likely involved, their activation is thought to require negative energy balance. To investigate this, we implemented long-term, continuous in vivo fiber-photometry recordings in mice. We discovered new forms of AgRP neuron regulation, including fast pre-ingestive decreases in activity and unexpectedly rapid activation by fasting. Furthermore, AgRP neuron activity has a circadian rhythm that peaks concurrent with the daily feeding onset. Importantly, this rhythm persists when nutrition is provided via constant-rate gastric infusions. Hence, it is not secondary to a circadian feeding rhythm. The AgRP neuron rhythm is driven by the circadian clock, the suprachiasmatic nucleus (SCN), as SCN ablation abolishes the circadian rhythm in AgRP neuron activity and feeding. The SCN activates AgRP neurons via excitatory afferents from thyrotrophin-releasing hormone-expressing neurons in the dorsomedial hypothalamus (DMHTrh neurons) to drive daily feeding rhythms.},
  author       = {Douglass, Amelia May Barnett and Kucukdereli, Hakan and Madara, Joseph C. and Wang, Daqing and Wu, Chen and Lowenstein, Elijah D. and Tao, Jenkang and Lowell, Bradford B.},
  issn         = {1550-4131},
  journal      = {Cell Metabolism},
  number       = {3},
  pages        = {708--722.e5},
  publisher    = {Elsevier},
  title        = {{Acute and circadian feedforward regulation of agouti-related peptide hunger neurons}},
  doi          = {10.1016/j.cmet.2024.11.009},
  volume       = {37},
  year         = {2024},
}

@article{19471,
  abstract     = {Fasting initiates a multitude of adaptations to allow survival. Activation of the hypothalamic–pituitary–adrenal (HPA) axis and subsequent release of glucocorticoid hormones is a key response that mobilizes fuel stores to meet energy demands1,2,3,4,5. Despite the importance of the HPA axis response, the neural mechanisms that drive its activation during energy deficit are unknown. Here, we show that fasting-activated hypothalamic agouti-related peptide (AgRP)-expressing neurons trigger and are essential for fasting-induced HPA axis activation. AgRP neurons do so through projections to the paraventricular hypothalamus (PVH), where, in a mechanism not previously described for AgRP neurons, they presynaptically inhibit the terminals of tonically active GABAergic afferents from the bed nucleus of the stria terminalis (BNST) that otherwise restrain activity of corticotrophin-releasing hormone (CRH)-expressing neurons. This disinhibition of PVHCrh neurons requires γ-aminobutyric acid (GABA)/GABA-B receptor signalling and potently activates the HPA axis. Notably, stimulation of the HPA axis by AgRP neurons is independent of their induction of hunger, showing that these canonical ‘hunger neurons’ drive many distinctly different adaptations to the fasted state. Together, our findings identify the neural basis for fasting-induced HPA axis activation and uncover a unique means by which AgRP neurons activate downstream neurons: through presynaptic inhibition of GABAergic afferents. Given the potency of this disinhibition of tonically active BNST afferents, other activators of the HPA axis, such as psychological stress, may also work by reducing BNST inhibitory tone onto PVHCrh neurons.},
  author       = {Douglass, Amelia May Barnett and Resch, Jon M. and Madara, Joseph C. and Kucukdereli, Hakan and Yizhar, Ofer and Grama, Abhinav and Yamagata, Masahito and Yang, Zongfang and Lowell, Bradford B.},
  issn         = {1476-4687},
  journal      = {Nature},
  number       = {7972},
  pages        = {154--162},
  publisher    = {Springer Nature},
  title        = {{Neural basis for fasting activation of the hypothalamic–pituitary–adrenal axis}},
  doi          = {10.1038/s41586-023-06358-0},
  volume       = {620},
  year         = {2023},
}

@article{19472,
  abstract     = {The forebrain hemispheres are predominantly separated during embryogenesis by the interhemispheric fissure (IHF). Radial astroglia remodel the IHF to form a continuous substrate between the hemispheres for midline crossing of the corpus callosum (CC) and hippocampal commissure (HC). Deleted in colorectal carcinoma (DCC) and netrin 1 (NTN1) are molecules that have an evolutionarily conserved function in commissural axon guidance. The CC and HC are absent in <jats:italic>Dcc</jats:italic> and <jats:italic>Ntn1</jats:italic> knockout mice, while other commissures are only partially affected, suggesting an additional aetiology in forebrain commissure formation. Here, we find that these molecules play a critical role in regulating astroglial development and IHF remodelling during CC and HC formation. Human subjects with <jats:italic>DCC</jats:italic> mutations display disrupted IHF remodelling associated with CC and HC malformations. Thus, axon guidance molecules such as DCC and NTN1 first regulate the formation of a midline substrate for dorsal commissures prior to their role in regulating axonal growth and guidance across it.},
  author       = {Morcom, Laura and Gobius, Ilan and Marsh, Ashley PL and Suárez, Rodrigo and Lim, Jonathan WC and Bridges, Caitlin and Ye, Yunan and Fenlon, Laura R and Zagar, Yvrick and Douglass, Amelia May Barnett and Donahoo, Amber-Lee S and Fothergill, Thomas and Shaikh, Samreen and Kozulin, Peter and Edwards, Timothy J and Cooper, Helen M and Sherr, Elliott H and Chédotal, Alain and Leventer, Richard J and Lockhart, Paul J and Richards, Linda J},
  issn         = {2050-084X},
  journal      = {eLife},
  publisher    = {eLife Sciences Publications},
  title        = {{DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation}},
  doi          = {10.7554/elife.61769},
  volume       = {10},
  year         = {2021},
}

@article{19473,
  abstract     = {Leptin informs the brain about sufficiency of fuel stores. When insufficient, leptin levels fall, triggering compensatory increases in appetite. Falling leptin is first sensed by hypothalamic neurons, which then initiate adaptive responses. With regard to hunger, it is thought that leptin-sensing neurons work entirely via circuits within the central nervous system (CNS). Very unexpectedly, however, we now show this is not the case. Instead, stimulation of hunger requires an intervening endocrine step, namely activation of the hypothalamic–pituitary–adrenocortical (HPA) axis. Increased corticosterone then activates AgRP neurons to fully increase hunger. Importantly, this is true for 2 forms of low leptin-induced hunger, fasting and poorly controlled type 1 diabetes. Hypoglycemia, which also stimulates hunger by activating CNS neurons, albeit independently of leptin, similarly recruits and requires this pathway by which HPA axis activity stimulates AgRP neurons. Thus, HPA axis regulation of AgRP neurons is a previously underappreciated step in homeostatic regulation of hunger.},
  author       = {Perry, Rachel J. and Resch, Jon M. and Douglass, Amelia May Barnett and Madara, Joseph C. and Rabin-Court, Aviva and Kucukdereli, Hakan and Wu, Chen and Song, Joongyu D. and Lowell, Bradford B. and Shulman, Gerald I.},
  issn         = {1091-6490},
  journal      = {Proceedings of the National Academy of Sciences},
  number       = {27},
  pages        = {13670--13679},
  publisher    = {National Academy of Sciences},
  title        = {{Leptin’s hunger-suppressing effects are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents}},
  doi          = {10.1073/pnas.1901795116},
  volume       = {116},
  year         = {2019},
}

@article{19474,
  abstract     = {The complex behaviors underlying reward seeking and consumption are integral to organism survival. The hypothalamus and mesolimbic dopamine system are key mediators of these behaviors, yet regulation of appetitive and consummatory behaviors outside of these regions is poorly understood. The central nucleus of the amygdala (CeA) has been implicated in feeding and reward, but the neurons and circuit mechanisms that positively regulate these behaviors remain unclear. Here, we defined the neuronal mechanisms by which CeA neurons promote food consumption. Using in vivo activity manipulations and Ca2+ imaging in mice, we found that GABAergic serotonin receptor 2a (Htr2a)-expressing CeA neurons modulate food consumption, promote positive reinforcement and are active in vivo during eating. We demonstrated electrophysiologically, anatomically and behaviorally that intra-CeA and long-range circuit mechanisms underlie these behaviors. Finally, we showed that CeAHtr2a neurons receive inputs from feeding-relevant brain regions. Our results illustrate how defined CeA neural circuits positively regulate food consumption.},
  author       = {Douglass, Amelia May Barnett and Kucukdereli, Hakan and Ponserre, Marion and Markovic, Milica and Gründemann, Jan and Strobel, Cornelia and Alcala Morales, Pilar L and Conzelmann, Karl-Klaus and Lüthi, Andreas and Klein, Rüdiger},
  issn         = {1546-1726},
  journal      = {Nature Neuroscience},
  number       = {10},
  pages        = {1384--1394},
  publisher    = {Springer Nature},
  title        = {{Central amygdala circuits modulate food consumption through a positive-valence mechanism}},
  doi          = {10.1038/nn.4623},
  volume       = {20},
  year         = {2017},
}

@article{19475,
  abstract     = {The left and right sides of the nervous system communicate via commissural axons that cross the midline during development using evolutionarily conserved molecules. These guidance cues have been particularly well studied in the mammalian spinal cord, but it remains unclear whether these guidance mechanisms for commissural axons are similar in the developing forebrain, in particular for the corpus callosum, the largest and most important commissure for cortical function. Here, we show that Netrin1 initially attracts callosal pioneering axons derived from the cingulate cortex, but surprisingly is not attractive for the neocortical callosal axons that make up the bulk of the projection. Instead, we show that Netrin-deleted in colorectal cancer signaling acts in a fundamentally different manner, to prevent the Slit2-mediated repulsion of precrossing axons thereby allowing them to approach and cross the midline. These results provide the first evidence for how callosal axons integrate multiple guidance cues to navigate the midline.},
  author       = {Fothergill, Thomas and Donahoo, Amber-Lee S. and Douglass, Amelia May Barnett and Zalucki, Oressia and Yuan, Jiajia and Shu, Tianzhi and Goodhill, Geoffrey J. and Richards, Linda J.},
  issn         = {1460-2199},
  journal      = {Cerebral Cortex},
  number       = {5},
  pages        = {1138--1151},
  publisher    = {Oxford University Press},
  title        = {{Netrin-DCC signaling regulates corpus callosum formation through attraction of pioneering axons and by modulating Slit2-mediated repulsion}},
  doi          = {10.1093/cercor/bhs395},
  volume       = {24},
  year         = {2014},
}