Author
Listed:
- B. Sofia Beas
(Unit on the Neurobiology of Affective Memory, National Institute of Mental Health)
- Xinglong Gu
(National Institute of Dental and Craniofacial Research)
- Yan Leng
(Unit on the Neurobiology of Affective Memory, National Institute of Mental Health)
- Omar Koita
(Unit on the Neurobiology of Affective Memory, National Institute of Mental Health)
- Shakira Rodriguez-Gonzalez
(Unit on the Neurobiology of Affective Memory, National Institute of Mental Health)
- Morgan Kindel
(Unit on the Neurobiology of Affective Memory, National Institute of Mental Health)
- Bridget A. Matikainen-Ankney
(National Institute of Diabetes and Digestive and Kidney Diseases)
- Rylan S. Larsen
(Allen Institute for Brain Science)
- Alexxai V. Kravitz
(National Institute of Diabetes and Digestive and Kidney Diseases
Washington University School of Medicine)
- Mark A. Hoon
(National Institute of Dental and Craniofacial Research)
- Mario A. Penzo
(Unit on the Neurobiology of Affective Memory, National Institute of Mental Health)
Abstract
Marked deficits in glucose availability, or glucoprivation, elicit organism-wide counter-regulatory responses whose purpose is to restore glucose homeostasis. However, while catecholamine neurons of the ventrolateral medulla (VLMCA) are thought to orchestrate these responses, the circuit and cellular mechanisms underlying specific counter-regulatory responses are largely unknown. Here, we combined anatomical, imaging, optogenetic and behavioral approaches to interrogate the circuit mechanisms by which VLMCA neurons orchestrate glucoprivation-induced food seeking behavior. Using these approaches, we found that VLMCA neurons form functional connections with nucleus accumbens (NAc)-projecting neurons of the posterior portion of the paraventricular nucleus of the thalamus (pPVT). Importantly, optogenetic manipulations revealed that while activation of VLMCA projections to the pPVT was sufficient to elicit robust feeding behavior in well fed mice, inhibition of VLMCA–pPVT communication significantly impaired glucoprivation-induced feeding while leaving other major counterregulatory responses intact. Collectively our findings identify the VLMCA–pPVT–NAc pathway as a previously-neglected node selectively controlling glucoprivation-induced food seeking. Moreover, by identifying the ventrolateral medulla as a direct source of metabolic information to the midline thalamus, our results support a growing body of literature on the role of the PVT in homeostatic regulation.
Suggested Citation
B. Sofia Beas & Xinglong Gu & Yan Leng & Omar Koita & Shakira Rodriguez-Gonzalez & Morgan Kindel & Bridget A. Matikainen-Ankney & Rylan S. Larsen & Alexxai V. Kravitz & Mark A. Hoon & Mario A. Penzo, 2020.
"A ventrolateral medulla-midline thalamic circuit for hypoglycemic feeding,"
Nature Communications, Nature, vol. 11(1), pages 1-13, December.
Handle:
RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19980-7
DOI: 10.1038/s41467-020-19980-7
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Cited by:
- Kelsey M. Vollmer & Lisa M. Green & Roger I. Grant & Kion T. Winston & Elizabeth M. Doncheck & Christopher W. Bowen & Jacqueline E. Paniccia & Rachel E. Clarke & Annika Tiller & Preston N. Siegler & B, 2022.
"An opioid-gated thalamoaccumbal circuit for the suppression of reward seeking in mice,"
Nature Communications, Nature, vol. 13(1), pages 1-16, December.
- Nilufer Sayar-Atasoy & Connor Laule & Iltan Aklan & Hyojin Kim & Yavuz Yavuz & Tayfun Ates & Ilknur Coban & Fulya Koksalar-Alkan & Jacob Rysted & Debbie Davis & Uday Singh & Muhammed Ikbal Alp & Bayra, 2023.
"Adrenergic modulation of melanocortin pathway by hunger signals,"
Nature Communications, Nature, vol. 14(1), pages 1-15, December.
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