ArticleEndocrinology2015
Hindbrain Catecholamine Neurons Activate Orexin Neurons During Systemic Glucoprivation in Male Rats.
Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Repeated chemogenetic activation of C1 catecholamine neurons reduces subsequent glucoprivic responses and mimics HAAF.Endocrinology · 2026Article
- The hindbrain-hypothalamic noradrenergic pathway controls homeostatic food intake but not cue-induced appetitive behaviors.Journal of neuroendocrinology · 2026Article
- CCK-sensitive C fibers activate NTS leptin receptor-expressing neurons via NMDA receptors.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Lesion of NPY Receptor-expressing Neurons in Perifornical Lateral Hypothalamus Attenuates Glucoprivic Feeding.Endocrinology · 2024Article
- Chemogenetic activation of ventral medullary astrocytes enhances feeding and corticosterone release in response to mild glucoprivation.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Nucleus of the solitary tract A2 neurons control feeding behaviors via projections to the paraventricular hypothalamus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Article
- Paraventricular nucleus-Medullary interactions: How they help enable endocrine responses to metabolic stress.Current opinion in endocrine and metabolic research · 2022Article
- The physiological control of eating: signals, neurons, and networks.Physiological reviews · 2022 · on this mapArticle
- Article
- Central nervous system regulation of organismal energy and glucose homeostasis.Nature metabolism · 2021Review
- Insulin actions on hypothalamic glucose-sensing neurones.Journal of neuroendocrinology · 2021Review
- Repeated Pharmacogenetic Catecholamine Neuron Activation in the Ventrolateral Medulla Attenuates Subsequent Glucoregulatory Responses.Diabetes · 2020Article
- NTS Catecholamine Neurons Mediate Hypoglycemic Hunger via Medial Hypothalamic Feeding Pathways.Cell metabolism · 2020Article
- Evidence that hindbrain astrocytes in the rat detect low glucose with a glucose transporter 2-phospholipase C-calcium release mechanism.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Ventromedial hypothalamus glucose-inhibited neurones: A role in glucose and energy homeostasis?Journal of neuroendocrinology · 2020Review
- Hindbrain glucoregulatory mechanisms: Critical role of catecholamine neurons in the ventrolateral medulla.Physiology & behavior · 2019Review
- The Effects of Amphetamine and Methamphetamine on the Release of Norepinephrine, Dopamine and Acetylcholine From the Brainstem Reticular Formation.Frontiers in neuroanatomy · 2019Article
- Activation of catecholamine neurons in the ventral medulla reduces CCK-induced hypophagia and c-Fos activation in dorsal medullary catecholamine neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Response of catecholaminergic neurons in the mouse hindbrain to glucoprivic stimuli is astrocyte dependent.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hindbrain catecholamine neurons are required for elicitation of feeding responses to glucose deficit, but the forebrain circuitry required for these responses is incompletely understood. Here we examined interactions of catecholamine and orexin neurons in eliciting glucoprivic feeding. Orexin neurons, located in the perifornical lateral hypothalamus (PeFLH), are heavily innervated by hindbrain catecholamine neurons, stimulate food intake, and increase arousal and behavioral activation. Orexin neurons may therefore contribute importantly to appetitive responses, such as food seeking, during glucoprivation. Retrograde tracing results showed that nearly all innervation of the PeFLH from the hindbrain originated from catecholamine neurons and some raphe nuclei. Results also suggested that many catecholamine neurons project collaterally to the PeFLH and paraventricular hypothalamic nucleus. Systemic administration of the antiglycolytic agent, 2-deoxy-D-glucose, increased food intake and c-Fos expression in orexin neurons. Both responses were eliminated by a lesion of catecholamine neurons innervating orexin neurons using the retrogradely transported immunotoxin, anti-dopamine-β-hydroxylase saporin, which is specifically internalized by dopamine-β-hydroxylase-expressing catecholamine neurons. Using designer receptors exclusively activated by designer drugs in transgenic rats expressing Cre recombinase under the control of tyrosine hydroxylase promoter, catecholamine neurons in cell groups A1 and C1 of the ventrolateral medulla were activated selectively by peripheral injection of clozapine-N-oxide. Clozapine-N-oxide injection increased food intake and c-Fos expression in PeFLH orexin neurons as well as in paraventricular hypothalamic nucleus neurons. In summary, catecholamine neurons are required for the activation of orexin neurons during glucoprivation. Activation of orexin neurons may contribute to appetitive responses required for glucoprivic feeding.
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