Inhibition of noradrenergic locus coeruleus neurons by C1 adrenergic cells in the rostral ventral medulla

Aston‐Jones, Gary; Astier, Bernadette; Ennis, Matthew

doi:10.1016/0306-4522(92)90497-p

Cited by 63 publications

(27 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5) was originally thought to be inhibitory and mediated by catecholamines, but a reinvestigation of this issue with optogenetic techniques in vivo has suggested that the C1 cells actually excite the LC by releasing glutamate (2,14). We recently confirmed the monosynaptic and glutamatergic nature of this input using optogenetics in mouse brain slices (B.…”

Section: Activation Of Cns Noradrenergic Neurons By the C1 Neuronsmentioning

confidence: 85%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

248

262

View full text Add to dashboard Cite

The C1 neurons reside in the rostral and intermediate portions of the ventrolateral medulla (RVLM, IVLM). They use glutamate as a fast transmitter and synthesize catecholamines plus various neuropeptides. These neurons regulate the hypothalamic pituitary axis via direct projections to the paraventricular nucleus and regulate the autonomic nervous system via projections to sympathetic and parasympathetic preganglionic neurons. The presympathetic C1 cells, located in the RVLM, are probably organized in a roughly viscerotopic manner and most of them regulate the circulation. C1 cells are variously activated by hypoglycemia, infection or inflammation, hypoxia, nociception, and hypotension and contribute to most glucoprivic responses. C1 cells also stimulate breathing and activate brain stem noradrenergic neurons including the locus coeruleus. Based on the various effects attributed to the C1 cells, their axonal projections and what is currently known of their synaptic inputs, subsets of C1 cells appear to be differentially recruited by pain, hypoxia, infection/inflammation, hemorrhage, and hypoglycemia to produce a repertoire of stereotyped autonomic, metabolic, and neuroendocrine responses that help the organism survive physical injury and its associated cohort of acute infection, hypoxia, hypotension, and blood loss. C1 cells may also contribute to glucose and cardiovascular homeostasis in the absence of such physical stresses, and C1 cell hyperactivity may contribute to the increase in sympathetic nerve activity associated with diseases such as hypertension. C1 neurons; blood pressure; brain stem BEST KNOWN for their contribution to the control of arterial pressure (AP), the C1 neurons have also been implicated in many other physiological processes ranging from neuroendocrine responses to infection and inflammation, glucose homeostasis, reproduction, breathing, thermoregulation, hypothalamo-pituitary axis (HPA)-mediated stress responses, and food consumption. The purpose of this review is to summarize the most salient information concerning the C1 cells, to point out some of the remaining gaps in our current knowledge, and to suggest a few unifying physiological principles that could account for these seemingly disparate observations. Based on the various effects attributed to the C1 cells and what is currently known of their synaptic inputs, we propose that these neurons are, figuratively speaking, the body's "emergency medical technicians." By this we imply that these neurons produce stereotyped autonomic, metabolic, and neuroendocrine responses designed to help the organism survive major acute physical stresses such as accidental, pathological, or dive-related hypoxia or physical injury and its associated cohort of acute infection, blood loss, and hypotension. These emergency responses include, in the short term and depending on the stress, vasoconstriction, cardioinhibition, or acceleration, breathing stimulation, antidiuresis, changes in metabolism, and gastrointestinal (GI) functions designed to conserve pe...

show abstract

Section: Activation Of Cns Noradrenergic Neurons By the C1 Neuronsmentioning

confidence: 85%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

248

262

View full text Add to dashboard Cite

show abstract

“…This is supported by our finding that focal injection of yohimbine at bilateral A7 and A5 neurons produced similar beneficial effects on HM activity and obstructive apnea-induced hLTF, as did systemic yohimbine (Figure 6), suggesting that postsynaptic α 2 -adrenoceptors on the dendrites and/or cell bodies of these pontine noradrenergic neurons (rather than α 2 -autoceptors on their distal axonal terminals presynaptic to the HMs) were likely the sites of action of yohimbine therapy. Indeed, certain medullary adrenergic neurons (such as the C1 cell group) are known to be active during REM sleep and exert inhibitory influences on pontine noradrenergic neurons via α 2 -adrenoceptors (44,45), although recent studies revealed that a subset of C1 neurons may paradoxically also exert stimulation frequency-dependent excitatory influences on pontine noradrenergic neurons (46). Of note, previous studies have shown that HMs may be subject to an α 2C -adrenoceptor (but not α 2A -adrenoceptor) subtype-mediated inhibition (47,48).…”

Section: Discussionmentioning

confidence: 99%

α2-Adrenergic blockade rescues hypoglossal motor defense against obstructive sleep apnea

Song¹,

Poon²

2017

JCI Insight

View full text Add to dashboard Cite

“…First, the identity and properties of the neurons supplying EPI to the above brain regions is not yet clearly established. Second, excitation of EPI-containing neurons in the C1 area of the medulla has been found to inhibit rather than excite neuronal activity in the LC (Aston- Jones et al, 1992). Third, in the PNMT-inhibitor-treated mice ivt.…”

Section: Epi As An Endogenous Neurotransmitter At a 1 -Receptorsmentioning

confidence: 99%

Emerging Evidence for a Central Epinephrine-Innervated α1-Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression

Stone

Yang

Rosengarten

et al. 2003

Neuropsychopharmacol

View full text Add to dashboard Cite

Currently, most basic and clinical research on depression is focused on either central serotonergic, noradrenergic, or dopaminergic neurotransmission as affected by various etiological and predisposing factors. Recent evidence suggests that there is another system that consists of a subset of brain a 1B -adrenoceptors innervated primarily by brain epinephrine (EPI) that potentially modulates the above three monoamine systems in parallel and plays a critical role in depression. The present review covers the evidence for this system and includes findings that brain a 1 -adrenoceptors are instrumental in behavioral activation, are located near the major monoamine cell groups or target areas, receive EPI as their neurotransmitter, are impaired or inhibited in depressed patients or after stress in animal models, and are restored by a number of antidepressants. This 'EPI-a 1 system' may therefore represent a new target system for this disorder.

show abstract

Inhibition of noradrenergic locus coeruleus neurons by C1 adrenergic cells in the rostral ventral medulla

Cited by 63 publications

References 70 publications

C1 neurons: the body's EMTs

C1 neurons: the body's EMTs

α2-Adrenergic blockade rescues hypoglossal motor defense against obstructive sleep apnea

Emerging Evidence for a Central Epinephrine-Innervated α1-Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression

Contact Info

Product

Resources

About