A critical role for the parabrachial nucleus in generating central nervous system responses elicited by a systemic immune challenge

Buller, Kathryn M.; Allen, T. O.; Wilson, Lori D.; Munro, F. L.; Day, Trevor A.

doi:10.1016/j.jneuroim.2004.03.013

Cited by 28 publications

(23 citation statements)

References 72 publications

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“…PGE 2 presumably reaches the C1 neurons by diffusion and activates these cells via EP3 receptors (155,163). Lesions of the lateral parabrachial nuclei attenuate the activation of the A1 neurons by systemic administration of IL-1␤ but, based on Fos expression, these lesions have no effect on the activation of C1 and PVH neurons elicited by the same stimulus (26). This observation reinforces the notion that some of the C1 cells are a primary target of circulating IL-1 and that these cells rather than the A1 neurons mediate the activation of CRH-producing parvovellular PVH neurons by an immune challenge.…”

Section: Control Of the Crh-acth-corticosterone Cascade By The C1 Neumentioning

confidence: 99%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

234

262

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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...

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Section: Control Of the Crh-acth-corticosterone Cascade By The C1 Neumentioning

confidence: 99%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

234

262

View full text Add to dashboard Cite

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“…The increase in Fos expression (detection of which is used as an indicator of recent activation of neurons) that is seen following stress exposure in several forebrain limbic structures such as the medial amygdala, lateral septum, and cingulate cortex is significantly reduced in late pregnant rats (da Costa et al 1996). Brainstem A1 and A2 noradrenergic neurons in the ventrolateral medulla and nucleus tractus solitarii (NTS), respectively, are activated by physical stressors, including cytokine challenge (Ericsson et al 1994;Xu et al 1999;Buller et al 2001Buller et al , 2004. These neurons project both directly and indirectly (via the parabrachial nucleus or central nucleus of the amygdala and bed nucleus of the stria terminalis) to the PVN and provide excitatory input to the CRH neurons.…”

Section: Mechanisms Of Reduced Hpa Axis Responses To Stress In Late Pmentioning

confidence: 99%

Allopregnanolone and suppressed hypothalamo–pituitary–adrenal axis stress responses in late pregnancy in the rat

Brunton

Russell

2010

Stress

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In rats, late pregnancy is associated with suppressed hypothalamo-pituitary-adrenal (HPA) axis responses to a variety of stressful stimuli. The result is reduced corticosterone secretion following stress, which is considered to give some protection to the fetuses from adverse glucocorticoid programming and limits the catabolic effect of corticosterone, hence minimizing maternal energy expenditure. We have used a model of immune challenge in which systemic administration of the cytokine, interleukin-1β (IL-1β), allows study of the mechanisms underlying HPA axis hyporesponsiveness in late pregnancy. Suppressed responsiveness of parvocellular paraventricular nucleus (pPVN) corticotropin-releasing hormone neurons, and hence the HPA axis, following IL-1β in late pregnancy is evidently explained by presynaptic inhibition of noradrenaline release in the pPVN, owing to increased endogenous opioid peptide enkephalin production in brainstem nucleus tractus solitarii neurons. Allopregnanolone, a neurosteroid metabolite of progesterone, signals the pregnancy status of the animal to the brain and stimulates opioid production in the brainstem. In this review, we discuss the supporting evidence for these mechanisms.

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“…The functional involvement of the PMT in this cholinergicallyinduced long-term behavioral response adds a novel finding to the known behavioral and autonomic responses of this pontine region [5,26,[43][44][45]50,69,73].…”

Section: Introductionmentioning

confidence: 79%

From synapse to gene product: prolonged expression of c-fos induced by a single microinjection of carbachol in the pontomesencephalic tegmentum

Quattrochi

Bazalakova

Hobson

2005

Molecular Brain Research

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It is not known how the brain modifies its regulatory systems in response to the application of a drug, especially over the long term of weeks and months. We have developed a model system approach to this question by manipulating cholinergic cell groups of the laterodorsal and pedunculopontine tegmental (LDT/PPT) nuclei in the pontomesencephalic tegmentum (PMT), which are known to be actively involved in the timing and quantity of rapid eye movement (REM) sleep. In a freely moving feline model, a single microinjection of the cholinergic agonist carbachol conjugated to a latex nanosphere delivery system into the caudolateral PMT elicits a long-term enhancement of one distinguishing phasic event of REM sleep, ponto-geniculo-occipital (PGO) waves, lasting 5 days but without any significant change in REM sleep or other behavioral state. Here, we test the hypothesis that cholinergic activation within the caudolateral PMT alters the postsynaptic excitability of the PGO network, stimulating the prolonged expression of c-fos that underlies this long-term PGO enhancement (LTPE) effect. Using quantitative Fos immunohistochemistry, we found that the number of Fos-immunoreactive (Fos-IR) neurons surrounding the caudolateral PMT injection site decreased sharply by postcarbachol day 03, while the number of Fos-IR neurons in the more rostral LDT/PPT increased >30-fold and remained at a high level following the course of LTPE. These results demonstrate a sustained c-fos expression in response to pharmacological stimulation of the brain and suggest that carbachol's acute effects induce LTPE via cholinergic receptors, with subsequent transsynaptic activation of the LDT/PPT maintaining the LTPE effect.

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A critical role for the parabrachial nucleus in generating central nervous system responses elicited by a systemic immune challenge

Cited by 28 publications

References 72 publications

C1 neurons: the body's EMTs

C1 neurons: the body's EMTs

Allopregnanolone and suppressed hypothalamo–pituitary–adrenal axis stress responses in late pregnancy in the rat

From synapse to gene product: prolonged expression of c-fos induced by a single microinjection of carbachol in the pontomesencephalic tegmentum

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