Sympathetic reflexes after depletion of bulbospinal catecholaminergic neurons with anti-DβH-saporin

Schreihofer, Ann M.; Guyenet, Patrice G.

doi:10.1152/ajpregu.2000.279.2.r729

Cited by 95 publications

(171 citation statements)

References 29 publications

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“…3 B and C). At early survival intervals, the majority of these neurons were concentrated in the rostral portion of the RVLM that is the principal source of descending C1 projections to SPGs in the IML of the thoracic spinal cord (27,28). A day later, neurons throughout the RVLM exhibited yellow, green, and cyan fluorescence, either alone or in combination.…”

Section: Resultsmentioning

confidence: 99%

Microdissection of neural networks by conditional reporter expression from a Brainbow herpesvirus

Card

Kobiler

McCambridge

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Transneuronal transport of neurotropic viruses is widely used to define the organization of neural circuitry in the mature and developing nervous system. However, interconnectivity within complex circuits limits the ability of viral tracing to define connections specifically linked to a subpopulation of neurons within a network. Here we demonstrate a unique viral tracing technology that highlights connections to defined populations of neurons within a larger labeled network. This technology was accomplished by constructing a replication-competent strain of pseudorabies virus (PRV-263) that changes the profile of fluorescent reporter expression in the presence of Cre recombinase (Cre). The viral genome carries a Brainbow cassette that expresses a default red reporter in infected cells. However, in the presence of Cre, the red reporter gene is excised from the genome and expression of yellow or cyan reporters is enabled. We used PRV-263 in combination with a unique lentivirus vector that produces Cre expression in catecholamine neurons. Projection-specific infection of central circuits containing these Cre-expressing catecholamine neurons with PRV-263 resulted in Cre-mediated recombination of the PRV-263 genome and conditional expression of cyan/yellow reporters. Replication and transneuronal transport of recombined virus produced conditional reporter expression in neurons synaptically linked to the Cre-expressing catecholamine neurons. This unique technology highlights connections specific to phenotypically defined neurons within larger networks infected by retrograde transneuronal transport of virus from a defined projection target. The availability of other technologies that restrict Cre expression to defined populations of neurons indicates that this approach can be widely applied across functionally defined systems.

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Section: Resultsmentioning

confidence: 99%

Microdissection of neural networks by conditional reporter expression from a Brainbow herpesvirus

Card

Kobiler

McCambridge

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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“…The primary response of most RVLM presympathetic barosensitive neurons to carotid body stimulation (cyanide or brief hypoxia) in rodents is a vigorous activation (93,144,179), although this response can be modified by the baroreflex (93) and central respiratory generator drive (71,113). Consistent with this observation, a large proportion of C1 neurons express Fos in conscious mammals exposed to hypoxia (54,73), and sympathetic nerve activation elicited by carotid body stimulation is severely depressed after selective lesions of the C1 neurons (157). The pathway between the carotid bodies and the C1 cells may involve a single interneuron located within the commissural part of the NTS (7,37,151).…”

Section: C1 Neurons and Responses To Hypoxiamentioning

confidence: 87%

“…However, there was a substantial reduction in the rise of plasma norepinephrine, vasopressin, and oxytocin following hydralazine-induced hypotension (respectively ϳ40%, 73%, and 40%), indicating permanent deficits in the neuroendocrine adjustments to baroreceptor unloading (110). In other experiments, the presympathetic C1 neurons (and A5 neurons) were destroyed by injecting the same toxin into the spinal cord (157,161). These lesions spared the bulbospinal barosensitive non-C1 RVLM neurons (161) and, as in the above-mentioned studies of Madden and Sved (110,111), had inconsequential effects on resting AP (157).…”

Section: C1 Cells Hypotension and Baroreflexesmentioning

confidence: 91%

“…In other experiments, the presympathetic C1 neurons (and A5 neurons) were destroyed by injecting the same toxin into the spinal cord (157,161). These lesions spared the bulbospinal barosensitive non-C1 RVLM neurons (161) and, as in the above-mentioned studies of Madden and Sved (110,111), had inconsequential effects on resting AP (157). However, sympathoexcitatory responses evoked by electrical stimulation of the RVLM were severely attenuated as were the baroreflex and the increase in sympathetic nerve activity (SNA) elicited by carotid body stimulation.…”

Section: C1 Cells Hypotension and Baroreflexesmentioning

confidence: 99%

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C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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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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“…Sympathoexcitation evoked by chemoreceptor activation is significantly attenuated when catecholaminergic bulbospinal neurons are lesioned 33 but abolished when muscimol is injected into the RVLM. 29 Because sst2A receptors are found on a subpopulation of catecholamine-containing bulbospinal neurons, chemoreceptor reflex attenuation was unsurprising.…”

Section: Discussionmentioning

confidence: 98%

Somatostatin 2A Receptor-Expressing Presympathetic Neurons in the Rostral Ventrolateral Medulla Maintain Blood Pressure

Burke

Costin

et al. 2008

Hypertension

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Abstract-Bulbospinal neurons in the rostral ventrolateral medulla (RVLM) are critical for the maintenance of sympathetic vasomotor tone and normal cardiovascular reflex function. So far, selectively eliminating/inhibiting distinct subpopulations of RVLM neurons has not significantly altered arterial pressure. Here we show that RVLM presympathetic neurons that express somatostatin 2A receptors are essential for maintaining and potentially generating sympathetic vasomotor tone. Combined immunocytochemistry and in situ hybridization were used to map the expression of somatostatin receptors 1, 2A, 2B, 3, and 4 (sst1 through 4, respectively) in the rat RVLM. sst1 and sst2B were absent; sst3 and sst4 were sparse. However, sst2A was found postsynaptically and detected in 35Ϯ5% of bulbospinal RVLM neurons a population that included 54Ϯ4% of catecholaminergic and 30Ϯ3% of enkephalinergic neurons. Bilateral microinjection into the RVLM of either somatostatin or the receptor-selective agonist lanreotide evoked dramatic, dose-dependent sympathoinhibition, hypotension, and bradycardia that were blocked by the sst2 receptor antagonist BIM-23627 in anesthetized rats. Bilateral RVLM microinjection of somatostatin also attenuated chemoreceptor and somatosympathetic reflex function. Somatostatin only eliminated the first sympathoexcitatory peak evoked by somatosympathetic reflex activation, whereas muscimol abolished both excitatory peaks providing functional evidence that the activity of only a subpopulation of RVLM presympathetic neurons is inhibited by somatostatin. We suggest that the subpopulation of bulbospinal RVLM neurons that expresses the sst2A receptor sets sympathetic vasomotor output. These neurons are essential for maintaining resting blood pressure under anesthesia and contribute to adaptive reflexes mediated through the RVLM. Key Words: cardiovascular Ⅲ sympathetic vasomotor tone Ⅲ catecholamine Ⅲ enkephalin Ⅲ respiration P resympathetic neurons within the rostral ventrolateral medulla (RVLM) contain catecholamines and/or preproenkephalin (PPE) and are critical for the tonic and reflex control of arterial pressure (AP). [1][2][3] Inputs regulating RVLM presympathetic neuronal activity release amino acids and/or a range of modulatory neurochemicals, including peptides. [2][3][4][5][6] These underlie the ability to provide a differentiated sympathetic drive to the various vascular beds, 6 alter the responses to reflex activation, 5 and set the level of AP. 1,3,5 Identification of neurons responsible for generating and maintaining sympathetic vasomotor tone and, therefore, setting the level of AP would be a major breakthrough in understanding circulatory control.The inhibitory neuropeptide somatostatin (SST) is distributed widely in regions of the central nervous system involved in motor, cognitive, autonomic, and neuroendocrine processes. 7,8 Two biologically active forms of SST, SST 14 and SST 28, are cleaved from preprosomatostatin and bind to all of the SST receptors with similar affinity. 8 Six G protein-couple...

show abstract

Sympathetic reflexes after depletion of bulbospinal catecholaminergic neurons with anti-DβH-saporin

Cited by 95 publications

References 29 publications

Microdissection of neural networks by conditional reporter expression from a Brainbow herpesvirus

Microdissection of neural networks by conditional reporter expression from a Brainbow herpesvirus

C1 neurons: the body's EMTs

Somatostatin 2A Receptor-Expressing Presympathetic Neurons in the Rostral Ventrolateral Medulla Maintain Blood Pressure

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