Depressor area within caudal ventrolateral medulla of the rat does not correspond to the A1 catecholamine cell group

Day, Trevor A.; Ro, A. I.; Renaud, Leo P.

doi:10.1016/0006-8993(83)90197-x

Cited by 56 publications

(21 citation statements)

References 7 publications

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“…Catecholamine neurons in the ventrolateral medulla are distributed within a caudal medullary area known as the cardiovascular depressor zone (18,19) and a rostral medullary area known as the cardiovascular pressor zone (20,21). Glucoprivation is a potent stimulus for adrenal medullary secretion, which could potentially alter cardiovascular function and lead to changes in Fos expression in these cardiovascular areas.…”

Section: Discussionmentioning

confidence: 99%

“…Finally, catecholamine neurons activated by 2DG appear to be anatomically distinct from the neurons with cardiovascular function. In the caudal ventrolateral medulla, the majority of the baroreceptive neurons in the cardiovascular depressor zone express the GABAergic, not the catecholaminergic, phenotype (18,19). Catecholamine neurons in the rostral ventrolateral medulla in the cardiovascular pressor zone express Fos in response to sustained hypertension and may be involved in cardiovascular regulation.…”

Section: Discussionmentioning

confidence: 99%

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Repeated 2-deoxy-D-glucose-induced glucoprivation attenuates Fos expression and glucoregulatory responses during subsequent glucoprivation.

Sanders

Ritter

2000

Diabetes

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A condition of reduced responsiveness to hypoglycemia, known as hypoglycemia-associated autonomic failure (HAAF), occurs in diabetic patients in the wake of a prior hypoglycemic episode. This condition suggests that hypoglycemia alters central glucose-sensing mechanisms. This experiment examined the effects of repeated 2-deoxy-D-glucose (2DG)-induced glucoprivation on subsequent 2DG-induced feeding and hyperglycemic responses in rats. Fos immunoreactivity (ir) in adrenal medulla and brain sites involved in these responses was also examined. Rats were injected daily for 10 days with 2DG (200 mg/kg) or saline (0.9%) or were handled. On day 11, rats were injected with 2DG (200 mg/kg). After injection, food intake was measured in one group. In another group, food was withheld, and multiple blood samples were collected for glucose determination. In a third group, food was withheld, and rats were killed after 2 h for evaluation of Fos-ir. Prior repeated glucoprivation reduced subsequent feeding and hyperglycemia responses to 2DG to baseline levels. Double-label immunohistochemistry showed that Fos-ir was reduced or abolished in catecholamine cell groups A1, A1/C1, C1, C3, and A6 and in the paraventricular nucleus of the hypothalamus and adrenal medulla. In other brain sites, 2DG-induced Fos-ir was diminished or unaffected by prior glucoprivation. Sites in which Fos-ir was abolished have been implicated previously in glucoprivic control of feeding and adrenal medullary secretion. Therefore, the present findings may identify crucial neuroanatomical sites that are altered by prior glucoprivation and that mediate some of the physiological deficits observed in HAAF.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Repeated 2-deoxy-D-glucose-induced glucoprivation attenuates Fos expression and glucoregulatory responses during subsequent glucoprivation.

Sanders

Ritter

2000

Diabetes

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“…During hypoxia and hypercapnia, CVLM neurons could be activated by (also labeled) caudal NTS neurons, which are known to project to A1-cells and to noncatecholaminergic neurons in this medullary region (Sawchenko and Swanson, 1981;Ross et al, 1985). The methods used in this study do not have the resolution to discriminate between the following possible sequelae of activation by hypoxia and hypercapnia of noradrenergic A1 and neighbouring noncatecholaminergic neurons: (1) activation of vasopressin-synthesizing neurons in the hypothalamus to which A1-cells project (e.g., Sawchenko and Swanson, 1982;Cunningham and Sawchenko, 1988); (2) reflex inhibition of sympathetic output from RVLM (C1) neurons to which noncatecholaminergic neurons of the CVLM project (e.g., Day et al, 1983); (3) activation (and labeling) of adjacent retroambigual cells of the caudal ventral respiratory group (CVRG), with which A1 neurons in fact are intermingled Sun et al, 1994). Part of the labeled noncatecholaminergic cells in CVLM may be cells projecting to the phrenic motor nucleus or to respiratory neurons in the PGCl or KF nuclei (Loewy et al, 1981;McKellar and Loewy, 1982).…”

Section: Ventral Medullamentioning

confidence: 97%

Expression of c‐fos in the rat brainstem after exposure to hypoxia and to normoxic and hyperoxic hypercapnia

et al. 1997

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In this study, Fos immunohistochemistry was used to map brainstem neuronal pathways activated during hypercapnia and hypoxia. Conscious rats were exposed to six different gas mixtures: (a) air; (b) 8% CO2 in air; (c) 10% CO2 in air; (d) 15% CO2 in air; (e) 15% CO2 + 60% O2, balance N2; (f) 9% O2, balance N2. Double-staining was performed to show the presence of tyrosine hydroxylase. Hypercapnia, in a dose-dependent way caused Fos expression in the following areas: caudal nucleus tractus solitarius (NTS), with few labeled A2 noradrenergic neurons; noradrenergic A1 cells and noncatecholaminergic neurons in the caudal ventrolateral medulla; raphe magnus and gigantocellular nucleus pars alpha (GiA); many noncatecholaminergic (and relatively few C1) neurons in the lateral paragigantocellular nucleus (PGCl), and in the retrotrapezoid nucleus (RTN); locus coeruleus (LC), external lateral parabrachial and Kölliker-Fuse nuclei, and A5 noradrenergic neurons at pontine level; and in caudal mesencephalon, the ventrolateral column of the periaqueductal gray (vlPAG). In most of these nuclei, hypoxia also induced Fos expression, albeit generally less than after hypercapnia. However, hypoxia did not cause labeling in RTN, juxtafacial PGCl, GiA, LC, or vlPAG. After normoxic hypercapnia, more labeled cells were present in NTS and PGCl than after hyperoxic hypercapnia. Part of the observed labeling could be caused by stress- or cardiovascular-related sequelae of hypoxia and hypercapnia. Possible implications for the neural control of breathing are also discussed, particularly with regard to the finding that several nuclei, not belonging to the classical brainstem respiratory centres, contained labeled cells.

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“…For example, the distribution of A1 neurons has recently been shown to overlap in part with those of bulbospinal and propriobulbar neurons of the ventral respiratory group (Ellenberger et al, 1990). In addition, physiologic studies have defined a so-called "depressor region" of the caudal ventrolateral medulla that participates in baroreflex circuitry by inhibiting the activity of reticulospinal neurons in the C1 region both tonically and reflexively, in response to increased arterial blood pressure (e.g., Day et al, 1983;Agarwal et al, 1990;Cravo et al, 1991;Jeske et al, 1993). The topography of depressor sites in the caudal ventrolateral medulla appears to overlap in part with that of hypothalamically projecting A1 neurons, though it has been demonstrated that the two populations are distinct (Day et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, physiologic studies have defined a so-called "depressor region" of the caudal ventrolateral medulla that participates in baroreflex circuitry by inhibiting the activity of reticulospinal neurons in the C1 region both tonically and reflexively, in response to increased arterial blood pressure (e.g., Day et al, 1983;Agarwal et al, 1990;Cravo et al, 1991;Jeske et al, 1993). The topography of depressor sites in the caudal ventrolateral medulla appears to overlap in part with that of hypothalamically projecting A1 neurons, though it has been demonstrated that the two populations are distinct (Day et al, 1983). In line with this, we have recently found that the distribution of neurons in the caudal ventrolateral medulla exhibiting cellular activation (i.e., immediate-early gene induction) in response to intravenous injection of the vasoconstrictor drug, phenylephrine, conforms with physiologically generated maps of depressor sites in the region, and that affected cells are overwhelmingly noncatecholaminergic (Chan and Sawchenko, 199413).…”

Section: Discussionmentioning

confidence: 99%

A1 catecholamine cell group: Fine structure and synaptic input from the nucleus of the solitary tract

Chan

Peto

Sawchenko

1995

J of Comparative Neurology

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Preembedding immunoperoxidase staining methods were used to characterize tyrosine hydroxylase-immunoreactive (TH-ir) elements in the caudal ventrolateral medulla, and to determine the extent to which neurons of the A1 cell group are directly innervated by projections of the nucleus of the solitary tract (NTS). TH-ir neurons in the A1 region were medium-sized and multipolar. They possessed rounded nuclei with infrequent invaginations, well-developed Golgi apparati, high cytoplasmic densities of mitochondria, and a low to moderate tendency for rough endoplasmic reticulum (RER) to align in parallel stacks. A1 cell bodies were commonly juxtaposed to TH-positive and TH-negative neurons, myelinated profiles, glia and/or vascular elements, but close membrane appositions were only seen with glial elements. Synaptic input to A1 neurons was predominantly asymmetric, provided virtually exclusively by non-TH-ir terminals, and directed principally to dendritic shafts; A1 somata are relatively sparsely innervated. In a second experiment, silver-intensified immunogold localization of TH-ir was combined with immunoperoxidase labeling for anterogradely transported Phaseolus vulgaris-leucoagglutinin (PHA-L), following tracer injections in the caudal aspect of the medial division of the NTS. These experiments revealed a small proportion of PHA-L-labeled axon terminals that made asymmetric contacts with dendritic shafts of TH-ir neurons. These results suggest that the fine structure and synaptic input of A1 neurons are somewhat distinct from that of rostrally situated C1 catecholamine cells. In addition, while they document a direct NTS-A1 projection that may participate in the interoceptive control of vasopressin secretion, the bulk of ventrolaterally directed projections from the caudomedial NTS contact noncatecholaminergic elements in the A1 region, some of which may correspond to so-called depressor neurons implicated in the baroreflex control of sympathetic outflow and vasopressin secretion.

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Depressor area within caudal ventrolateral medulla of the rat does not correspond to the A1 catecholamine cell group

Cited by 56 publications

References 7 publications

Repeated 2-deoxy-D-glucose-induced glucoprivation attenuates Fos expression and glucoregulatory responses during subsequent glucoprivation.

Repeated 2-deoxy-D-glucose-induced glucoprivation attenuates Fos expression and glucoregulatory responses during subsequent glucoprivation.

Expression of c‐fos in the rat brainstem after exposure to hypoxia and to normoxic and hyperoxic hypercapnia

A1 catecholamine cell group: Fine structure and synaptic input from the nucleus of the solitary tract

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