Adrenergic and non-adrenergic spinal projections of a cardiovascular-active pressor area of medulla oblongata: quantitative topographic analysis

Ruggiero, David A.; Cravo, Sérgio L.; Golanov, Eugene V.; Gómez, Roberto; Anwar, Mumtaz Ali; Reis, Donald J.

doi:10.1016/0006-8993(94)90468-5

Cited by 83 publications

(85 citation statements)

References 43 publications

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“…To test whether retrograde transduction can be used for efficient and selective targeting of noradrenergic neurons from their projection areas, we injected AdPRSx8EGFP into the IML (a known target area for C1 adrenergic neurons in the rostral ventrolateral medulla, RVLM; 24,30,31,39). This resulted in numerous EGFP-expressing neurons in the RVLM (Fig.…”

Section: Patterns Of Transduction Following Adhcmvegfp Adsyn1egfp-whmentioning

confidence: 99%

Targeting brain stem centers of cardiovascular control using adenoviral vectors: impact of promoters on transgene expression

Lonergan

Teschemacher

Hwang

et al. 2005

Physiological Genomics

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Adenoviral vectors (AVV) are widely used as tools for exploring gene function in studies of the central autonomic control, but the cellular specificity of the promoters commonly used in these vectors has not been studied. We evaluated AVV with four “wide-spectrum” promoters, human cytomegalovirus promoter (HCMV), synapsin-1 promoter (Syn1), tubulin-α1 promoter (Tα1), and neuron-specific enolase (NSE) for their ability to express enhanced green fluorescent protein (EGFP) within the dorsal vagal complex and the adjacent brain stem. They were compared with the PRSx8 promoter, specifically designed to target catecholaminergic neurons. AdHCMVEGFP, AdSyn1EGFP-WHE (woodchuck hepatitis enhancer element), AdTα1EGFP, and AdNSEEGFP were unable to drive expression of EGFP in dopamine β-hydroxylase-immunoreactive neurons of the A2 cell group, although the adjacent dorsal vagal motonucleus and especially hypoglossal motoneurons did express high levels of EGFP. AdPRSx8EGFP efficiently drove EGFP expression in the A2 cell group but also in choline acetyltransferase-positive vagal motoneurons. However, catecholaminergic neurons could be selectively and efficiently transduced via a retrograde route by injecting the vector into their target areas. Thus AVV with “wide-spectrum” promoters have strikingly different activity in the diverse cellular populations within brain stem cardiovascular control centers. The PRSx8 promoter is a valuable tool for the study of the role of catecholaminergic neurons.

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Section: Patterns Of Transduction Following Adhcmvegfp Adsyn1egfp-whmentioning

confidence: 99%

Targeting brain stem centers of cardiovascular control using adenoviral vectors: impact of promoters on transgene expression

Lonergan

Teschemacher

Hwang

et al. 2005

Physiological Genomics

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“…Anatomical studies have shown that the PVH, A6, and adrenal medullary preganglionic neurons are all heavily innervated by catecholamine neurons in C1 through C3. Spinal and hypothalamic projections arise from separate populations of epinephrine neurons in these cell groups (23)(24)(25)(26)(27)(28)(29). Based on these anatomical connections, it is possible that the loss of 2DG-induced Fos expression could be due to a selective effect of the antecedent glucoprivation on these epinephrine neurons and the resulting inability of these neurons to activate their target sites in the PVH and intermediolateral column.…”

Section: A B C Dmentioning

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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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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“…This difficulty is compounded by the fact that the total number of RVL bulbospinal neurons is ϳ200 per side, and only a fraction of these cells can be retrogradely labeled (Ruggiero et al 1994). The practical limitation imposed by the small number of cells that can be recorded per rat, even in the neonate, compelled us to limit the number of experimental protocols to the strict minimum and, in particular, prevented us from testing the effects of multiple antagonists.…”

Section: Technical Considerations and Experimental Limitationsmentioning

confidence: 99%

“…In brief, the main evidence is that RVL neurons that are retrogradely labeled from the thoracic spinal cord are known to innervate selectively the intermediolateral cell column (Ross et al 1984;Ruggiero et al 1994). In addition, the majority of recorded neurons are catecholaminergic C1 cells which project monosynaptically to sympathetic preganglionic neurons (for review, see Guyenet et al 1996).…”

Section: Technical Considerations and Experimental Limitationsmentioning

confidence: 99%

Prototypical Imidazoline-1 Receptor Ligand Moxonidine Activates Alpha2-Adrenoceptors in Bulbospinal Neurons of the RVL

Hayar

Guyenet

2000

Journal of Neurophysiology

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Hayar, Abdallah and Patrice G. Guyenet. Prototypical imidazoline-1 receptor ligand moxonidine activates alpha2-adrenoceptors in bulbospinal neurons of the RVL. J. Neurophysiol. 83: 766 -776, 2000. Moxonidine is an antihypertensive drug that lowers sympathetic vasomotor tone by stimulating either alpha2-adrenergic (␣2-AR) or imidazoline I1 receptors within the rostral ventrolateral medulla (RVL). In this study, we investigated the effects of moxonidine (10 M) on RVL neurons in brain stem slices of neonatal rats. We recorded mainly from retrogradely labeled RVL bulbospinal neurons (putative presympathetic neurons) except for some extracellular recordings. Prazosin was used to block alpha1-adrenoceptors. Moxonidine inhibited the extracellularly recorded discharges of all spontaneously active RVL neurons tested (bulbospinal and unidentified). This effect was reversed or blocked by the selective ␣2-AR antagonist SKF 86466 (10 M). In contrast, the I1 imidazoline ligand AGN 192403 (10 M) had no effect on the spontaneous activity. In whole cell recordings (holding potential Ϫ70 mV), moxonidine produced a small and variable outward current (mean 7 pA). This current was observed in both tyrosine hydroxylase-immunoreactive and other bulbospinal neurons and was blocked by SKF 86466. Excitatory postsynaptic currents (EPSCs) evoked by focal electrical stimulation were isolated by incubation with gabazine and strychnine, and inhibitory postsynaptic currents (IPSCs) were isolated with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Moxonidine reduced the amplitude of the evoked EPSCs (EC 50 ϭ 1 M; 53% inhibition at 10 M) but not their decay time constant (5.6 ms). The effect of moxonidine on EPSCs persisted in barium (300 M) and was reduced ϳ80% by SKF 86466. Moxonidine also reduced the amplitude of evoked IPSCs by 63%. In conclusion, moxonidine inhibits putative RVL presympathetic neurons both presynaptically and postsynaptically. All observed effects in the present study are consistent with an ␣2-AR agonist activity of moxonidine. I N T R O D U C T I O NCentrally acting antihypertensive drugs with an imidazoline structure, like clonidine and moxonidine, are effective in treating moderate to severe forms of hypertension (Armah et al. 1988;Prichard et al. 1997;Schafer et al. 1995;Ziegler et al. 1996). There is general agreement that a major site of action of these drugs is within the rostral ventrolateral medulla (RVL) (Punnen et al. 1987; reviewed by Reis 1996), but their specific neuronal targets are unknown. The RVL is critical for sympathetic tone generation and blood pressure control because it contains bulbospinal neurons (presympathetic neurons) that contribute the major excitatory drive to sympathetic vasoconstrictor and cardiac preganglionic neurons (McAllen et al. 1997;Sun 1995). The presympathetic neurons include a catecholaminergic cell group (C1 cells) that express the A subtype of ␣2-ARs (Guyenet et al. 1994). Activation of ␣2-ARs by norepinephrine (NE) in RVL bulbospinal neurons in vitro (C1 cells and others) acti...

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Adrenergic and non-adrenergic spinal projections of a cardiovascular-active pressor area of medulla oblongata: quantitative topographic analysis

Cited by 83 publications

References 43 publications

Targeting brain stem centers of cardiovascular control using adenoviral vectors: impact of promoters on transgene expression

Targeting brain stem centers of cardiovascular control using adenoviral vectors: impact of promoters on transgene expression

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

Prototypical Imidazoline-1 Receptor Ligand Moxonidine Activates Alpha2-Adrenoceptors in Bulbospinal Neurons of the RVL

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