scholarly journals Catecholamines modulate podocyte function.

1998 ◽  
Vol 9 (3) ◽  
pp. 335-345 ◽  
Author(s):  
T B Huber ◽  
J Gloy ◽  
A Henger ◽  
P Schollmeyer ◽  
R Greger ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Patch Clamp Technique ◽  
Extracellular Solution ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Beta 2 ◽  
Cl Conductance ◽  
Stimulation Of ◽  
Ion Conductances

The aim of this study was to investigate the influence of adrenoceptor agonists on the intracellular calcium activity ([Ca2+]i), membrane voltage (Vm), and ion conductances (Gm) in differentiated mouse podocytes. [Ca2+]i was measured by the Fura-2 fluorescence method in single podocytes. Noradrenaline and the alpha 1-adrenoceptor agonist phenylephrine induced a reversible and concentration-dependent biphasic increase of [Ca2+]i in podocytes (EC50 approximately 0.1 microM for peak and plateau), whereas the alpha 2-adrenoceptor agonist UK 14.304 did not influence [Ca2+]i. The [Ca2+]i response induced by noradrenaline was completely inhibited by the alpha 1-adrenoceptor antagonist prazosin (10 nM). In a solution with a high extracellular K+ (72.5 mM), [Ca2+]i was unchanged and the [Ca2+]i increase induced by noradrenaline was not inhibited by the L-type Ca2+ channel blocker nicardipine (1 microM). Vm and Gm were examined with the patch-clamp technique in the slow whole-cell configuration. Isoproterenol, phenylephrine, and noradrenaline depolarized podocytes and increased Gm. The order of potency for the adrenoceptor agonists was isoproterenol (EC50 approximately 1 nM) > noradrenaline (EC50 approximately 0.3 microM) > phenylephrine (EC50 approximately 0.5 microM). The beta 2-adrenoceptor antagonist ICI 118.551 (5 to 100 nM) inhibited the effect of isoproterenol on Vm. Stimulation of adenylate cyclase by forskolin mimicked the effect of isoproterenol on Vm and Gm (EC50 approximately 40 nM). Isoproterenol induced a time- and concentration-dependent increase of cAMP in podocytes. The effect of isoproterenol was unchanged in the absence of Na+ or in an extracellular solution with a reduced Ca2+ concentration, whereas it was significantly increased in an extracellular solution with a reduced Cl- concentration (from 145 to 32 mM). The data indicate that adrenoceptor agonists regulate podocyte function: They increase [Ca2+]i via an alpha 1-adrenoceptor and induce a depolarization via a beta 2-adrenoceptor. The depolarization is probably due to an opening of a cAMP-dependent Cl- conductance.

Testosterone-augmented contractile responses to α1- and β1-adrenoceptor stimulation are associated with increased activities of RyR, SERCA, and NCX in the heart

2009 ◽  
Vol 296 (4) ◽  
pp. C766-C782 ◽  
Author(s):  
Sharon Tsang ◽  
Stanley S. C. Wong ◽  
Song Wu ◽  
Gennadi M. Kravtsov ◽  
Tak-Ming Wong
Keyword(s):  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Contractile Responses ◽  
Adrenoceptor Antagonist ◽  
Cardiac Contractile ◽  
Plasmic Reticulum ◽  
Adrenoceptor Agonist ◽  
Intracellular Ca ◽  
Developed Pressure ◽  
Stimulation Of

We hypothesized that testosterone at physiological levels enhances cardiac contractile responses to stimulation of both α1- and β1-adrenoceptors by increasing Ca2+ release from the sarcoplasmic reticulum (SR) and speedier removal of Ca2+ from cytosol via Ca2+-regulatory proteins. We first determined the left ventricular developed pressure, velocity of contraction and relaxation, and heart rate in perfused hearts isolated from control rats, orchiectomized rats, and orchiectomized rats without and with testosterone replacement (200 μg/100 g body wt) in the presence of norepinephrine (10−7 M), the α1-adrenoceptor agonist phenylephrine (10−6 M), or the nonselective β-adrenoceptor agonist isoprenaline (10−7 M) in the presence of 5 × 10−7 M ICI-118,551, a β2-adrenoceptor antagonist. Next, we determined the amplitudes of intracellular Ca2+ concentration transients induced by electrical stimulation or caffeine, which represent, respectively, Ca2+ release via the ryanodine receptor (RyR) or releasable Ca2+ in the SR, in ventricular myocytes isolated from the three groups of rats. We also measured 45Ca2+ release via the RyR. We then determined the time to 50% decay of both transients, which represents, respectively, Ca2+ reuptake by sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and removal via the sarcolemmal Na+/Ca2+ exchanger (NCX). We correlated Ca2+ removal from the cytosol with activities of SERCA and its regulator phospholamban as well as NCX. The results showed that testosterone at physiological levels enhanced positive inotropic and lusitropic responses to stimulation of α1- and β1-adrenoceptors via the androgen receptor. The increased contractility and speedier relaxation were associated with increased Ca2+ release via the RyR and faster Ca2+ removal out of the cytosol via SERCA and NCX.

Effects of α-adrenoceptor agonists and antagonists on thyroid hormone secretion

1985 ◽  
Vol 108 (2) ◽  
pp. 184-191 ◽  
Author(s):  
Bo Ahrén
Keyword(s):  
Thyroid Hormone ◽  
Dose Level ◽  
Hormone Secretion ◽  
High Dose ◽  
Inhibitory Effects ◽  
High Dose Level ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists

Abstract. The effects of various α-adrenoceptor agonists and antagonists on blood radioiodine levels were studied in mice pre-treated with 125I and thyroxine. The non-selective α-adrenoceptor agonist noradrenaline and the selective α1-adrenoceptor agonist phenylephrine both enhanced blood radioiodine levels. Noradrenaline was more potent than phenylephrine. Contrary, the selective α2-adrenoceptor agonist clonidine depressed basal levels of blood radioiodine. The non-selective α-adrenoceptor antagonist phentolamine and the selective α1-adrenoceptor antagonist prazosin both inhibited the noradrenaline-induced elevation of radioiodine levels, whereas the α2-adrenoceptor antagonist yohimbine had no such effect, except at a high dose level. All three α-adrenoceptor agonists, noradrenaline, phenylephrine and clonidine, inhibited the radioiodine response to TSH. In addition, TSH-induced increase in radioiodine levels was inhibited by prazosin, whereas yohimbine had no effect. Phentolamine inhibited the radioiodine response to TSH when given 2 h prior to TSH, whereas when given 15 min prior to TSH the response to TSH was potentiated by Phentolamine. It is concluded, that under in vivo conditions in the mouse, α1-adrenoceptor activation stimulates basal thyroid hormone secretion and inhibits TSH-induced thyroid hormone secretion. Further, α2-adrenoceptor activation inhibits basal thyroid hormone secretion. In addition, TSH-induced thyroid hormone secretion is inhibited by α1-adrenoceptor antagonism. Thus, α-adrenoceptors induce both stimulatory and inhibitory effects of thyroid function.

Beta adrenoceptors mediate the catecholamine-induced stimulation of oxytocin secretion from cultured bovine granulosa cells

1991 ◽  
Vol 3 (6) ◽  
pp. 715 ◽  
Author(s):  
MR Luck ◽  
M Munker
Keyword(s):  
Granulosa Cells ◽  
Receptor Subtype ◽  
Alpha Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Ici 118,551 ◽  
Beta 2 ◽  
Term Response

Bovine granulosa cells were treated in culture with alpha- and beta-adrenoceptor ligands to determine the receptor subtype mediating their response to catecholamines. The secretion of oxytocin by granulosa cells in serum-free medium was measured on the fourth day of culture (during the period of acquisition of a luteal phenotype). Cultures were performed in the presence of 0.5 mM ascorbic acid, which increased hormone output and potentiated the response to catecholamines. The effects of adrenaline and noradrenaline on oxytocin secretion were concentration-dependent; maximum stimulation was over 700% with adrenalin (EC50 92 nM) and 500% with noradrenaline (EC50 87 nM). The response to noradrenaline (10(-6) M) and adrenaline (10(-6) M) could be blocked by propranolol but not by phentolamine, suggesting that beta- rather than alpha-adrenoceptors were involved. Blockade by metoprolol and practolol (beta 1-adrenoceptor antagonists) was poor and dobutamine (beta 1-agonist) was weakly stimulatory. A concentration-dependent stimulatory response (EC50 200 nM) was obtained with salbutamol (beta 2-adrenoceptor agonist) and stimulation by adrenaline or salbutamol could be blocked by a selective beta 2-adrenoceptor antagonist (ICI 118,551). It is concluded that, during luteinization, the long-term response of bovine granulosa cells to stimulation induced by catecholamines is mediated through beta- rather than alpha-adrenoceptors. Although the beta 2-subtype is probably involved, the similar potencies of adrenaline and noradrenaline are uncharacteristic of beta 2-adrenoceptors and may be peculiar to the long-term response shown by these cells.

The Effect of Imidazoline Receptors and α2-adrenoceptors on the Anesthetic Requirement (MAC) for Halothane in Rats 

1997 ◽  
Vol 87 (4) ◽  
pp. 963-967 ◽  
Author(s):  
Kiyokazu Kagawa ◽  
Tadanori Mammoto ◽  
Yukio Hayashi ◽  
Takahiko Kamibayashi ◽  
Takashi Mashimo ◽  
...  
Keyword(s):  
Minimum Alveolar Concentration ◽  
Inhibitory Effect ◽  
Imidazoline Receptors ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
The Central Nervous System ◽  
Anesthetic Requirement ◽  
Alpha2 Adrenoceptor ◽  
Pharmacologic Actions

Background Recent evidences have documented that several pharmacologic actions of alpha2-adrenoceptor agonists are mediated via activation of not only alpha2-adrenoceptors, but also by imidazoline receptors, which are nonadrenergic receptors in the central nervous system. However, the effect of imidazoline receptors on the anesthesia is not well known, and it is important to clarify the effects of both receptors on anesthesia. Methods Seventy-two rats were anesthetized with halothane, and the anesthetic requirement for halothane was evaluated as minimum alveolar concentration (MAC). The MAC for halothane was determined in the presence of dexmedetomidine (0, 10, 20, and 30 microg/kg, intraperitoneally [IP]), a selective alpha2-adrenoceptor agonist with weak affinity for imidazoline receptors. Then, the authors evaluated the inhibitory effect of rauwolscine (20 mg/kg, IP), an alpha2-adrenoceptor antagonist with little affinity for imidazoline receptors, on the MAC-reducing action of dexmedetomidine (30 microg/kg). Further, the effect of rilmenidine (20, 50, 100, 1000 microg/kg, IP), a selective imidazoline receptor agonist, on the MAC for halothane was also investigated. Results Dexmedetomidine decreased the MAC for halothane dose-dependently, and this MAC-reducing action of dexmedetomidine was completely blocked by rauwolscine. Rilmenidine alone did not change the MAC for halothane. Conclusions The present data indicate that the anesthetic sparing action of dexmedetomidine is most likely mediated through alpha2- adrenoceptors, and the stimulation of imidazoline receptors exerts little effect on the anesthetic requirement for halothane.

scholarly journals Effect of compound D-600 (methoxyverapamil) on gluconeogenesis and on acceleration of the process by α-adrenergic stimuli in rat kidney tubules

1980 ◽  
Vol 190 (2) ◽  
pp. 283-291 ◽  
Author(s):  
E D Saggerson ◽  
C A Carpenter
Keyword(s):  
Renal Cortex ◽  
Rat Kidney ◽  
Sodium Lactate ◽  
Kidney Tubules ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Blocker ◽  
Glucose Formation ◽  
Stimulation Of

1. Tubule fragments were isolated from renal cortex of fed rats and glucose formation was measured after incubation with 5 mM-sodium lactate. 20 Compound D-600 (10-100 microM) decreased gluconeogenesis from lactate. This inhibition of the process by compound D-600 increased with increasing extracellular Ca2+ concentration, was overridden by noradrenaline and diminished by starvation for 24 h. 3. Inhibition of lactate-supported gluconeogenesis by compound D-600 was not prevented by the alpha 1-adrenoceptor antagonist thymoxamine. 4. Compound D-600 had little effect on gluconeogenesis from 2-oxoglutarate and increased gluconeogenesis from succinate. 5. Compound D-600 opposed stimulation of gluconeogenesis by noradrenaline or oxymetazoline (a selective alpha-adrenoceptor agonist) in a manner suggesting that compound D-600 is an alpha-adrenoceptor blocker. Oxymetazoline was more sensitive than noradrenaline to blockade by both compound D-600 and by the conventional alpha-adrenoceptor antagonist phentolamine. Noradrenaline became more sensitive to blockade by compound D-600 when extracellular Ca2+ was decreased. 6. Compound D-600 did not block stimulation of gluconeogenesis by angiotensin or cyclic AMP.

Noradrenaline Excites and Inhibits GABAergic Transmission in Parvocellular Neurons of Rat Hypothalamic Paraventricular Nucleus

2002 ◽  
Vol 87 (5) ◽  
pp. 2287-2296 ◽  
Author(s):  
Seong Kyu Han ◽  
Wonee Chong ◽  
Long Hua Li ◽  
In Se Lee ◽  
Kazuyuki Murase ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Synaptic Activity ◽  
Hypothalamic Paraventricular Nucleus ◽  
Anatomical Location ◽  
Type Ii ◽  
Inhibitory Effects ◽  
Patch Clamp Technique ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Parvocellular Neurons

Noradrenaline (NA) is a major neurotransmitter that regulates many neuroendocrine and sympathetic autonomic functions of the hypothalamic paraventricular nucleus (PVN). Previously NA has been shown to increase the frequency of excitatory synaptic activity of parvocellular neurons within the PVN, but little is known about its effects on inhibitory synaptic activity. In this work, we studied the effects of NA (1–100 μM) on the spontaneous inhibitory synaptic currents (sIPSC) of type II PVN neurons in brain slices of the rat using the whole cell patch-clamp technique. Spontaneous IPSCs were observed from most type II neurons ( n = 121) identified by their anatomical location within the PVN and their electrophysiological properties. Bath application of NA (100 μM) increased sIPSC frequency by 256% in 59% of the neurons. This effect was blocked by prazosin (2–20 μM), the α1-adrenoceptor antagonist and mimicked by phenylephrine (10–100 μM), the α1-adrenoceptor agonist. However, in 33% of the neurons, NA decreased sIPSC frequency by 54%, and this effect was blocked by yohimbine (2–20 μM), the α2-adrenoceptor antagonist and mimicked by clonidine (50 μM), the α2-adrenoceptor agonist. The Na+ channel blocker, tetrodotoxin (0.1 μM) blocked the α1-adrenoceptor–mediated effect, but not the α2-adreonoceptor–mediated one. Both of the stimulatory and inhibitory effects of NA on sIPSC frequency were observed in individual neurons when tested with NA alone, or both phenylephrine and clonidine. Furthermore, in most neurons that showed the stimulatory effects, the inhibitory effects of NA were unmasked after blocking the stimulatory effects by prazosin or tetrodotoxin. These data indicate that tonic GABAergic inputs to the majority of type II PVN neurons are under a dual noradrenergic modulation, the increase in sIPSC frequency via somatic or dendritic α1-adrenoceptors and the decrease in sIPSC frequency via axonal terminal α2-adrenoceptors on the presynaptic GABAergic neurons.

Interaction between epinephrine and renal nerves in control of renin secretion rate

1986 ◽  
Vol 250 (6) ◽  
pp. F999-F1007 ◽  
Author(s):  
U. C. Kopp ◽  
G. F. DiBona
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Urinary Sodium Excretion ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Beta 2 ◽  
Renal Innervation

To determine whether the increase in renin secretion rate (RSR) produced by the beta 2-adrenoceptor agonist epinephrine was dependent on intact renal innervation, epinephrine (10 ng X kg-1 X min-1) was infused bilaterally into an innervated and a denervated kidney (ira) of the same anesthetized dog at spontaneous and reduced renal arterial pressure (decreases RAP, 100 mmHg). Epinephrine ira did not affect mean arterial pressure, renal hemodynamics, or urinary sodium excretion of either kidney. At spontaneous RAP epinephrine ira increased RSR from 633 +/- 134 to 926 +/- 137 ng/min in innervated kidneys but did not change RSR in denervated kidneys. decreases RAP in the presence of epinephrine ira resulted in an increase in RSR from 969 +/- 248 to 2,564 +/- 630 ng/min in innervated kidneys, which was greater than that produced in the absence of epinephrine, from 741 +/- 244 to 1,606 +/- 431 ng/min. In denervated kidneys decreases RAP resulted in similar increases in RSR in the absence and presence of epinephrine ira from 41 +/- 15 to 166 +/- 60 ng/min and from 59 +/- 210 to 235 +/- 78 ng/min, respectively. These results demonstrate that the increase in RSR produced by epinephrine is dependent on intact renal innervation at spontaneous and decreases RAP and suggest that epinephrine increases RSR by a prejunctional mechanism. The beta 1-adrenoceptor antagonist metoprolol (0.3-0.5 microgram X kg-1 X min-1 ira) abolished the enhanced RSR response to decreases RAP produced by epinephrine ira. Similarly, the beta 2-adrenoceptor antagonist ICI 118551 (0.005-0.25 microgram X kg-1 X min-1 ira) abolished the enhanced RSR response to decreases RAP produced by epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of alpha-adrenergic agonists on intracellular and intramitochondrial pH in rat proximal nephrons

1989 ◽  
Vol 257 (4) ◽  
pp. F623-F630 ◽  
Author(s):  
F. A. Gesek ◽  
A. C. Schoolwerth
Keyword(s):  
Specific Inhibitor ◽  
Weak Acid ◽  
Adrenergic Agonists ◽  
Acetoxymethyl Ester ◽  
Maximum Increase ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Agonist ◽  
Proximal Tubular ◽  
Adrenoceptor Agonists ◽  
Stimulation Of

Rat proximal tubular segments were used to examine alpha-adrenoceptor alterations in Na+-H+ exchange by monitoring intracellular pH (pHi) and mitochondrial matrix pH (pHm). To obtain pHi, tubules were incubated with the cell-permeant fluorescent probe, 2',7'-bis(2-carboxyethyl)-5(6) carboxyfluorescein acetoxymethyl ester in a HCO3--free Na+ buffer. The intracellular distribution of the weak acid [2-14C] 5,5-dimethyloxazolidine-2,4-dione was used to calculate pHm, using values of medium pH, pHi, cell volume, and matrix content. Several selective alpha 1- and alpha 2-adrenoceptor agonists and the endogenous mixed agonist, norepinephrine, all produced dose-related increases in pHi. With each of the agonists tested, a maximum increase in pHi was observed at 1 microM final concentrations, with peak effects occurring in less than 1 min. Pretreatment with ethylisopropyl amiloride (EIPA, 10 microM), a specific inhibitor of proximal Na+-H+ exchange, blocked receptor-stimulated increases in pHi, as well as stimulation of Na+-H+ exchange by phorbol ester (PMA, 0.1 microM). Similarly, selective alpha 1- (prazosin, 0.1 microM) and alpha 2-(idazoxan, 0.1 microM) adrenoceptor antagonists inhibited alterations in agonist-induced pHi changes, whereas PMA-stimulated increases in pHi remained unaffected. Neither alpha 1- nor alpha 2-adrenoceptor agonists produced differences in pHm. Adrenoceptor agonist-induced pHi changes were also assessed at various concentrations of external Na+ (0-135 mM). It was observed that 0 and 10 mM external Na+ concentrations significantly reduced alpha 1- and alpha 2-adrenoceptor-stimulated pHi changes; Km values for the alpha 1-agonist phenylephrine and the alpha 2-agonist B-HT 933 were 18.0 +/- 2.1 and 22.7 +/- 2.6, respectively. In summary, stimulation by alpha-adrenergic agonists may be blocked at the receptor level with specific alpha-antagonists or at the exchanger with EIPA. The increase in cellular pH induced by these agonists is sensitive to external Na+ and reflects alpha-adrenoceptor activation of the Na+-H+ exchanger.

scholarly journals Adrenal and sympathetic catecholamines in exercising rats

1989 ◽  
Vol 256 (1) ◽  
pp. R155-R160 ◽  
Author(s):  
A. J. Scheurink ◽  
A. B. Steffens ◽  
H. Bouritius ◽  
G. H. Dreteler ◽  
R. Bruntink ◽  
...  
Keyword(s):  
Marked Reduction ◽  
Plasma Epinephrine ◽  
Blood Samples ◽  
Adrenoceptor Antagonist ◽  
Selective Agonist ◽  
Adrenoceptor Agonists ◽  
Sympathetic Nervous ◽  
Beta 2 ◽  
Exercise Induced ◽  
Intact Rats

The effects of adrenodemedullation and/or adrenoceptor agonists and antagonists on plasma epinephrine (E) and norepinephrine (NE) concentrations during exercise were investigated in rats. Exercise consisted of strenuous swimming against a countercurrent for 15 min in a pool with water of 33 degrees C. Before, during, and after swimming, blood samples were taken through a permanent heart catheter. E was not detectable in plasma of adrenodemedullated (Adm) rats. A marked reduction in the normal exercise-induced increase in plasma NE concentrations occurred in both Adm rats as well as in intact rats injected with the beta 2-selective adrenoceptor antagonist ICI 118551. Intravenous infusion of either E or the beta 2-selective agonist fenoterol restored the increase in plasma NE in Adm rats. Injection of the alpha 2-selective antagonist yohimbine in combination with infusion of the beta 2-selective agonist fenoterol into Adm rats caused an enormous increase in plasma NE. It is concluded that all NE in plasma as released during exercise originates from the peripheral nerve endings of the sympathetic nervous system. Adrenal E influences the release of NE via activation of presynaptic beta 2-adrenoceptors.

Central catecholaminergic neurons are involved in expression of the 10-Hz rhythm in SND

1996 ◽  
Vol 270 (2) ◽  
pp. R333-R341 ◽  
Author(s):  
H. S. Orer ◽  
S. Zhong ◽  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Intravenous Administration ◽  
Sympathetic Nerve ◽  
Ventrolateral Medulla ◽  
Imidazoline Receptors ◽  
Catecholaminergic Neurons ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Nerve Discharge ◽  
Lower Frequencies

We studied the effects of adrenoceptor agonists and antagonists on sympathetic nerve discharge (SND) of urethan-anesthetized, baroreceptor-denervated cats. In cats in which a 10-Hz rhythm coexisted with irregular 2- to 6-Hz oscillations in SND, intravenous clonidine, an alpha 2-adrenoceptor agonist, blocked the 10-Hz rhythm without affecting power at lower frequencies. In contrast, power at frequencies < or = 6 Hz was depressed by clonidine in cats in which the 10-Hz rhythm was absent. These effects were reversed by intravenous administration of alpha 2-adrenoceptor antagonists, idazoxan and rauwolscine. Rauwolscine is devoid of affinity for imidazoline receptors. Furthermore, in cats untreated with clonidine, idazoxan and rauwolscine enhanced or induced the 10-Hz rhythm without affecting power at lower frequencies. Prazosin, an alpha 1-adrenoceptor antagonist, selectively blocked the 10-Hz rhythm in SND. Finally, the 10-Hz rhythm in SND was blocked by microinjection of clonidine into the rostral or caudal ventrolateral medulla. The results support the view that central catecholaminergic neurons play a role in expression of the 10-Hz rhythm in SND.

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