Hypoxia and acidosis increase the secretion of catecholamines in the neonatal rat adrenal medulla: an in vitro study

2005 ◽  
Vol 289 (6) ◽  
pp. C1417-C1425 ◽  
Author(s):  
A. J. Rico ◽  
J. Prieto-Lloret ◽  
C. Gonzalez ◽  
R. Rigual
Keyword(s):  
Adrenal Medulla ◽  
In Vitro Study ◽  
Neonatal Rat ◽  
Hypercapnic Acidosis ◽  
Hypoxic Response ◽  
High K ◽  
Old Rats ◽  
The Subject ◽  
Direct Sensitivity

Hypoxia elicits catecholamine (CA) secretion from the adrenal medulla (AM) in perinatal animals by acting directly on chromaffin cells. However, whether innervation of the AM, which in the rat occurs in the second postnatal week, suppresses this direct hypoxic response is the subject of debate. Opioid peptides have been proposed as mediators of this suppression. To resolve these controversies, we have compared CA-secretory responses with high external concentrations of K+ ([K+]e) and hypoxia in the AM of neonatal (1- to 2-day-old) and juvenile (14- or 15- and 30-day-old) rats subjected to superfusion in vitro. In addition, we studied the effect of hypercapnic acidosis on the CA-secretory responses in the AM during postnatal development and the possible interaction between acidic and hypoxic stimuli. Responses to high [K+]e were comparable at all ages, but responses to hypoxia and hypercapnic acidosis were maximal in neonatal animals. Suppression of the hypoxic response in the rat AM was not mediated by opioids, because their agonists did not affect the hypoxic CA response. The association of hypercapnic acidosis and hypoxia, mimicking the episodes of asphyxia occurring during delivery, generates a more than additive secretory response in the neonatal rat AM. Our data confirm the loss of the direct sensitivity to hypoxia of the AM in the initial weeks of life and demonstrate a direct response of neonatal AM to hypercapnic acidosis. The synergistic effect of hypoxia and acidosis would explain the CA outburst crucial for adaptation to extrauterine life observed in naturally delivered mammals.

scholarly journals Effects of N-Methyl-D-Aspartate, Glutamate, and Glycine on the Dorsal Column Axons of Neonatal Rat Spinal Cord: In Vitro Study

2005 ◽  
Vol 45 (2) ◽  
pp. 73-81 ◽  
Author(s):  
Masato MATSUMOTO ◽  
Tatsuya SASAKI ◽  
Hiroyasu NAGASHIMA ◽  
Edward S. AHN ◽  
Wise YOUNG ◽  
...  
Keyword(s):  
Spinal Cord ◽  
In Vitro Study ◽  
Dorsal Column ◽  
Vitro Study ◽  
Neonatal Rat ◽  
Rat Spinal Cord

Neonatal hypoxic hyperlipidemia in the rat: effects on aldosterone and corticosterone synthesis in vitro

2000 ◽  
Vol 278 (3) ◽  
pp. R663-R668 ◽  
Author(s):  
Hershel Raff ◽  
Eric D. Bruder ◽  
Barbara M. Jankowski ◽  
Theodore L. Goodfriend
Keyword(s):  
Fatty Acids ◽  
Adrenal Glands ◽  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Neonatal Rat ◽  
Nonesterified Fatty Acids ◽  
Aldosterone Production ◽  
Old Rats ◽  
In Cells

Neonatal hypoxia increases aldosterone production and plasma lipids. Because fatty acids can inhibit aldosterone synthesis, we hypothesized that increases in plasma lipids restrain aldosteronogenesis in the hypoxic neonate. We exposed rats to 7 days of hypoxia from birth to 7 days of age (suckling) or from 28 to 35 days of age (weaned at day 21). Plasma was analyzed for lipid content, and steroidogenesis was studied in dispersed whole adrenal glands untreated and treated to wash away lipids. Hypoxia increased plasma cholesterol, triglycerides, and nonesterified fatty acids in the suckling neonatal rat only. Washing away lipids increased aldosterone production in cells from 7-day-old rats exposed to hypoxia, but not in cells from normoxic 7-day-old rats or from normoxic or hypoxic 35-day-old rats. Addition of oleic or linolenic acid to washed cells inhibited both aldosterone and corticosterone production, although cells from hypoxic 7-day-old rats were less sensitive. We conclude that hypoxia induces hyperlipidemia in the suckling neonate and that elevated nonesterified fatty acids inhibit aldosteronogenesis.

Extracellular K+ Induces Locomotor-Like Patterns in the Rat Spinal Cord In Vitro: Comparison With NMDA or 5-HT Induced Activity

1998 ◽  
Vol 79 (5) ◽  
pp. 2643-2652 ◽  
Author(s):  
E. Bracci ◽  
M. Beato ◽  
A. Nistri
Keyword(s):  
Spinal Cord ◽  
Threshold Concentration ◽  
Pattern Generation ◽  
Neonatal Rat ◽  
Rat Spinal Cord ◽  
Motor Patterns ◽  
Pattern Frequency ◽  
High K ◽  
In Vitro Comparison

Bracci, E., M. Beato, and A. Nistri. Extracellular K+ induces locomotor-like patterns in the rat spinal cord in vitro: comparison with NMDA or 5-HT induced activity. J. Neurophysiol. 79: 2643–2652, 1998. Bath-application of increasing concentrations of extracellular K+ elicited alternating motor patterns recorded from pairs of various lumbar ventral roots of the neonatal rat (0–2 days old) spinal cord in vitro. The threshold concentration of K+ for this effect was 7.9 ± 0.8 mM (mean ± SD). The suprathreshold concentration range useful to evoke persistent motor patterns (lasting ≥10 min) was very narrow (∼1 mM) as further increments elicited only rhythmic activity lasting from 20 s to a few minutes. On average, the fastest period of rhythmic patterns was 1.1 ± 0.3 s. Intracellular recording from lumbar motoneurons showed that raised extracellular K+ elicited membrane potential oscillations with superimposed repetitive firing. In the presence of N-methyl-d-aspartate (NMDA) or non-NMDA receptor blockers [ R(−)-2-amino-phosphonovaleric acid or 6-cyano-7-nitroquinoxaline-2,3-dione, respectively] extracellular K+ increases could still induce motor patterns although the threshold concentration was raised. Serotonin (5-HT) also induced alternating motor patterns (threshold 15 ± 7 μM) that were consistently slower than those induced by high K+ or NMDA. Ritanserin (1 μM) prevented the locomotor-like activity of 5-HT but not that of high K+ provided the concentration of the latter was further increased. Subthreshold concentrations of K+ became effective in the presence of subthreshold doses of 5-HT or NMDA, indicating mutual facilitation between these substances. The fastest pattern frequency was observed by raising K+ or by adding NMDA. In the presence of 5-HT, the pattern frequency was never as fast even if NMDA (or high K+) was coapplied. Furthermore, application of 5-HT significantly slowed down the K+- or NMDA-induced rhythm, an effect strongly potentiated in the presence of ritanserin. It is suggested that the operation of the spinal locomotor network was activated by rises in extracellular K+, which presumably led to a broad increase in neuronal excitability. Whenever the efficiency of excitatory synaptic transmission was diminished (for example by glutamate receptor antagonism), a larger concentration of K+ was required to evoke locomotor-like patterns. The complex effect (comprising stimulation and inhibition) of 5-HT on alternating pattern generation appeared to result from a dual action of this substance on the spinal locomotor network.

Developmental changes in neuromuscular transmission in the rat diaphragm

1991 ◽  
Vol 71 (1) ◽  
pp. 280-286 ◽  
Author(s):  
J. D. Feldman ◽  
A. R. Bazzy ◽  
T. R. Cummins ◽  
G. G. Haddad
Keyword(s):  
Phrenic Nerve ◽  
Neuromuscular Transmission ◽  
Peak Force ◽  
Neonatal Rat ◽  
Maximum Force ◽  
Muscle Stimulation ◽  
Rat Diaphragm ◽  
Stimulus Train ◽  
Old Rats

Neuromuscular transmission was studied in diaphragms from rats of three ages, 4–7 days old, 11–12 days old, and adults with the use of an in vitro phrenic nerve-hemidiaphragm preparation. Each hemidiaphragm was stimulated via either muscle or nerve with 1-s stimulus trains at frequencies from 10 to 100 Hz. The patterns of force development obtained in response to the two routes of stimulation were compared for each group. Diaphragms from adults developed maximum force in response to stimulation of approximately 40 Hz with no significant decrease in force at higher frequencies. Within each stimulus train, once peak force was achieved, it was maintained for the remainder of the stimulus and responses to nerve and muscle stimulation were almost identical. In contrast, diaphragms from 4- to 7-day-old rats developed maximum force at approximately 20 Hz; stimulation at greater than or equal to 60 Hz induced significantly less peak force. This decrease in peak force at higher frequencies was significantly larger for nerve than for muscle stimulation. In addition, during each nerve stimulus train diaphragms from 4- to 7-day-old rats were unable to maintain peak force, which decreased at frequencies greater than 20 Hz. The decrease in force reached approximately 50% of peak at stimulation frequencies greater than or equal to 60 Hz. Diaphragms from 11- to 12-day-old rats showed intermediate responses. Based on the responses to phrenic nerve stimulation, we conclude that the neonatal rat diaphragm shows marked neuromuscular transmission failure that is not seen in the adult.(ABSTRACT TRUNCATED AT 250 WORDS)

Serotonergic inhibition of phrenic motoneuron activity: an in vitro study in neonatal rat

1997 ◽  
Vol 230 (1) ◽  
pp. 29-32 ◽  
Author(s):  
Eric Di Pasquale ◽  
Amy Lindsay ◽  
Jack Feldman ◽  
Roger Monteau ◽  
Gérard Hilaire
Keyword(s):  
In Vitro Study ◽  
Vitro Study ◽  
Neonatal Rat ◽  
Motoneuron Activity ◽  
Phrenic Motoneuron

scholarly journals Developmental changes in rat blood choline concentration

1981 ◽  
Vol 198 (3) ◽  
pp. 565-570 ◽  
Author(s):  
S H Zeisel ◽  
R J Wurtman
Keyword(s):  
High Serum ◽  
Choline Oxidase ◽  
Neonatal Rat ◽  
Betaine Aldehyde Dehydrogenase ◽  
Choline Dehydrogenase ◽  
Rat Pups ◽  
Age Related ◽  
Old Rats

1. Serum choline concentration in the newborn rat is extremely high and declines as the rat matures until adult values are attained at 20 days of age. 2. Rat milk is a rich source of choline, and rat pups denied access to milk had significantly lower serum choline concentrations than did fed littermates. We conclude that dietary intake of choline contributes to the maintenance of high serum choline concentrations in the neonatal rat. 3. In vivo, choline disappears with a half-life of 70 min. It is converted into betaine, phosphocholine and phosphatidylcholine. The rate of phosphocholine formation is identical in 3- and 10-day-old rats (3.3 mumol/h), whereas the rate of betaine formation is slower in younger animals (0.15 mumol/h at 3 days versus 0.69 mumol/h at 10 days). In vitro, choline oxidase activity [choline dehydrogenase (EC 1.1.99.1) and betaine aldehyde dehydrogenase (EC 1.2.1.8)] increased between birth and 40 days of age. The age-related acceleration in choline's conversion into betaine probably tends to diminish unesterified choline concentration in the rat.

scholarly journals Experimental and Modeling Studies of Novel Bursts Induced by Blocking Na+ Pump and Synaptic Inhibition in the Rat Spinal Cord

2002 ◽  
Vol 88 (2) ◽  
pp. 676-691 ◽  
Author(s):  
Aldo Rozzo ◽  
Laura Ballerini ◽  
Gilda Abbate ◽  
Andrea Nistri
Keyword(s):  
Spinal Cord ◽  
Time Course ◽  
Synaptic Depression ◽  
Neonatal Rat ◽  
Pump Operation ◽  
High K ◽  
Close Sequence ◽  
Activity Dependent ◽  
Dependent Processes

This study addressed some electrophysiological mechanisms enabling neonatal rat spinal networks in vitro to generate spontaneous rhythmicity. Networks, made up by excitatory connections only after block of GABAergic and glycinergic transmission, develop regular bursting (disinhibited bursts) suppressed by the Na+ pump blocker strophanthidin. Thus the Na+ pump is considered important to control bursts. This study, however, shows that, after about 1 h in strophanthidin solution, networks of the rat isolated spinal cord surprisingly resumed spontaneous bursting (“strophanthidin bursting”), which consisted of slow depolarizations with repeated oscillations. This pattern, recorded from lumbar ventral roots, was synchronous on both sides, of irregular periodicity, and lasted for ≥12 h. Assays of 86Rb+uptake by spinal tissue confirmed Na+ pump block by strophanthidin. The strophanthidin rhythm was abolished by glutamate receptor antagonists or tetrodotoxin, indicating its network origin. N-methyl-d-aspartate (NMDA), serotonin, or high K+ could not accelerate it. The size of each burst was linearly related to the length of the preceding pause. Bursts could also be generated by dorsal root electrical stimulation and possessed similar dependence on the preceding pause. Conversely, disinhibited bursts could be evoked at short intervals from the preceding one unless repeated pulses were applied in close sequence. These data suggest that rhythmicity expressed by excitatory spinal networks could be controlled by Na+ pump activity or slow synaptic depression. A model based on the differential time course of pump operation and synaptic depression could simulate disinhibited and strophanthidin bursting, indicating two fundamental, activity-dependent processes for regulating network discharge.

In vitro study of antral gastrin biosynthesis in response to weaning and corticosterone acetate in rats

1986 ◽  
Vol 111 (4) ◽  
pp. 539-545 ◽  
Author(s):  
Hiroyasu Okahata ◽  
Yoshikazu Nishi ◽  
Kotaro Muraki ◽  
Koji Sumii ◽  
Ko Tanaka ◽  
...  
Keyword(s):  
Single Dose ◽  
Breast Milk ◽  
Gel Filtration ◽  
In Vitro Study ◽  
Physiological Saline ◽  
Solid Food ◽  
Adult Level ◽  
Old Rats ◽  
Corticosterone Treatment

Abstract. The effects of weaning (abrupt dietary changes from breast milk to solid food) and corticosterone injection on antral gastrin-like immunoreactivity (G-LI) concentrations and antral G-LI biosynthesis were studied in rats. A single dose of corticosterone acetate was injected in one group of 7 day old rats, and a single dose of physiological saline was injected in another. Each group of rats was divided into two subgroups, one fed only rat breast milk until 25 days old and the other weaned at day 21. In non-corticosterone treated unweaned rats, antral G-LI did not increase. In non-corticosterone treated weaned rats, antral G-LI was constant before weaning, then increased 4-fold to the adult level. In corticosterone treated unweaned rats, the antral G-LI on day 11 was twice than on day 7, and thereafter remained constant. In corticosterone treated weaned rats, antral G-LI increased after corticosterone treatment and increased again after weaning to reach the adult level at day 25. Gel filtration of pulse-chase incubated antral samples with l-[methyl-3H]methionine from unweaned rats without corticosterone administration showed Vo, fraction 19 (Fr. 19) and gastrin-34 (G34) peaks, but no gastrin-17 (G17) peak after 60 min of chase incubation, but at 120 min of chase incubation a G17 peak was present; corticosterone-treated and/or weaned (solid food alone) rat samples showed Vo, Fr. 19, G34 and G17 peaks at 30 min of pulse incubation.

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