GABA augments basal and electrically stimulated 3H-norepinephrine release in hypothalamic, preoptic area and cortical slices of female rats

1997 ◽  
Vol 31 (6) ◽  
pp. 769-780 ◽  
Author(s):  
J Fiber
1989 ◽  
Vol 257 (4) ◽  
pp. R765-R770 ◽  
Author(s):  
K. T. Nakamura ◽  
J. M. Klinkefus ◽  
F. G. Smith ◽  
T. Sato ◽  
J. E. Robillard

The role of renal nerves and norepinephrine release on renin secretion during fetal and postnatal maturation has not been studied. Experiments were performed to determine the effect of veratridine, a substance known to promote norepinephrine release from nerve terminals, on active and inactive renin secretion from renal cortical slices of fetal (134-138 days gestation; term is 145 days), newborn (4-9 days of age), and adult nonpregnant sheep. Veratridine (10-300 microM) significantly increased active renin secretion and produced a small but nonsignificant rise in inactive renin secretion in all three groups of animals (P less than 0.05). The percent rise in active renin secretion during veratridine stimulation was similar among all groups. Veratridine-stimulated (300 microM) active renin secretion was antagonized by tetrodotoxin (0.5 and 5.0 microM) and DL-propranolol (1 microM) in fetal renal cortical slices. However, neither tetrodotoxin nor propranolol completely inhibited the stimulatory effect of veratridine on active renin secretion. These results suggest that 1) norepinephrine released from nerve terminals may regulate active renin secretion early during development; 2) the effect of veratridine on active renin secretion was similar in fetal, newborn, and adult sheep; 3) veratridine had no significant effect on inactive renin secretion; and 4) active renin secretion due to depolarization of nerve terminals in fetal sheep is dependent on activation of beta-adrenoceptors as it is in adults.


Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 323-335 ◽  
Author(s):  
Bruna Kalil ◽  
Aline B. Ribeiro ◽  
Cristiane M. Leite ◽  
Ernane T. Uchôa ◽  
Ruither O. Carolino ◽  
...  

Abstract In rodents, kisspeptin neurons in the rostral periventricular area of the third ventricle (RP3V) of the preoptic area are considered to provide a major stimulatory input to the GnRH neuronal network that is responsible for triggering the preovulatory LH surge. Noradrenaline (NA) is one of the main modulators of GnRH release, and NA fibers are found in close apposition to kisspeptin neurons in the RP3V. Our objective was to interrogate the role of NA signaling in the kisspeptin control of GnRH secretion during the estradiol induced LH surge in ovariectomized rats, using prazosin, an α1-adrenergic receptor antagonist. In control rats, the estradiol-induced LH surge at 17 hours was associated with a significant increase in GnRH and kisspeptin content in the median eminence with the increase in kisspeptin preceding that of GnRH and LH. Prazosin, administered 5 and 3 hours prior to the predicted time of the LH surge truncated the LH surge and abolished the rise in GnRH and kisspeptin in the median eminence. In the preoptic area, prazosin blocked the increases in Kiss1 gene expression and kisspeptin content in association with a disruption in the expression of the clock genes, Per1 and Bmal1. Together these findings demonstrate for the first time that NA modulates kisspeptin synthesis in the RP3V through the activation of α1-adrenergic receptors prior to the initiation of the LH surge and indicate a potential role of α1-adrenergic signaling in the circadian-controlled pathway timing of the preovulatory LH surge.


1993 ◽  
Vol 71 (5-6) ◽  
pp. 414-424 ◽  
Author(s):  
C.W. Simpson ◽  
W. D. Ruwe ◽  
R. D. Myers

The neuroanatomical distribution of sites in the diencephalon and mesencephalon within which a prostaglandin (PG) of the E series elicits hyperthermia was characterized in Macaca mulatta and Macaca nemestrina. In 420 experiments undertaken in 13 animals, 225 loci were examined for their reactivity to PGE1 microinjected in a dose of 30 or 100 ng given in a volume of 1.0–1.5 μL. The regions of the brainstem for injection extended rostrally from the thermosensitive cells of the anterior hypothalamic, preoptic area (AH/POA) to the caudal border of the mesencephalon. Colonic and skin temperatures of the monkeys were measured continuously by thermistor probes. A hyperthermic response of ≥0.5 °C and a latency of ≤45 min was evoked by PGE1 within sites located primarily in the AH/POA. When PGE1 was microinjected at loci located caudal to the AH/POA, the elevation in body temperature (Tb) not only was less intense but rose at a slower rate. A higher concentration of PGE1 in these caudal regions was required to induce hyperthermia comparable with that elicited at loci within the AH/POA. In a second series of experiments either 1.0–5.0 μg 5-hydroxytryptamine (serotonin) or a concentration of 108 organisms/mL of Escherichia coli was microinjected at PGE1-reactive sites. A close anatomical concordance within the AH/POA of the animal was found in terms of the temporal characteristics and magnitude of the hyperthermia evoked by the indoleamine or lipopolysaccharide. The present results coincide with the reported neuroanatomical distribution of sites in the diencephalon and mesencephalon of other species in which PGE1 causes hyperthermia. Furthermore, these findings support the concept that the local neuronal mechanism of action of a pyrogen in the brainstem of the primate may involve phasic changes in the endogenous activity of both the serotonergic pathway and cyclo-oxygenase system in the AH/POA. In turn, their commonality of action suggests a functional similarity in their effect of shifting the set point for Tb.Key words: prostaglandin E1, hyperthermia, serotonin, Escherichia coli, anterior hypothalamus, thermoregulation, bacterial pyrogen, preoptic area, neuroanatomical localization, Macaca nemestrina, Macaca mulatta.


2015 ◽  
Vol 42 (12) ◽  
pp. 3138-3148 ◽  
Author(s):  
M. Dean Graham ◽  
James Gardner Gregory ◽  
Dema Hussain ◽  
Wayne G. Brake ◽  
James G. Pfaus

2021 ◽  
Vol 50 (2) ◽  
pp. 42-46
Author(s):  
G. O. Kerkeshko

Experiments on chronic administration of melatonin with and without chronic inhalation of toluene dosed at both maximal permissible concentration (50 mg/ml) and limited chronical range (500 mg/m3) have been carried out on female rats to discover their effects on biogenic amines system in hypothalamic structures related to gonadoliberin synthesis and secretion - preoptic area (PA) and median eminence (ME). Contents of biogenic amines in ME and especially in PA have been shown to have circadian variations with maximum in the morning in control group of rats.The chronic effect of synchronizing agent melatonin (administered dissolved in drinking water in concentration of 10 pg/m l, at night during 2 months) on neotransmitters and their circadian variations in both hypothalamic structures proved surprisingly to be much alike the effect of toluene. Both chemicals cause the disturbances of normal circadian variations o f norepinephrine, dopamine and serotonine in PA and dopamine in ME. The simultaneous administration of toluene and melatonin showed likewise no synchronizing ability of the latter under the conditions described.


2004 ◽  
Vol 26 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Shaw-Lang Yang ◽  
Yu-Yang Chen ◽  
Ya-Lun Hsieh ◽  
Su-Hwa Jin ◽  
Hseng-Kuang Hsu ◽  
...  

2021 ◽  
Vol 15 ◽  
Author(s):  
Sarah L. Reitz ◽  
Max B. Kelz

The role of the hypothalamic preoptic area (POA) in arousal state regulation has been studied since Constantin von Economo first recognized its importance in the early twentieth century. Over the intervening decades, the POA has been shown to modulate arousal in both natural (sleep and wake) as well as drug-induced (anesthetic-induced unconsciousness) states. While the POA is well known for its role in sleep promotion, populations of wake-promoting neurons within the region have also been identified. However, the complexity and molecular heterogeneity of the POA has made distinguishing these two populations difficult. Though multiple lines of evidence demonstrate that general anesthetics modulate the activity of the POA, the region’s heterogeneity has also made it challenging to determine whether the same neurons involved in sleep/wake regulation also modulate arousal in response to general anesthetics. While a number of studies show that sleep-promoting POA neurons are activated by various anesthetics, recent work suggests this is not universal to all arousal-regulating POA neurons. Technical innovations are making it increasingly possible to classify and distinguish the molecular identities of neurons involved in sleep/wake regulation as well as anesthetic-induced unconsciousness. Here, we review the current understanding of the POA’s role in arousal state regulation of both natural and drug-induced forms of unconsciousness, including its molecular organization and connectivity to other known sleep and wake promoting regions. Further insights into the molecular identities and connectivity of arousal-regulating POA neurons will be critical in fully understanding how this complex region regulates arousal states.


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