Anatomical distribution of brainstem sites where PGE1 induces hyperthermia in macaque species

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.

1978 ◽  
Vol 235 (1) ◽  
pp. R29-R34 ◽  
Author(s):  
P. R. McHugh ◽  
T. H. Moran

In seven male monkeys, Macaca mulatta, the infusion of nutrients into the stomach just prior to or 20 h before a 4-h feeding period reduced the feeding by an amount comparable to the calories infused. Pure carbohydrates, fat, protein, and mixtures were employed as infusions and given in a random fashion over a caloric range of 75-300 kcal. In a second series of experiments, monkeys were partially fasted on 1 day and in this way deprived of 75, 150, 300, or 450 kcal. On successive days, they overate to compensate for this deprivation. The smaller deprivations (75 and 150 kcal) were corrected on the first recovery day. The 300-kcal deprivation required 2 days to be corrected while the 450-kcal deficit was only partially restored. These experiments demonstrate the capacities of the monkey to respond with precision to caloric supply and deprivation so as to maintain a constant caloric intake.


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.


Vision ◽  
2019 ◽  
Vol 3 (3) ◽  
pp. 40 ◽  
Author(s):  
Alfred Lim ◽  
Vivian Eng ◽  
Caitlyn Osborne ◽  
Steve M. J. Janssen ◽  
Jason Satel

Inhibition of return is characterized by delayed responses to previously attended locations when the cue-target onset asynchrony (CTOA) is long enough. However, when cues are predictive of a target’s location, faster reaction times to cued as compared to uncued targets are normally observed. In this series of experiments investigating saccadic reaction times, we manipulated the cue predictability to 25% (counterpredictive), 50% (nonpredictive), and 75% (predictive) to investigate the interaction between predictive endogenous facilitatory (FCEs) and inhibitory cueing effects (ICEs). Overall, larger ICEs were seen in the counterpredictive condition than in the nonpredictive condition, and no ICE was found in the predictive condition. Based on the hypothesized additivity of FCEs and ICEs, we reasoned that the null ICEs observed in the predictive condition are the result of two opposing mechanisms balancing each other out, and the large ICEs observed with counterpredictive cueing can be attributed to the combination of endogenous facilitation at uncued locations with inhibition at cued locations. Our findings suggest that the endogenous activity contributed by cue predictability can reduce the overall inhibition observed when the mechanisms occur at the same location, or enhance behavioral inhibition when the mechanisms occur at opposite locations.


2019 ◽  
Vol 36 ◽  
Author(s):  
William H. Ridder ◽  
Kai Ming Zhang ◽  
Apoorva Karsolia ◽  
Michael Engles ◽  
James Burke

AbstractContrast sensitivity functions reveal information about a subject’s overall visual ability and have been investigated in several species of nonhuman primates (NHPs) with experimentally induced amblyopia and glaucoma. However, there are no published studies comparing contrast sensitivity functions across these species of normal NHPs. The purpose of this investigation was to compare contrast sensitivity across these primates to determine whether they are similar. Ten normal humans and eight normal NHPs (Macaca fascicularis) took part in this project. Previously published data from Macaca mulatta and Macaca nemestrina were also compared. Threshold was operationally defined as two misses in a row for a descending method of limits. A similar paradigm was used for the humans except that the descending method of limits was combined with a spatial, two-alternative forced choice (2-AFC) technique. The contrast sensitivity functions were fit with a double exponential function. The averaged peak contrast sensitivity, peak spatial frequency, acuity, and area under the curve for the humans were 268.9, 3.40 cpd, 27.3 cpd, and 2345.4 and for the Macaca fascicularis were 99.2, 3.93 cpd, 26.1 cpd, and 980.9. A two-sample t-test indicated that the peak contrast sensitivities (P = 0.001) and areas under the curve (P = 0.010) were significantly different. The peak spatial frequencies (P = 0.150) and the extrapolated visual acuities (P = 0.763) were not different. The contrast sensitivities for the Macaca fascicularis, Macaca mulatta, and Macaca nemestrina were qualitatively and quantitatively similar. The contrast sensitivity functions for the NHPs had lower peak contrast sensitivities and areas under the curve than the humans. Even though different methods have been used to measure contrast sensitivity in different species of NHP, the functions are similar. The contrast sensitivity differences and similarities between humans and NHPs need to be considered when using NHPs to study human disease.


1990 ◽  
Vol 258 (1) ◽  
pp. E163-E171 ◽  
Author(s):  
G. Katsuura ◽  
A. Arimura ◽  
K. Koves ◽  
P. E. Gottschall

Intravenous administration of recombinant human interleukin 1 beta (IL-1 beta, 1 micrograms/100 g body wt) resulted in a marked elevation of plasma adrenocorticotropic hormone (ACTH) levels, with peak levels at 10 min, in conscious unrestrained rats. One week after the placement of a lesion by radiofrequency or microinjection of kainic acid in the organum vasculosum of lamina terminalis (OVLT) but not in subfornical organ, ACTH response to intravenous IL-1 beta was enhanced, whereas both radiofrequency-induced lesion and kainic acid in the preoptic area (POA) suppressed the response. Indomethacin or a prostaglandin E (PGE) antagonist microinjected into the OVLT or POA suppressed or abolished the response. On the other hand, PGE, but not PGD2, microinjected into the POA increased plasma ACTH levels. These results suggest an important role for the OVLT, which lacks blood-brain barrier, as a possible site of entry of blood-borne IL-1 beta into the brain and for the POA, which may contain the neurons required for the response. Involvement of PGE in the OVLT and POA in the ACTH response to intravenous IL-1 beta is also suggested.


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