Role of an excitatory preoptic-raphé pathway in febrile vasoconstriction of the rat's tail

2013 ◽  
Vol 305 (12) ◽  
pp. R1479-R1489 ◽  
Author(s):  
Mutsumi Tanaka ◽  
Michael J. McKinley ◽  
Robin M. McAllen
Keyword(s):  
Sympathetic Nerve Activity ◽  
Heat Dissipation ◽  
Preoptic Area ◽  
Preoptic Region ◽  
Glutamate Receptor Antagonist ◽  
Vasoconstrictor Response ◽  
Medullary Raphe ◽  
Premotor Neurons ◽  
Lateral Cerebral Ventricle

Heat dissipation from the rat's tail is reduced in response to cold and during fever. The sympathetic premotor neurons for this mechanism, located in the medullary raphé, are under tonic inhibitory control from the preoptic area. In parallel with the inhibitory pathway, an excitatory pathway from the rostromedial preoptic region (RMPO) to the medullary raphé mediates the vasoconstrictor response to cold skin. Whether this applies also to the tail vasoconstrictor response in fever is unknown. Single- or a few-unit tail sympathetic nerve activity (SNA) was recorded in urethane-anesthetized, artificially ventilated rats. Experimental fever was induced by PGE2 injected into the lateral cerebral ventricle (50 ng in 1.5 μl icv) or into the RMPO (0.2 ng in 60 nl); in both cases, there was a robust increase in tail SNA and a delayed rise in core temperature. Microinjection of glutamate receptor antagonist kynurenate (50 mM, 120 nl) into the medullary raphé completely reversed the tail SNA response to intracerebroventricular or RMPO PGE2 injection. Inhibiting RMPO neurons by microinjecting glycine (0.5 M, 60 nl) or the GABAA receptor agonist, muscimol (2 mM, 30–60 nl), reduced the tail SNA response to PGE2 injected into the same site by approximately half. Vehicle injections into the medullary raphé or RMPO were without effect. These results suggest that the tail vasoconstrictor response during experimental fever depends on a glutamatergic excitatory synaptic relay in the medullary raphé and that an excitatory output signal from the RMPO contributes to the tail vasoconstrictor response during fever.

Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever

1998 ◽  
Vol 274 (3) ◽  
pp. R783-R789 ◽  
Author(s):  
Thomas E. Scammell ◽  
John D. Griffin ◽  
Joel K. Elmquist ◽  
Clifford B. Saper
Keyword(s):  
Cerebrospinal Fluid ◽  
Body Temperature ◽  
Preoptic Area ◽  
Prostaglandin Synthesis ◽  
Cyclooxygenase Inhibitor ◽  
Preoptic Region ◽  
Considerable Evidence ◽  
Artificial Cerebrospinal Fluid ◽  
Intravenous Ketorolac

Considerable evidence supports the role of prostaglandins in fever production, but the neuroanatomic sites of prostaglandin synthesis that produce fever remain unknown. With the use of a novel microinjection technique, we injected the cyclooxygenase inhibitor ketorolac into the preoptic area (POA) to determine which preoptic regions produce the prostaglandins required for fever. Initial experiments demonstrated that intravenous ketorolac blocked the fever normally produced by lipopolysaccharide (LPS) 5 μg/kg iv. Microinjection of ketorolac into the POA had no effect on body temperature, and injection of artificial cerebrospinal fluid into the POA did not alter LPS fever. Injection of ketorolac into the anteroventral POA markedly decreased the fever produced by LPS, compared with injections into more rostral, caudal, or dorsal locations. These observations indicate that prostaglandin synthesis in the anteroventral preoptic region is necessary for the production of fever.

Role of median preoptic area in vasopressin-mediated bradycardia

1988 ◽  
Vol 254 (6) ◽  
pp. H1172-H1178 ◽  
Author(s):  
K. P. Patel ◽  
P. G. Schmid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve Activity ◽  
Preoptic Area ◽  
Local Administration ◽  
Base Line ◽  
Preoptic Nucleus ◽  
Nerve Activity ◽  
Median Preoptic Nucleus

To determine whether neural traffic through the median preoptic nucleus (MnPO) is involved in arginine vasopressin (AVP)-mediated bradycardia and sympathoinhibition, we recorded reflex decreases in heart rate (HR) and lumbar sympathetic nerve activity, in response to increases in arterial pressure induced either by intravenous phenylephrine (PE) or AVP before, during, and after local administration of lidocaine (200 nl, 2%) in the MnPO of chloralose-anesthetized rabbits. Base-line blood pressure and HR did not change in response to administration of lidocaine into the MnPO. Blockade of neural traffic (by lidocaine) in the MnPO produced an attenuation of AVP-mediated bradycardia but not the baroreflex-mediated bradycardia caused by PE. Lidocaine in the MnPO did not alter the sympathoinhibition produced with AVP. These results indicate that part of the bradycardia produced by AVP is mediated via forebrain structures such as the MnPO and is selective for bradycardia. Additionally, this response was mimicked by administration of yohimbine, an alpha 2-antagonist, into the MnPO, which suggests that noradrenergic mechanisms are involved in the baroreflex-mediated facilitation of bradycardia by AVP at the level of the MnPO.

Febrile nonresponsiveness of vagotomized animals: is it due to endotoxin translocation from the gut and tolerance?

1998 ◽  
Vol 275 (3) ◽  
pp. R933-R935 ◽  
Author(s):  
Andrej A. Romanovsky
Keyword(s):  
Cerebrospinal Fluid ◽  
Preoptic Area ◽  
Prostaglandin Synthesis ◽  
Cyclooxygenase Inhibitor ◽  
Preoptic Region ◽  
Considerable Evidence ◽  
Artificial Cerebrospinal Fluid ◽  
Endotoxin Translocation ◽  
Intravenous Ketorolac

The following is the abstract of the article discussed in the subsequent letter: Scammell, Thomas E., John D. Griffin, Joel K. Elmquist, and Clifford B. Saper. Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever. Am. J. Physiol.274 ( Regulatory Integrative Comp. Physiol. 43): R933–R935, 1998.—Considerable evidence supports the role of prostaglandins in fever production, but the neuroanatomic sites of prostaglandin synthesis that produce fever remain unknown. With the use of a novel microinjection technique, we injected the cyclooxygenase inhibitor ketorolac into the preoptic area (POA) to determine which preoptic regions produce the prostaglandins required for fever. Initial experiments demonstrated that intravenous ketorolac blocked the fever normally produced by lipopolysaccharide (LPS) 5 μg/kg iv. Microinjection of ketorolac into the POA had no effect on body temperature, and injection of artificial cerebrospinal fluid into the POA did not alter LPS fever. Injection of ketorolac into the anteroventral POA markedly decreased the fever produced by LPS, compared with injections into more rostral, caudal, or dorsal locations. These observations indicate that prostaglandin synthesis in the anteroventral preoptic region is necessary for the production of fever.

A subsidiary fever center in the medullary raphé?

2005 ◽  
Vol 289 (6) ◽  
pp. R1592-R1598 ◽  
Author(s):  
Mutsumi Tanaka ◽  
Robin M. McAllen
Keyword(s):  
Heart Rate ◽  
Body Temperature ◽  
Preoptic Area ◽  
Sympathetic Nerves ◽  
Prostaglandin E ◽  
Brown Adipose ◽  
Medullary Raphe ◽  
Premotor Neurons ◽  
Heat Conservation ◽  
Cutaneous Vasoconstriction

In fever, as in normal thermoregulation, signals from the preoptic area drive both cutaneous vasoconstriction and thermogenesis by brown adipose tissue (BAT). Both of these responses are mediated by sympathetic nerves whose premotor neurons are located in the medullary raphé. EP3 receptors, key prostaglandin E2 (PGE2) receptors responsible for fever induction, are expressed in this same medullary raphé region. To investigate whether PGE2 in the medullary raphé might contribute to the febrile response, we tested whether direct injections of PGE2 into the medullary raphé could drive sympathetic nerve activity (SNA) to BAT and cutaneous (tail) vessels in anesthetized rats. Microinjections of glutamate (50 mM, 60–180 nl) into the medullary raphé activated both tail and BAT SNA, as did cooling the trunk skin. PGE2 injections (150–500 ng in 300–1,000 nl) into the medullary raphé had no effect on tail SNA, BAT SNA, body temperature, or heart rate. By contrast, 150 ng PGE2 injected into the preoptic area caused large increases in both tail and BAT SNA (+60 ± 17 spikes/15 s and 1,591 ± 150% of control, respectively), increased body temperature (+1.8 ± 0.2°C), blood pressure (+17 ± 2 mmHg), and heart rate (+124 ± 19 beats/min). These results suggest that despite expression of EP3 receptors, neurons in the medullary raphé are unable to drive febrile responses of tail and BAT SNA independently of the preoptic area. Rather, they appear merely to transmit signals for heat production and heat conservation originating from the preoptic area.

scholarly journals Transcriptome Sequencing in the Preoptic Region of Rat Dams Reveals a Role of Androgen Receptor in the Control of Maternal Behavior

2021 ◽  
Vol 22 (4) ◽  
pp. 1517
Author(s):  
András H. Lékó ◽  
Rashmi Kumari ◽  
Fanni Dóra ◽  
Dávid Keller ◽  
Edina B. Udvari ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Maternal Behavior ◽  
Transcriptome Sequencing ◽  
Preoptic Area ◽  
Control Group ◽  
Preoptic Region ◽  
Protein Levels ◽  
Repeat Domain ◽  
High Level

(1) Background: Preoptic region of hypothalamus is responsible to control maternal behavior, which was hypothesized to be associated with gene expressional changes. (2) Methods: Transcriptome sequencing was first applied in the preoptic region of rat dams in comparison to a control group of mothers whose pups were taken away immediately after parturition and did not exhibit caring behavior 10 days later. (3) Results: Differentially expressed genes were found and validated by quantitative RT-PCR, among them NACHT and WD repeat domain containing 1 (Nwd1) is known to control androgen receptor (AR) protein levels. The distribution of Nwd1 mRNA and AR was similar in the preoptic area. Therefore, we focused on this steroid hormone receptor and found its reduced protein level in rat dams. To establish the function of AR in maternal behavior, its antagonist was administered intracerebroventricularly into mother rats and increased pup-directed behavior of the animals. (4) Conclusions: AR levels are suppressed in the preoptic area of mothers possibly mediated by altered Nwd1 expression in order to allow sustained high-level care for the pups. Thus, our study first implicated the AR in the control of maternal behaviors.

Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man

1995 ◽  
Vol 133 (6) ◽  
pp. 723-728 ◽  
Author(s):  
Ettore C degli Uberti ◽  
Maria R Ambrosio ◽  
Marta Bondanelli ◽  
Giorgio Transforini ◽  
Alberto Valentini ◽  
...  
Keyword(s):  
Heart Rate ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Heart Rate Response ◽  
Statistical Significance ◽  
Inhibitory Effect ◽  
Amino Acid Residues ◽  
Nerve Activity ◽  
Receptor Stimulation

degli Uberti EC, Ambrosio MR, Bondanelli M, Trasforini G, Valentini A, Rossi R, Margutti A, Campo M. Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man. Eur J Endocrinol 1995;133:723–8. ISSN 0804–4643 Human galanin (hGAL) is a neuropeptide with 30 amino acid residues that has been found in the peripheral and central nervous system, where it often co-exists with catecholamines. In order to clarify the possible role of hGAL in the regulation of sympathoadrenomedullary function, the effect of a 60 min infusion of hGAL (80 pmol·kg−1 · min−1) on plasma epinephrine and norepinephrine responses to insulin-induced hypoglycemia in nine healthy subjects was investigated. Human GAL administration significantly reduced both the release of basal norepinephrine and the response to insulin-induced hypoglycemia, whereas it attenuated the epinephrine response by 26%, with the hGAL-induced decrease in epinephrine release failing to achieve statistical significance. Human GAL significantly increased the heart rate in resting conditions and clearly exaggerated the heart rate response to insulin-induced hypoglycemia, whereas it had no effect on the blood pressure. We conclude that GAL receptor stimulation exerts an inhibitory effect on basal and insulin-induced hypoglycemia-stimulated release of norepinephrine. These findings provide further evidence that GAL may modulate sympathetic nerve activity in man but that it does not play an important role in the regulation of adrenal medullary function. Ettore C degli Uberti, Chair of Endocrinology, University of Ferrara, Via Savonarola 9, I-44100 Ferrara, Italy

scholarly journals A Scientometric Approach to Review the Role of the Medial Preoptic Area (MPOA) in Parental Behavior

2021 ◽  
Vol 11 (3) ◽  
pp. 393
Author(s):  
Alessandro Carollo ◽  
Jan Paolo Macapinlac Balagtas ◽  
Michelle Jin-Yee Neoh ◽  
Gianluca Esposito
Keyword(s):  
Preoptic Area ◽  
Parental Behavior ◽  
Neural Substrates ◽  
Medial Preoptic Area ◽  
Brain Network ◽  
Scientometric Analysis ◽  
Parental Behaviour ◽  
Scientific Papers ◽  
The Relationship

Research investigating the neural substrates underpinning parental behaviour has recently gained momentum. Particularly, the hypothalamic medial preoptic area (MPOA) has been identified as a crucial region for parenting. The current study conducted a scientometric analysis of publications from 1 January 1972 to 19 January 2021 using CiteSpace software to determine trends in the scientific literature exploring the relationship between MPOA and parental behaviour. In total, 677 scientific papers were analysed, producing a network of 1509 nodes and 5498 links. Four major clusters were identified: “C-Fos Expression”, “Lactating Rat”, “Medial Preoptic Area Interaction” and “Parental Behavior”. Their content suggests an initial trend in which the properties of the MPOA in response to parental behavior were studied, followed by a growing attention towards the presence of a brain network, including the reward circuits, regulating such behavior. Furthermore, while attention was initially directed uniquely to maternal behavior, it has recently been extended to the understanding of paternal behaviors as well. Finally, although the majority of the studies were conducted on rodents, recent publications broaden the implications of previous documents to human parental behavior, giving insight into the mechanisms underlying postpartum depression. Potential directions in future works were also discussed.

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