The influence of dorsomedial hypothalamic nucleus on contralateral paraventricular nucleus in NMDA-mediated cardiovascular responses

2003 ◽  
Vol 968 (2) ◽  
pp. 219-226 ◽  
Author(s):  
M.Zafer Gören ◽  
H.Raci Yananlı ◽  
Kemal Berkman ◽  
Filiz Onat ◽  
Rezzan Aker
2018 ◽  
Vol 74 (2) ◽  
pp. 325-334
Author(s):  
M. V. López-González ◽  
A. Díaz-Casares ◽  
M. González-García ◽  
C. A. Peinado-Aragonés ◽  
M. A. Barbancho ◽  
...  

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Eric Murillo-Rodríguez ◽  
Diana Millán-Aldaco ◽  
Gloria Arankowsky-Sandoval ◽  
Tetsuya Yamamoto ◽  
Roger G. Pertwee ◽  
...  

Abstract Background Cannabidiol (CBD), the non-psychotropic compound from Cannabis sativa, shows positive results on controlling several health disturbances; however, comparable data regarding additional chemical from C. sativa, such as cannabidiolic acid (CBDA), is scarce due to its instability. To address this limitation, a stable CBDA analogue, CBDA methyl ester (HU-580), was synthetized and showed CBDA-like effects. Recently, we described that HU-580 increased wakefulness and wake-related neurochemicals. Objective To extend the comprehension of HU-580´s properties on waking, the c-Fos and NeuN expression in a wake-linked brain area, the hypothalamus was evaluated. Methods c-Fos and NeuN expression in hypothalamic sections were analyzed after the injections of HU-580 (0.1 or 100 μg/kg, i.p.). Results Systemic administrations of HU-580 increased c-Fos and neuronal nuclei (NeuN) expression in hypothalamic nuclei, including the dorsomedial hypothalamic nucleus dorsal part, dorsomedial hypothalamic nucleus compact part, and dorsomedial hypothalamic nucleus ventral part. Conclusion HU-580 increased c-Fos and NeuN immunoreactivity in hypothalamus nuclei suggesting that this drug might modulate the sleep–wake cycle by engaging the hypothalamus.


2007 ◽  
Vol 22 (6) ◽  
pp. 467-478 ◽  
Author(s):  
Glenn J. Landry ◽  
Glenn R. Yamakawa ◽  
Ian C. Webb ◽  
Rhiannon J. Mear ◽  
Ralph E. Mistlberger

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yuko Maejima ◽  
Shoko Yokota ◽  
Masaru Shimizu ◽  
Shoichiro Horita ◽  
Daisuke Kobayashi ◽  
...  

Abstract Background Feeding rhythm disruption contributes to the development of obesity. The receptors of glucagon-like peptide-1 (GLP-1) are distributed in the wide regions of the brain. Among these regions, GLP-1 receptors (GLP-1R) are expressed in the dorsomedial hypothalamic nucleus (DMH) which are known to be associated with thermogenesis and circadian rhythm development. However, the physiological roles of GLP-1R expressing neurons in the DMH remain elusive. Methods To examine the physiological role of GLP-1R expressing neurons in the DMH, saporin-conjugated exenatide4 was injected into rat brain DMH to delete GLP-1R-positive neurons. Subsequently, locomotor activity, diurnal feeding pattern, amount of food intake and body weight were measured. Results This deletion of GLP-1R-positive neurons in the DMH induced hyperphagia, the disruption of diurnal feeding pattern, and obesity. The deletion of GLP-1R expressing neurons also reduced glutamic acid decarboxylase 67 and cholecystokinin A receptor mRNA levels in the DMH. Also, it reduced the c-fos expression after refeeding in the suprachiasmatic nucleus (SCN). Thirty percent of DMH neurons projecting to the SCN expressed GLP-1R. Functionally, refeeding after fasting induced c-fos expression in the SCN projecting neurons in the DMH. As for the projection to the DMH, neurons in the nucleus tractus solitarius (NTS) were found to be projecting to the DMH, with 33% of those neurons being GLP-1-positive. Refeeding induced c-fos expression in the DMH projecting neurons in the NTS. Conclusion These findings suggest that GLP-1R expressing neurons in the DMH may mediate feeding termination. In addition, this meal signal may be transmitted to SCN neurons and change the neural activities.


2011 ◽  
Vol 1393 ◽  
pp. 31-43 ◽  
Author(s):  
Fernando H.F. Alves ◽  
Carlos C. Crestani ◽  
Cristiane Busnardo ◽  
José Antunes-Rodrigues ◽  
Felipe V. Gomes ◽  
...  

1990 ◽  
Vol 259 (3) ◽  
pp. R579-R584 ◽  
Author(s):  
S. Rivest ◽  
D. Richard

The effects of a hypothalamic paraventricular nucleus (PVN) lesion on energy balance were investigated in exercise-trained rats. Male Wistar rats weighing initially 250 g were divided into four groups. Two groups of rats underwent a bilateral PVN lesion, whereas the two remaining groups were sham operated. The PVN lesions were done electrolytically. One group from each surgical treatment was exercised, while the other group was kept in sedentary conditions. Rats were exercised on a rodent motor-driven treadmill at moderate intensity, 1 h/day for 21 consecutive days. Food intake and body weight were measured each day during the study. At the end of the treatment period, rats were killed, and carcasses were analyzed for their energy content. Serum corticosterone was measured by a competitive protein-binding assay. Energy gain and energy intake were lower in exercised rats than in sedentary controls, regardless of whether they were sham or PVN lesioned. Concurrently, there was no difference in the energy gain between PVN-lesioned and sham-operated rats, despite the fact that PVN-lesioned rats ended the experiment with a larger body weight than the sham-lesioned animals. Serum corticosterone levels were lower in PVN-lesioned rats than in sham-lesioned rats. In conclusion, the present results indicate that the PVN, the hypothalamic nucleus predominantly controlling the pituitary-adrenal axis activity, is not a prominent structure in the regulation of energy balance in exercised male Wistar rats.


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