Nocturnal increase in pineal melatonin production in two lemming species, Dicrostonyx hudsonius and D. groenlandicus

1990 ◽  
Vol 78 (2) ◽  
pp. 322-325 ◽  
Author(s):  
Russel J. Reiter ◽  
Juan M. Guerrero ◽  
Celsa Santana
2021 ◽  
Vol 4 (1) ◽  
pp. 99-114
Author(s):  
Janaína B Garcia ◽  
Fernanda G Do Amaral ◽  
Daniela C Buonfiglio ◽  
Rafaela FA Vendrame ◽  
Patrícia L Alves ◽  
...  

The pineal gland synthesizes melatonin exclusively at night, which gives melatonin the characteristic of a temporal synchronizer of the physiological systems. Melatonin is a regulator of insulin activities centrally and also peripherally and its synthesis is reduced in diabetes.  Since monosodium glutamate (MSG) is often used to induce the type 2 diabetic and metabolic syndrome in animal models, the purpose of this work is to evaluate the potential effects of MSG given to neonates on the pineal melatonin synthesis in different aged male and female rats. Wistar rats were subcutaneously injected with MSG (4mg/g/day) or saline solution (0.9%) from the second to eighth post-natal day. The circadian profiles both melatonin levels and AANAT activity were monitored at different ages. Body weight, naso-anal length, adipose tissues weight, GTT, ITT and serum insulin levels were also evaluated. Typical obesity with the neonatal MSG treatment was observed, indicated by a great increase in adipose depots without a concurrent increase in body weight. MSG treatment did not cause hyperglycemia or glucose intolerance, but induced insulin resistance. An increase of melatonin synthesis at ZT 15 with phase advance was observed in in some animals. The AANAT activity was positively parallel to the melatonin circadian profile. It seems that MSG causes hypothalamic obesity which may increase AANAT activity and melatonin production in pineal gland. These effects were not temporally correlated with insulin resistance and hyperinsulinemia indicating the hypothalamic lesions, particularly in arcuate nucleus induced by MSG in early age, as the principal cause of the increase in melatonin production.


2002 ◽  
Vol 282 (2) ◽  
pp. R358-R365 ◽  
Author(s):  
D. J. Kennaway ◽  
A. Voultsios ◽  
T. J. Varcoe ◽  
R. W. Moyer

There has been relatively little research conducted on pineal melatonin production in laboratory mice, in part, due to the lack of appropriate assays. We studied the pineal and plasma rhythm, response to light, adrenergic stimulation, and metabolism of melatonin in CBA mice. With the use of a sensitive and specific melatonin RIA, melatonin was detected in the pineal glands at all times of the day >21 fmol/gland in CBA mice but not in C57Bl mice. Both plasma and pineal melatonin levels peaked 2 h before dawn in a 12:12-h light-dark photoperiod (162 ± 31 pM and 1,804 ± 514 fmol/gland, respectively). A brief light pulse (200 lx/15 min), 2 h before lights on, suppressed both plasma and pineal melatonin to near basal levels within 30 min. Exposure to light pulses 4 h after lights off or 2 h before lights on resulted in delays and advances, respectively, in the early morning decline of plasma and pineal melatonin on the next cycle. Administration of the β-adrenergic agonist isoproterenol (20 mg/kg) 2 and 4 h after lights on in the morning resulted in a fivefold increase in plasma and pineal melatonin 2.5 to 3 h after the first injection. In the mouse, unlike the rat, melatonin was shown to be metabolized almost exclusively to 6-glucuronylmelatonin rather than 6-sulphatoxymelatonin. These studies have shown that the appropriate methodological tools are now available for studying melatonin rhythms in mice.


1994 ◽  
Vol 719 (1 The Aging Clo) ◽  
pp. 43-63 ◽  
Author(s):  
WILLY HUMBERT ◽  
PAUL PEVET

1988 ◽  
Vol 475 (2) ◽  
pp. 393-396 ◽  
Author(s):  
A. Gonzalez-Brito ◽  
R.J. Reiter ◽  
C. Santana ◽  
A. Menedez-Pelaez ◽  
J.M. Guerrero

1990 ◽  
Vol 119 (1) ◽  
pp. 12-14 ◽  
Author(s):  
F. Moujir ◽  
R. Bordón ◽  
C. Santana ◽  
P. Abreu ◽  
G. Hernandez ◽  
...  

1992 ◽  
Vol 263 (3) ◽  
pp. E481-E488
Author(s):  
A. K. Ho ◽  
C. L. Chik

In rat pinealocytes, amiloride can modulate adrenergic-stimulated cyclic nucleotide accumulation. In this study, the effect of amiloride on melatonin production was characterized. Addition of 5-(N,N-hexamethylene)amiloride, a potent inhibitor of the Na(+)-H+ antiport, dose dependently inhibited norepinephrine- and isoproterenol-stimulated N-acetyltransferase (NAT) activity and melatonin production. Similar inhibition was also observed when pineal melatonin synthesis was stimulated directly with forskolin or dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP), suggesting that the site of inhibition is distal to cAMP accumulation. Similarities between the inhibitory potencies of amiloride derivatives on the Na(+)-H+ antiport and pineal melatonin synthesis indicate that the observed inhibition on pineal melatonin synthesis by amilorides may be secondary to their actions on the Na(+)-H+ antiport. Further studies also indicate that the inhibitory effect of amilorides was not secondary to its cytotoxic actions and that amilorides had no direct antagonistic action on NAT activity. Our findings, therefore, suggest that, in addition to their effects on cyclic nucleotide accumulation, the Na(+)-H+ antiport also plays an important role in the cAMP-mediated melatonin synthesis in the rat pineal gland.


Melatonin ◽  
2020 ◽  
pp. 73-105
Author(s):  
Rafael Alonso ◽  
Pedro Abreu ◽  
Natalia Fajardo

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