The role of glutamate in the photic regulation of the suprachiasmatic nucleus

1996 ◽  
Vol 50 (2-3) ◽  
pp. 109-132 ◽  
Author(s):  
F EBLING
Keyword(s):  
Suprachiasmatic Nucleus

Role of nociceptin and opioid receptor like 1 on entrainment function in the rat suprachiasmatic nucleus

Neuroscience ◽  
2006 ◽  
Vol 137 (2) ◽  
pp. 537-544 ◽  
Author(s):  
T. Sugino ◽  
T. Shimazoe ◽  
M. Ikeda ◽  
S. Watanabe
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Opioid Receptor

The role of PPARβ/δ in the regulation of glutamatergic signaling in the hamster suprachiasmatic nucleus

2012 ◽  
Vol 70 (11) ◽  
pp. 2003-2014 ◽  
Author(s):  
Etienne Challet ◽  
Isabelle Denis ◽  
Violaine Rochet ◽  
Josiane Aïoun ◽  
Sylviane Gourmelen ◽  
...  
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Glutamatergic Signaling

scholarly journals Role of Intracellular Na+ in the Regulation of [Ca2+]i in the Rat Suprachiasmatic Nucleus Neurons

2019 ◽  
Vol 20 (19) ◽  
pp. 4868
Author(s):  
Ruo-Ciao Cheng ◽  
Pi-Cheng Cheng ◽  
Yi-Chi Wang ◽  
Rong-Chi Huang
Keyword(s):  
Decay Rate ◽  
Suprachiasmatic Nucleus ◽  
Cardiac Glycoside ◽  
Spontaneous Firing ◽  
Fast Decay ◽  
Slow Decay ◽  
Central Clock ◽  
Ca2 Channels ◽  
Ionophore Monensin

Transmembrane Ca2+ influx is essential to the proper functioning of the central clock in the suprachiasmatic nucleus (SCN). In the rat SCN neurons, the clearance of somatic Ca2+ following depolarization-induced Ca2+ transients involves Ca2+ extrusion via Na+/Ca2+ exchanger (NCX) and mitochondrial Ca2+ buffering. Here we show an important role of intracellular Na+ in the regulation of [Ca2+]i in these neurons. The effect of Na+ loading on [Ca2+]i was determined with the Na+ ionophore monensin and the cardiac glycoside ouabain to block Na+/K+-ATPase (NKA). Ratiometric Na+ and Ca2+ imaging was used to measure the change in [Na+]i and [Ca2+]i, and cell-attached recordings to investigate the effects of monensin and ouabain on spontaneous firing. Our results show that in spite of opposite effects on spontaneous firing and basal [Ca2+], both monensin and ouabain induced Na+ loading, and increased the peak amplitude, slowed the fast decay rate, and enhanced the slow decay phase of 20 mM K+-evoked Ca2+ transients. Furthermore, both ouabain and monensin preferentially enhanced nimodipine-insensitive Ca2+ transients. Together, our results indicate that in the SCN neurons the NKA plays an important role in regulating [Ca2+]i, in particular, associated with nimodipine-insensitive Ca2+ channels.

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