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SCNs of both WT and Lhx1 SCN-KO mice showed no apparent difference in the firing frequency, supporting the notion that Lhx1 SCN-KO has no discernible developmental defects in the SCN.
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Taken together, these data indicate that increased apoptosis and neuron loss are likely secondary to defects in SCN terminal differentiation in Six3-Cre Lhx1lox/lox SCN.
The gene expression in the SCN, however, looked normal.
VIP and VPAC2 receptor are down regulated in R6/2 animals in the SCN (Fahrenkrug et al., 2007).
In the SCN, the photic signal activates mTOR signaling and promotes the translation of VIP by repressing 4E-BP1.
They did this by stimulating or suppressing neurons in the SCN, effectively "resetting" the biological clock.
Action potentials in the SCN are necessary for normal circadian timing of behavior [4], and spontaneous action potentials in the SCN show diurnal patterning.
The abundant presence of GABAergic neurons in the SCN nicely fits with such a prominent role for GABAergic SCN efferents [66], [67].
Little SAAS immunoreactivity is evident in the SCN of both rat and mouse (Fig. 1A F).
Consistent with this earlier work, CRGs are expressed in the SCN before birth.
Neuropeptides prominently and selectively expressed in the SCN are heavily implicated in the regulation of the SCN network.
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