Entrainment to Light-Dark Cycles Shorter than 24 H Involves Extracellular Nitric Oxide Communication within the Suprachiasmatic Nucleus.

PLANO, SA; CHIESA, JJ; GOLOMBEK, DA

EUROPEAN JOURNAL OF NEUROSCIENCE

WILEY-BLACKWELL PUBLISHING, INC

Año: 2010 vol. 31 p. 876 - 882

0953-816X

The ability to synchronize to light-dark cycles is an essential property of the circadian clock, located in mammals within the hypothalamic suprachiasmatic nuclei (SCN). Single light pulses activate nitric oxide intracellular signaling, leading to circadian phase shifts required for synchronization. In addition, extracellular nitric oxide has a role in the SCN paracrine communication of photic phase advances. In this work, the extracellular nitrergic transmission was assessed in the steady-state synchronization to light-dark cycles of locomotor rhythms in the golden hamster (Mesocricetus auratus). Extracellular nitric oxide levels were pharmacologically reduced in vivo with the specific scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (PTIO). Hamsters were subjected to light-dark cycles different from 24 h (i.e., T cycles), composed by a single 30-min light pulse presented either every 23 h (T23 cycles), or every 25 h (T25 cycles), thus allowing synchronization by advances or delays, respectively. Acute PTIO intracerebroventricular microinjections, delivered 30 min previous to the light pulse, inhibited synchronization by phase advances to T23 cycles, but did not alter phase delays under T25 cycles. In addition, nitric oxide scavenging inhibited light-induced expression of PERIOD1 protein at circadian time 18 (i.e., the time for light-induced phase advances). These findings demonstrate the role of extracellular nitric oxide communication within the SCN in the steady-state synchronization to light-dark cycles. Our data also suggest its role in the regional phase coupling of circadian oscillators during this process.