Cells and Circuits of the Suprachiasmatic Nucleus
| Rae Silver |
Columbia University , USA
|
Suprachiasmatic Nucleus (SCN) circuits are the key to its function as a daily and seasonal brain clock. In general, the cellular components of neural circuits require a large number of fast, durable, robust and stable connections. In addition, our work suggests that the emergent property of coherent rhythmicity on the time frame of a day, such as is seen in the SCN is achieved by additional circuit elements including gap junctions, oriented/directional wiring of cellular components, and incorporation of multiple oscillatory mechanisms.
Physiological evidence, elaborated in a mathematical model, indicates that “gate cells” are one component of the SCN circuit bearing a very small population of cells that lack detectable rhythmicity in clock gene expression and electrical activity. The gate cells receive direct input from the internal and external environment. One population of gate cells are small, bear extensive local dendritic arbors and axonal projections to intra and extra-SCN sites, and communicate by means of both synaptic and electrical connections. Functionally, they serve to narrow the phase dispersion of the individual cell-based SCN oscillators. Other circuit components of the SCN are constituted of more numerous, larger “oscillator” cells. Individual oscillator neurons are capable of circadian oscillation upon dissociation. In vivo however, they function in a coherent stereotypical spatially and temporally organized network. By measuring gene expression, we show that on a daily basis, SCN tissue oscillation begins at one pole of the nucleus and spreads in a time frame of hours through the entire oscillator population, and then slowly regresses. We suggest that the wiring of multiple feedback loops of component SCN circuits give rise to this activation pattern. The circuit organization of the SCN permits both robust and resilient function in the face of extreme natural and artificial environmental circumstances, and explains continued circadian function following experimental ablation of a significant proportion of SCN neuronal elements. Supported by NINDS 039719
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