Postinhibitory rebound spikes are modulated by the history of membrane hyperpolarization in the SCN.

The suprachiasmatic nucleus (SCN) of the hypothalamus regulates biological circadian time thereby directly impacting numerous physiological processes. The SCN is composed almost exclusively of gamma-aminobutyric acid (GABA)ergic neurons, many of which synapse with other GABAergic cells in the SCN to exert an inhibitory influence on their postsynaptic targets for most, if not all, phases of the circadian cycle. The overwhelmingly GABAergic nature of the SCN, along with its internal connectivity properties, provide a strong model to examine how inhibitory neurotransmission generates output signals. In the present work we show that hyperpolarizations that range from 5 to 1000 ms elicit rebound spikes in 63% of all SCN neurons tested in voltage-clamp in the SCN of adult rats and hamsters. In current-clamp recordings, hyperpolarizations led to rebound spike formation in all cells; however, low-amplitude or short-duration current injections failed to consistently activate rebound spikes. Increasing the duration of hyperpolarization from 5 to 1000 ms is strongly and positively correlated with enhanced spike probability. Additionally, the magnitude of hyperpolarization exerts a strong influence on both the amplitude of the spike, as revealed by voltage-clamp recordings, and the latency to peak current obtained in either voltage- or current-clamp mode. Our results suggest that SCN neurons may use rebound spikes as one means of producing output signals from a largely interconnected network of GABAergic neurons.