The effects of leptin on REM sleep and slow wave delta in rats are reversed by food deprivation

Leptin (ob protein) is an adipose tissue derived circulating hormone that a cts at specific receptors in the hypothalamus to reduce food intake. The pr otein is also critically involved in energy balance and metabolic status. H ere the effect of leptin on sleep architecture in rats was evaluated becaus e food consumption and metabolic status are known to influence sleep. Sprag ue-Dawley rats were chronically implanted with electrodes for EEG and EMG r ecording and diurnal sleep parameters were quantified over 9-h periods foll owing leptin administration. Murine recombinant leptin (rMuLep) was adminis tered systemically to rats that either had undergone 18 h of prior food dep rivation or had received food ad libitum. In the normally fed rats, leptin significantly decreased the duration of rapid eye movement sleep (REMS) by about 30% and increased the duration of slow wave sleep (SWS) by about 13%, the latter effect reflecting enhanced power in the delta frequency band. T hese results are consistent with studies that have linked changes in metabo lic rate with effects on sleep. Leptin administration has previously been s hown to alter neuroendocrine parameters that could have mediated these chan ges in sleep architecture. Unexpectedly, prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the signif icance of the apparent coupling between sleep parameters and energy status.