Hypocretin(orexin)-producing neurons in the lateral hypothalamic area are important for sleep regulation and their damage manifests clinically as narcolepsy in humans. In animal experiments, extensive lesions of these neurons confirmed and clarified their physiological importance. Smaller, partial lesions of hypocretinergic neurons may uncover more subtle mechanisms of function of hypocretin system and may help understand more delicate processes in early stages of pathogenesis of narcolepsy. In a lesioned group of rats (N=9) bilateral injections of hypocretin-2-saporin (Hcrt2-SAP) conjugate into the lateral hypothalamic area were performed. In control, sham operated group (N=10) analogous saline injections were administered. Hcrt2-SAP injection led to partial (~30%) decrease in number of hypocretin-producing neurons compared to the control group. We first characterized sleep architecture in natural, undisturbed sleep and wake cycle and then analyzed sleep and wake behavior after six hours of sleep deprivation. The lesions did not change the normal undisturbed sleep and wake pattern. The effects of lesions manifested under increased sleep pressure after six hours of sleep deprivation, when faster increase in compensatory slow wave sleep was observed in lesioned compared to control group. Preliminary analysis of electroencephalography signals indicated a decrease in theta power in REM sleep in the lesioned group compared to controls. In summary, the experiment revealed robustness of the hypocretinergic system, with no effect of partial lesion on undisturbed sleep and wake behavior. The experiment identified that sleep deprivation may expose early manifestations of partial hypocretin cell loss, and the partial lesions may manifest in changes in theta oscillations.